Reactive Oxygen Species in Signal Transduction and its applications
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Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling Applications for Drugs Targeted to Increase ROS in Cancer Treatment
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reactive oxygen species
damage caused by reactive oxygen species
formation of ros
functions of ros
oxidation and signal transduction
Reactive oxygen species & signal transduction 2
Reactive oxygen species (ROS) are produced during normal cellular processes and can act as signaling molecules by modifying receptors and proteins involved in cell signaling pathways. However, excessive ROS production causes oxidative stress and damage to lipids, proteins and DNA. ROS signaling is involved in processes like cell proliferation, apoptosis, and inflammatory responses through receptors like cytokine receptors, receptor tyrosine kinases, and G-protein coupled receptors. While low levels of ROS function in cell signaling, high levels contribute to disease states like cancer, neurodegeneration and cardiovascular diseases.
Reactive oxygen species
1. Reactive oxygen species (ROS) are generated through normal metabolic processes and can cause cell damage. Antioxidants help prevent this damage by neutralizing free radicals.
2. The document discusses various sources of ROS like mitochondria and inflammation, examples of ROS like superoxide and hydroxyl radicals, and the cell damage they can cause.
3. It also outlines the body's natural antioxidant protection systems including enzymes like superoxide dismutase and catalase, as well as dietary and plant-derived antioxidants. When antioxidant levels are insufficient to deal with ROS, oxidative stress can lead to diseases.
REACTIVE OXYGEN SPECIES
This document summarizes reactive oxygen species (ROS) and their role in periodontal disease. It begins by defining antioxidants, free radicals, and oxidative stress. It describes the various ROS like superoxide, hydroxyl radical, nitric oxide, and peroxynitrite. It outlines the sources of free radicals including internal sources like mitochondria and external sources like smoking. It details the effects of ROS on lipids, proteins, DNA and tissues. This causes cellular injury and death. Evidence shows elevated ROS in periodontal disease tissues and its role in tissue damage by affecting gingival cells, bone, ground substance, and collagen. The document also discusses antioxidant defense systems in the body like vitamins C and E, carotenoids,
reactive oxygen species in periodontal disease
This document summarizes the role of reactive oxygen species (ROS) and antioxidants in periodontal tissue destruction. It defines key terms like free radicals, oxidative stress, and antioxidants. It describes the major ROS molecules like superoxide, hydrogen peroxide, and hydroxyl radicals. These molecules are produced endogenously through metabolic pathways and phagocytosis, and can cause tissue damage by oxidizing lipids, proteins, and DNA. This oxidative damage disrupts cellular functions and structures. The document also discusses how ROS induce transcription factors and cytokine release to promote inflammation. Maintaining the pro-oxidant/antioxidant balance is important for periodontal health.
Reactive oxygen species
This document discusses reactive oxygen species (ROS) and their role in periodontal tissue damage. It begins with an introduction to periodontal diseases and defines ROS and free radicals. It describes the various ROS like superoxide, hydrogen peroxide, hydroxyl radicals, and lists sources of free radicals. Oxidative stress is defined. Mechanisms of tissue injury caused by ROS affecting proteins, lipids, DNA are outlined. Methods to measure ROS and oxidative damage in biological samples are presented. The role of ROS in periodontal tissue damage is discussed based on Halliwell's postulates. Several studies measuring local ROS in periodontitis are summarized. The antioxidant defense system and various antioxidants like vitamin C, vitamin E, carotenoids,
Oxidative stress
in this presentation, the light is focused on discussing the Reactive oxygen species, oxidative stress, how it forms, how it affects the body and what are the diseases that correlate with oxidative stress.
nevertheless, how it can be balanced by the antioxidants and what is their role in oxidative stress.
Free Radicals
This document discusses free radicals and their role in various diseases and conditions. It covers how free radicals are involved in cancer development, aging, and other diseases like diabetes, hypertension, neurological disorders, and cataracts. It also discusses how antioxidants from foods and supplements can help reduce free radical damage and risk or progression of these conditions. The document provides details on specific antioxidants like vitamins C and E and their effects. It also summarizes recent research on uses of antioxidants in treatments.
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reactive oxygen species
damage caused by reactive oxygen species
formation of ros
functions of ros
oxidation and signal transduction
Reactive oxygen species & signal transduction 2
Reactive oxygen species (ROS) are produced during normal cellular processes and can act as signaling molecules by modifying receptors and proteins involved in cell signaling pathways. However, excessive ROS production causes oxidative stress and damage to lipids, proteins and DNA. ROS signaling is involved in processes like cell proliferation, apoptosis, and inflammatory responses through receptors like cytokine receptors, receptor tyrosine kinases, and G-protein coupled receptors. While low levels of ROS function in cell signaling, high levels contribute to disease states like cancer, neurodegeneration and cardiovascular diseases.
Reactive oxygen species
1. Reactive oxygen species (ROS) are generated through normal metabolic processes and can cause cell damage. Antioxidants help prevent this damage by neutralizing free radicals.
2. The document discusses various sources of ROS like mitochondria and inflammation, examples of ROS like superoxide and hydroxyl radicals, and the cell damage they can cause.
3. It also outlines the body's natural antioxidant protection systems including enzymes like superoxide dismutase and catalase, as well as dietary and plant-derived antioxidants. When antioxidant levels are insufficient to deal with ROS, oxidative stress can lead to diseases.
REACTIVE OXYGEN SPECIES
This document summarizes reactive oxygen species (ROS) and their role in periodontal disease. It begins by defining antioxidants, free radicals, and oxidative stress. It describes the various ROS like superoxide, hydroxyl radical, nitric oxide, and peroxynitrite. It outlines the sources of free radicals including internal sources like mitochondria and external sources like smoking. It details the effects of ROS on lipids, proteins, DNA and tissues. This causes cellular injury and death. Evidence shows elevated ROS in periodontal disease tissues and its role in tissue damage by affecting gingival cells, bone, ground substance, and collagen. The document also discusses antioxidant defense systems in the body like vitamins C and E, carotenoids,
reactive oxygen species in periodontal disease
This document summarizes the role of reactive oxygen species (ROS) and antioxidants in periodontal tissue destruction. It defines key terms like free radicals, oxidative stress, and antioxidants. It describes the major ROS molecules like superoxide, hydrogen peroxide, and hydroxyl radicals. These molecules are produced endogenously through metabolic pathways and phagocytosis, and can cause tissue damage by oxidizing lipids, proteins, and DNA. This oxidative damage disrupts cellular functions and structures. The document also discusses how ROS induce transcription factors and cytokine release to promote inflammation. Maintaining the pro-oxidant/antioxidant balance is important for periodontal health.
Reactive oxygen species
This document discusses reactive oxygen species (ROS) and their role in periodontal tissue damage. It begins with an introduction to periodontal diseases and defines ROS and free radicals. It describes the various ROS like superoxide, hydrogen peroxide, hydroxyl radicals, and lists sources of free radicals. Oxidative stress is defined. Mechanisms of tissue injury caused by ROS affecting proteins, lipids, DNA are outlined. Methods to measure ROS and oxidative damage in biological samples are presented. The role of ROS in periodontal tissue damage is discussed based on Halliwell's postulates. Several studies measuring local ROS in periodontitis are summarized. The antioxidant defense system and various antioxidants like vitamin C, vitamin E, carotenoids,
Oxidative stress
in this presentation, the light is focused on discussing the Reactive oxygen species, oxidative stress, how it forms, how it affects the body and what are the diseases that correlate with oxidative stress.
nevertheless, how it can be balanced by the antioxidants and what is their role in oxidative stress.
Free Radicals
This document discusses free radicals and their role in various diseases and conditions. It covers how free radicals are involved in cancer development, aging, and other diseases like diabetes, hypertension, neurological disorders, and cataracts. It also discusses how antioxidants from foods and supplements can help reduce free radical damage and risk or progression of these conditions. The document provides details on specific antioxidants like vitamins C and E and their effects. It also summarizes recent research on uses of antioxidants in treatments.
Mechanisim and generation of free radicals
Free radicals are highly reactive molecules that are produced through normal cell metabolism and environmental exposures. They can damage cells by reacting with lipids, proteins, and DNA if produced in excess. The body has antioxidant defenses like enzymes and nutrients that neutralize free radicals. However, oxidative stress occurs when there is an imbalance between free radical production and antioxidant defenses, leading to chronic diseases. While free radicals play beneficial roles in small amounts for immune function, too many can contribute to conditions like cancer, cardiovascular disease, neurological disorders, and more.
Free radicals
Free radicals are unstable molecules that can damage cells. This document discusses free radicals, how they are produced in the body, and how they damage lipids, proteins, and DNA through oxidation. It also describes biomarkers that are used to measure free radical damage, such as markers of lipid peroxidation (MDA, HNE), protein oxidation (protein carbonyls), and DNA oxidation (8-OHdG). Antioxidants in the body help neutralize free radicals and prevent oxidative damage.
Free radicals & antioxidants
Free radicals are highly reactive molecules that are produced during normal cellular processes and can cause oxidative damage. Antioxidants help prevent this damage by neutralizing free radicals. Common sources of free radicals include mitochondria, inflammation, pollution, and radiation. Free radicals can damage cells by oxidizing lipids, proteins, and DNA, and are implicated in many diseases including cancer, atherosclerosis, and neurological conditions. Antioxidants help reduce oxidative stress and may protect against disease.
Reactive oxygen species
This document discusses reactive oxygen species (ROS) and antioxidants in biology and medicine. It defines key terms and explores the origins and effects of different ROS like superoxide, nitric oxide, and hydroxyl radicals. It also examines the mechanisms of tissue damage caused by ROS and the roles of antioxidant defense systems in preventing damage. Biomarkers of oxidative stress and lipid, DNA, and protein damage are reviewed. Evidence suggests ROS contribute to periodontal tissue destruction in periodontitis through lipid peroxidation and oxidative damage.
Antioxidants (1)
This document discusses reactive oxygen species (ROS) and antioxidants. It begins by defining ROS as unstable, highly reactive molecules that contain unpaired electrons, like hydrogen peroxide. ROS can damage cells by attacking macromolecules like DNA, proteins and lipids. This oxidative stress contributes to diseases like cancer and cardiovascular disease. The document then discusses the antioxidant defense system, including both enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase, and non-enzymatic antioxidants like vitamins C and E. It classifies antioxidants and describes their mechanisms of action in scavenging free radicals and preventing oxidative damage.
Hydrogen per oxide signaling in plants
Hydrogen peroxide acts as a signaling molecule in plants. It is produced in chloroplasts, peroxisomes, mitochondria, and other cellular locations in response to stresses. At low concentrations, H2O2 regulates processes like growth, development, and environmental responses, while higher amounts cause oxidative damage. It mediates responses to abiotic and biotic stresses by modulating calcium mobilization, protein phosphorylation, and gene expression. Plants have developed antioxidant defense systems involving enzymes like SOD, CAT, POD and APX to scavenge H2O2.
Final presantation mike
This document discusses reactive oxygen species (ROS), specifically superoxide. It defines ROS as chemically reactive molecules containing oxygen that are produced naturally during cellular metabolism. Superoxide is formed as a byproduct of mitochondrial electron transport and can damage cells when overproduced. The document describes how hydroethidine fluorescence is used to selectively detect superoxide levels in mitochondria, finding increased fluorescence with antimycin stimulation. It concludes that precise superoxide detection aids understanding of its role in signaling and damage.
Free Radical injury and acute phase reactants
Free radicals are unstable molecules that can cause oxidative damage. They play both beneficial and harmful roles in the body. Antioxidants help defend against free radical damage through enzymatic and non-enzymatic mechanisms. Acute phase proteins are hepatic proteins whose levels change in response to inflammation or infection, and include positive and negative proteins like C-reactive protein and haptoglobin. Oxidative stress and free radicals are implicated in many diseases while antioxidants may help prevent disease.
Response and tolerance strategies of microorganisms to oxidative
Microorganisms have developed various response and tolerance strategies to deal with oxidative stress caused by reactive oxygen species (ROS). These strategies include antioxidant enzymes like superoxide dismutase, catalase, and peroxidase that break down ROS. Microbes also induce genes encoding these enzymes and other stress response proteins through regulatory systems like SoxRS and OxyR in E. coli. Different groups of microbes utilize strategies like glutathione, mycothiol, efflux pumps, DNA repair, and avoidance mechanisms to tolerate oxidative stress.
Reactive Oxygen Species (ROS) an Activator of Apoptosis and Autophagy
This document summarizes the role of reactive oxygen species (ROS) in activating apoptosis and autophagy in cancer cells. It discusses how ROS are generated endogenously and exogenously, and how cells have antioxidant systems to maintain homeostasis. At high concentrations, ROS can induce apoptosis through both intrinsic and extrinsic pathways by modulating proteins like caspases, Bax, and Bcl-2. ROS have also been shown to induce autophagy by activating proteins involved in autophagosome formation like ATG4, Beclin-1, and modulating signaling pathways such as AMPK/mTOR. Many chemotherapy drugs and natural compounds exert their anticancer effects at least partially through increasing ROS levels and
Defence mechanism of antioxidant in Human Body
This document summarizes the antioxidant defense mechanism in the human body. It discusses what free radicals are and their main sources, as well as the antioxidant defense system that protects the body from free radical damage. The defense system includes antioxidant compounds and enzymes that act at different levels - prevention, interception, and repair - to neutralize free radicals. Some key antioxidant compounds and their roles are also described.
Oxidative stress 2013
Oxidative stress occurs when there is an imbalance between reactive oxygen species and antioxidants in cells. Reactive oxygen species are produced naturally in cells as byproducts, but can also be generated by external sources. Under normal conditions, cells balance ROS production with antioxidant defenses, but oxidative stress results from excess ROS or antioxidant depletion. This leads to oxidative damage of lipids, proteins and DNA. Cells defend against oxidative stress through antioxidant enzymes and pathways that upregulate antioxidant gene expression in response to oxidative stimuli. Detection of oxidative stress involves measuring ROS, antioxidant levels, and markers of oxidative damage. Gene expression studies can examine the antioxidant response and effects on cell fate pathways like apoptosis and autophagy under oxidative conditions.
Free Radical and Antioxidant
The document discusses free radicals and antioxidants. It begins by outlining the topics to be covered, including an introduction to antioxidants, types of antioxidants, and their mechanisms of action. It then explains that free radicals are generated endogenously through metabolic processes or exposure to external factors and can cause oxidative stress if not neutralized by antioxidants. The body has enzymatic and non-enzymatic antioxidant defenses to balance free radicals. When this balance is impaired, free radicals can damage biomolecules and trigger diseases. The document further describes different types of antioxidants, their classification, and mechanisms of scavenging or preventing free radicals.
Reactive oxygen species and anti-oxidants
This document discusses reactive oxygen species (ROS) and antioxidants. It begins with a brief history of the discovery of oxygen, free radicals, and their role in biology. ROS are classified and sources both endogenous and exogenous are described. The document outlines the origins and formation of ROS, as well as their beneficial roles in physiological functions and microbial destruction. However, excessive ROS can also cause tissue damage through lipid peroxidation and DNA damage. The body's antioxidant defense systems and how ROS levels impact periodontal health are examined. The conclusion discusses measuring ROS and antioxidants.
Super Males: Antioxidants boost male fertility and sperm viability in fruit f...
Antioxidants may improve male fertility in Drosophila melanogaster. The study investigated the effects of melatonin and lipoic acid antioxidants on sperm viability, mating behavior, and offspring production. Males fed antioxidants had higher sperm viability, increased mating rates, and produced more offspring than control-fed males. The antioxidants likely protected sperm from oxidative damage induced by paraquat, demonstrating their potential to boost male fertility.
Free radicals antioxidants
This document summarizes the roles of free radicals and antioxidants in health and disease. It discusses how free radicals are produced through normal cellular processes but can also be generated from external sources like pollution. At low levels, free radicals play beneficial roles but high levels can cause oxidative stress and damage to cells. Oxidative stress contributes to the development of many chronic diseases including cancer, cardiovascular disease, neurological disorders, and rheumatoid arthritis. The body produces antioxidants to counteract oxidative stress but supplementation may also be beneficial for health maintenance.
Oxidants and antioxidants
Oxidative reactions produce free radicals that can damage cells through chain reactions. Free radicals are unstable molecules with unpaired electrons that react with other molecules to become stabilized. Both deficiency and overproduction of free radicals can harm cells, so organisms maintain antioxidant defense systems to keep free radical levels in balance. Antioxidants terminate chain reactions by removing free radicals or preventing their formation and include enzymes like superoxide dismutase as well as nutrients obtained from foods.
The Role Of Transition Metals & Reactive Oxygen Species (ROS) In Alzheimer's ...
This powerpoint discusses the role of transition metals and amyloid plaque formation in Alzheimer’s disease (AD) and how metal ion chelators may be employed as therapeutic agents for AD. It describes the disorder, how it progresses and what happens to the brain tissue.
Furthermore, within the presentation I describe a drug which chelates metals including a description about the chemical formulation of these drugs and how the drug can be preventative of AD.
Oxidative stress and periodontal disease- Dr Harshavardhan Patwal
Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by reactive oxygen species (ROS) generated, e.g. O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide).Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling. Dr Harshavardhan Patwal , Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione.The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis.
Production of reactive oxygen species is a particularly destructive aspect of oxidative* stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage.Most long-term effects are caused by damage to DNA
Oxidative stress
This document defines oxidative stress as an imbalance between reactive oxygen species and antioxidants in cells. It describes how reactive oxygen species are naturally produced through processes like oxidative phosphorylation but can also come from external sources like pollution. The document lists some common reactive oxygen and nitrogen species and endogenous and exogenous antioxidants. It explains that damage from oxidative stress can lead to diseases like atherosclerosis, cancer, and cardiovascular diseases.
Reactive Oxygen Species
During favorable conditions, the level of reactive spices in the cell is limited to what is required for normal cellular activities. They act as important components of signaling pathways. Plants control some important processes such as defense, hormonal signaling and development by using them as signaling molecules. And An equilibrium is steblished between antioxidant system and ros formation. But when plant feels an external stress like, drought,cold, salt etc. the level of reactive specease increases above the basal level a situation that we call oxidative stress. These reactive molecules during oxidative stress, they react with biomolecules like as carbohydrates, unsaturated lipids, proteins, nucleic acids. Proteins are the most abundant cellular targets of the oxidative species, more than DNA and lipids, making up 68% of the oxidized molecules in the cell. Ros reacts with proteins which results in protein modification called redox PTMs.
Free Radicals
Reactive oxygen and nitrogen species (ROS/RNS) are highly reactive molecules that can damage cells. They include radicals like superoxide and hydroxyl, as well as non-radical species like hydrogen peroxide. ROS/RNS are produced through normal cellular processes but also from external sources like radiation and pollutants. They can cause oxidative damage to lipids, proteins, and DNA if not neutralized by antioxidant defenses. This oxidative stress has been linked to many diseases due to disruption of redox signaling and control in the cell.
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Mechanisim and generation of free radicals
Free radicals are highly reactive molecules that are produced through normal cell metabolism and environmental exposures. They can damage cells by reacting with lipids, proteins, and DNA if produced in excess. The body has antioxidant defenses like enzymes and nutrients that neutralize free radicals. However, oxidative stress occurs when there is an imbalance between free radical production and antioxidant defenses, leading to chronic diseases. While free radicals play beneficial roles in small amounts for immune function, too many can contribute to conditions like cancer, cardiovascular disease, neurological disorders, and more.
Free radicals
Free radicals are unstable molecules that can damage cells. This document discusses free radicals, how they are produced in the body, and how they damage lipids, proteins, and DNA through oxidation. It also describes biomarkers that are used to measure free radical damage, such as markers of lipid peroxidation (MDA, HNE), protein oxidation (protein carbonyls), and DNA oxidation (8-OHdG). Antioxidants in the body help neutralize free radicals and prevent oxidative damage.
Free radicals & antioxidants
Free radicals are highly reactive molecules that are produced during normal cellular processes and can cause oxidative damage. Antioxidants help prevent this damage by neutralizing free radicals. Common sources of free radicals include mitochondria, inflammation, pollution, and radiation. Free radicals can damage cells by oxidizing lipids, proteins, and DNA, and are implicated in many diseases including cancer, atherosclerosis, and neurological conditions. Antioxidants help reduce oxidative stress and may protect against disease.
Reactive oxygen species
This document discusses reactive oxygen species (ROS) and antioxidants in biology and medicine. It defines key terms and explores the origins and effects of different ROS like superoxide, nitric oxide, and hydroxyl radicals. It also examines the mechanisms of tissue damage caused by ROS and the roles of antioxidant defense systems in preventing damage. Biomarkers of oxidative stress and lipid, DNA, and protein damage are reviewed. Evidence suggests ROS contribute to periodontal tissue destruction in periodontitis through lipid peroxidation and oxidative damage.
Antioxidants (1)
This document discusses reactive oxygen species (ROS) and antioxidants. It begins by defining ROS as unstable, highly reactive molecules that contain unpaired electrons, like hydrogen peroxide. ROS can damage cells by attacking macromolecules like DNA, proteins and lipids. This oxidative stress contributes to diseases like cancer and cardiovascular disease. The document then discusses the antioxidant defense system, including both enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase, and non-enzymatic antioxidants like vitamins C and E. It classifies antioxidants and describes their mechanisms of action in scavenging free radicals and preventing oxidative damage.
Hydrogen per oxide signaling in plants
Hydrogen peroxide acts as a signaling molecule in plants. It is produced in chloroplasts, peroxisomes, mitochondria, and other cellular locations in response to stresses. At low concentrations, H2O2 regulates processes like growth, development, and environmental responses, while higher amounts cause oxidative damage. It mediates responses to abiotic and biotic stresses by modulating calcium mobilization, protein phosphorylation, and gene expression. Plants have developed antioxidant defense systems involving enzymes like SOD, CAT, POD and APX to scavenge H2O2.
Final presantation mike
This document discusses reactive oxygen species (ROS), specifically superoxide. It defines ROS as chemically reactive molecules containing oxygen that are produced naturally during cellular metabolism. Superoxide is formed as a byproduct of mitochondrial electron transport and can damage cells when overproduced. The document describes how hydroethidine fluorescence is used to selectively detect superoxide levels in mitochondria, finding increased fluorescence with antimycin stimulation. It concludes that precise superoxide detection aids understanding of its role in signaling and damage.
Free Radical injury and acute phase reactants
Free radicals are unstable molecules that can cause oxidative damage. They play both beneficial and harmful roles in the body. Antioxidants help defend against free radical damage through enzymatic and non-enzymatic mechanisms. Acute phase proteins are hepatic proteins whose levels change in response to inflammation or infection, and include positive and negative proteins like C-reactive protein and haptoglobin. Oxidative stress and free radicals are implicated in many diseases while antioxidants may help prevent disease.
Response and tolerance strategies of microorganisms to oxidative
Microorganisms have developed various response and tolerance strategies to deal with oxidative stress caused by reactive oxygen species (ROS). These strategies include antioxidant enzymes like superoxide dismutase, catalase, and peroxidase that break down ROS. Microbes also induce genes encoding these enzymes and other stress response proteins through regulatory systems like SoxRS and OxyR in E. coli. Different groups of microbes utilize strategies like glutathione, mycothiol, efflux pumps, DNA repair, and avoidance mechanisms to tolerate oxidative stress.
Reactive Oxygen Species (ROS) an Activator of Apoptosis and Autophagy
This document summarizes the role of reactive oxygen species (ROS) in activating apoptosis and autophagy in cancer cells. It discusses how ROS are generated endogenously and exogenously, and how cells have antioxidant systems to maintain homeostasis. At high concentrations, ROS can induce apoptosis through both intrinsic and extrinsic pathways by modulating proteins like caspases, Bax, and Bcl-2. ROS have also been shown to induce autophagy by activating proteins involved in autophagosome formation like ATG4, Beclin-1, and modulating signaling pathways such as AMPK/mTOR. Many chemotherapy drugs and natural compounds exert their anticancer effects at least partially through increasing ROS levels and
Defence mechanism of antioxidant in Human Body
This document summarizes the antioxidant defense mechanism in the human body. It discusses what free radicals are and their main sources, as well as the antioxidant defense system that protects the body from free radical damage. The defense system includes antioxidant compounds and enzymes that act at different levels - prevention, interception, and repair - to neutralize free radicals. Some key antioxidant compounds and their roles are also described.
Oxidative stress 2013
Oxidative stress occurs when there is an imbalance between reactive oxygen species and antioxidants in cells. Reactive oxygen species are produced naturally in cells as byproducts, but can also be generated by external sources. Under normal conditions, cells balance ROS production with antioxidant defenses, but oxidative stress results from excess ROS or antioxidant depletion. This leads to oxidative damage of lipids, proteins and DNA. Cells defend against oxidative stress through antioxidant enzymes and pathways that upregulate antioxidant gene expression in response to oxidative stimuli. Detection of oxidative stress involves measuring ROS, antioxidant levels, and markers of oxidative damage. Gene expression studies can examine the antioxidant response and effects on cell fate pathways like apoptosis and autophagy under oxidative conditions.
Free Radical and Antioxidant
The document discusses free radicals and antioxidants. It begins by outlining the topics to be covered, including an introduction to antioxidants, types of antioxidants, and their mechanisms of action. It then explains that free radicals are generated endogenously through metabolic processes or exposure to external factors and can cause oxidative stress if not neutralized by antioxidants. The body has enzymatic and non-enzymatic antioxidant defenses to balance free radicals. When this balance is impaired, free radicals can damage biomolecules and trigger diseases. The document further describes different types of antioxidants, their classification, and mechanisms of scavenging or preventing free radicals.
Reactive oxygen species and anti-oxidants
This document discusses reactive oxygen species (ROS) and antioxidants. It begins with a brief history of the discovery of oxygen, free radicals, and their role in biology. ROS are classified and sources both endogenous and exogenous are described. The document outlines the origins and formation of ROS, as well as their beneficial roles in physiological functions and microbial destruction. However, excessive ROS can also cause tissue damage through lipid peroxidation and DNA damage. The body's antioxidant defense systems and how ROS levels impact periodontal health are examined. The conclusion discusses measuring ROS and antioxidants.
Super Males: Antioxidants boost male fertility and sperm viability in fruit f...
Antioxidants may improve male fertility in Drosophila melanogaster. The study investigated the effects of melatonin and lipoic acid antioxidants on sperm viability, mating behavior, and offspring production. Males fed antioxidants had higher sperm viability, increased mating rates, and produced more offspring than control-fed males. The antioxidants likely protected sperm from oxidative damage induced by paraquat, demonstrating their potential to boost male fertility.
Free radicals antioxidants
This document summarizes the roles of free radicals and antioxidants in health and disease. It discusses how free radicals are produced through normal cellular processes but can also be generated from external sources like pollution. At low levels, free radicals play beneficial roles but high levels can cause oxidative stress and damage to cells. Oxidative stress contributes to the development of many chronic diseases including cancer, cardiovascular disease, neurological disorders, and rheumatoid arthritis. The body produces antioxidants to counteract oxidative stress but supplementation may also be beneficial for health maintenance.
Oxidants and antioxidants
Oxidative reactions produce free radicals that can damage cells through chain reactions. Free radicals are unstable molecules with unpaired electrons that react with other molecules to become stabilized. Both deficiency and overproduction of free radicals can harm cells, so organisms maintain antioxidant defense systems to keep free radical levels in balance. Antioxidants terminate chain reactions by removing free radicals or preventing their formation and include enzymes like superoxide dismutase as well as nutrients obtained from foods.
The Role Of Transition Metals & Reactive Oxygen Species (ROS) In Alzheimer's ...
This powerpoint discusses the role of transition metals and amyloid plaque formation in Alzheimer’s disease (AD) and how metal ion chelators may be employed as therapeutic agents for AD. It describes the disorder, how it progresses and what happens to the brain tissue.
Furthermore, within the presentation I describe a drug which chelates metals including a description about the chemical formulation of these drugs and how the drug can be preventative of AD.
Oxidative stress and periodontal disease- Dr Harshavardhan Patwal
Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA. Oxidative stress from oxidative metabolism causes base damage, as well as strand breaks in DNA. Base damage is mostly indirect and caused by reactive oxygen species (ROS) generated, e.g. O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide).Further, some reactive oxidative species act as cellular messengers in redox signaling. Thus, oxidative stress can cause disruptions in normal mechanisms of cellular signaling. Dr Harshavardhan Patwal , Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione.The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis.
Production of reactive oxygen species is a particularly destructive aspect of oxidative* stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage.Most long-term effects are caused by damage to DNA
Oxidative stress
This document defines oxidative stress as an imbalance between reactive oxygen species and antioxidants in cells. It describes how reactive oxygen species are naturally produced through processes like oxidative phosphorylation but can also come from external sources like pollution. The document lists some common reactive oxygen and nitrogen species and endogenous and exogenous antioxidants. It explains that damage from oxidative stress can lead to diseases like atherosclerosis, cancer, and cardiovascular diseases.
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Reactive Oxygen Species
During favorable conditions, the level of reactive spices in the cell is limited to what is required for normal cellular activities. They act as important components of signaling pathways. Plants control some important processes such as defense, hormonal signaling and development by using them as signaling molecules. And An equilibrium is steblished between antioxidant system and ros formation. But when plant feels an external stress like, drought,cold, salt etc. the level of reactive specease increases above the basal level a situation that we call oxidative stress. These reactive molecules during oxidative stress, they react with biomolecules like as carbohydrates, unsaturated lipids, proteins, nucleic acids. Proteins are the most abundant cellular targets of the oxidative species, more than DNA and lipids, making up 68% of the oxidized molecules in the cell. Ros reacts with proteins which results in protein modification called redox PTMs.
Free Radicals
Reactive oxygen and nitrogen species (ROS/RNS) are highly reactive molecules that can damage cells. They include radicals like superoxide and hydroxyl, as well as non-radical species like hydrogen peroxide. ROS/RNS are produced through normal cellular processes but also from external sources like radiation and pollutants. They can cause oxidative damage to lipids, proteins, and DNA if not neutralized by antioxidant defenses. This oxidative stress has been linked to many diseases due to disruption of redox signaling and control in the cell.
Oxidative stress
The document discusses oxidative stress and reactive oxygen species (ROS). It defines ROS and lists some examples like superoxide anion radical, hydroxyl radical, and hydrogen peroxide. It describes how ROS are produced endogenously through processes like mitochondrial electron transport, and exogenously through factors like pollution, radiation, and xenobiotics. The effects of ROS include DNA damage and modulation of signal transduction pathways. It also discusses antioxidants, dividing them into antioxidant enzymes like superoxide dismutase and catalase, chain breaking antioxidants like vitamins C and E, and transition metal binding proteins.
Free radicals and reactive oxygen species
Free radicals are highly reactive molecules with unpaired electrons that persist for very short durations. They react with other molecules by donating or abstracting electrons to achieve stability. Common types of free radicals include superoxide, hydrogen peroxide, and hydroxyl radicals. Antioxidants help scavenge free radicals and delay or inhibit oxidation, with one antioxidant typically reacting with one free radical. Enzymatic antioxidants include superoxide dismutase and catalase, while nutrient antioxidants include beta-carotene and vitamin E. Reactive oxygen species are oxygen metabolites produced from one-electron reductions of oxygen that can damage DNA, proteins, and lipids, potentially leading to diseases like cancer, diabetes, and age-related illnesses.
13. free radicals and antioxidants
Free radicals are unstable molecules that can damage cells. They are formed through normal metabolic processes but also due to environmental toxins and radiation. The body has antioxidant defenses against free radicals but an excess can lead to oxidative stress and disease. Endogenous free radicals include reactive oxygen species like superoxide, hydrogen peroxide, and hydroxyl radicals produced during metabolism. Exogenous sources include tobacco smoke, drugs, radiation, and air pollution. Free radical damage accumulates with age and is linked to many age-related diseases.
Free radicals and antioxidants
The document discusses free radicals and antioxidants. It defines free radicals as unstable chemical species with unpaired electrons that can cause oxidative damage. Free radicals are produced through normal cellular processes but can also be generated by external factors like radiation. They can cause lipid peroxidation, DNA and protein oxidation leading to cell damage associated with aging and diseases. Antioxidants help neutralize free radicals and prevent oxidative stress.
Free radicals
Free radicals are atoms, molecules, or ions with unpaired electrons that make them highly reactive. They are formed through processes like homolysis and oxidation-reduction reactions. Free radical stability is determined by factors like conjugation, hybridization, and hyperconjugation which disperse and stabilize the unpaired electron. Common examples of stable radicals include molecular oxygen and organic radicals within conjugated systems.
H2O2 in physiological and pathological states
This document discusses reactive oxygen species (ROS), specifically hydrogen peroxide (H2O2), in physiological and pathological conditions related to vascular diseases. It provides background on ROS, describing them as molecules containing unpaired electrons that are either free radicals like superoxide or non-radicals like H2O2. H2O2 is produced during normal cell metabolism and can act as a signaling molecule by oxidizing proteins, but also needs to be carefully regulated to prevent oxidative damage. The document then focuses on the roles and mechanisms of H2O2 in vasoconstriction and vasodilation, explaining it can cause both effects depending on conditions through pathways like activating potassium channels or the cyclooxygenase pathway.
Immunology iii immunoglobulins
This document discusses various topics related to immunoglobulins including their structure, function, production, genetic determination, and the clonal selection theory. It describes the variable and constant regions of immunoglobulin molecules, isotype switching, and the roles of different immunoglobulin isotypes such as IgG, IgM, IgA, and IgE.
Antioxidants and Fertility in The Common Fruit Fly
Antioxidants may improve male fertility in Drosophila melanogaster. The study investigated the effects of melatonin and lipoic acid antioxidants on mating behavior, sperm viability, and fertility when males were exposed to the oxidative stress of paraquat. Males fed antioxidants had higher mating rates, sperm viability over 70%, and produced more offspring than controls fed ethanol. The results suggest antioxidants protect sperm from oxidative damage and help maintain male fertility under stress.
Stress Repair Mechanism
Based on Capillary Gate Theory and Tissue Repair Theory, this presentation will explain the recently identified “Stress Repair Mechanism” (SRM) that enables the long-anticipated Universal Theory of Medicine postulated by Hans Selye in 1954. The SRM maintains and repairs vertebrate tissues and accounts for most of the mysterious manifestations of allostasis that remain unexplained by Hypothalamic-Pituitary-Axis (HPA) hormones. SRM activity explains hemodynamic physiology, capillary hemostasis, infarction, Korotkoff sounds, blood pressure, hypertension, diabetes, allostasis, allostatic load, anesthesia, analgesia, atherosclerosis, apoptosis, malignancy, eclampsia, sepsis, Multi-System Organ Failure (MSOF), the surgical stress syndrome, the fight or flight response, and numerous other manifestations of physiology, pathology, and allostasis. SRM function comprises the autonomic nervous system, the vascular endothelium, and the dynamic enzymatic interaction of blood-borne hepatic Factors VII, VIIIC, IX and X that produces thrombin, soluble fibrin and insoluble fibrin, whose combined effects account for all SRM manifestations. The vascular endothelium is a diaphanous neuroendocrine organ that lines all blood vessels and is the sole constituent of capillary walls. It secretes tissue factor into extravascular tissues, and insulates those tissues from the hepatic enzymes, so that tissue disruption exposes tissue factor to the enzymatic interaction and activates tissue repair. The vascular endothelium also releases nitric oxide and von Willebrand Factor into blood in accord with autonomic balance to regulate the enzymatic interaction to govern tissue perfusion and organ function. Therefore, continuously fluctuating combinations of nervous stimuli that affect autonomic balance and forces that disrupt tissues determine SRM activity.
Free redical vs antioxident
1. Free radicals are unstable molecules that react quickly to gain stability by capturing electrons from other compounds, causing damage. Common types include superoxide and hydroxyl radicals.
2. Free radicals are generated as a normal product of oxygen metabolism in cells and can also come from environmental exposures like pollution, smoking, and radiation. They cause oxidative damage to biomolecules like lipids, proteins, DNA and carbohydrates.
3. This damage is implicated in diseases such as cancer, heart disease, and neurological disorders. Antioxidants help counter the damaging effects of free radicals by reacting with and neutralizing them.
Ab diversity
The document discusses the molecular basis of antibody diversity. It describes how antibodies are produced by plasma cells and recognize and bind antigens. The immunoglobulin gene families for the heavy and light chains are located on different chromosomes and contain multiple gene segments. Gene rearrangement at the DNA and RNA level brings together gene segments to generate a diverse repertoire of antibodies. Mechanisms like combinatorial joining of variable region genes, junctional flexibility, and addition of nucleotides further increase diversity, as does somatic hypermutation in response to antigens. The associations between rearranged heavy and light chains also contribute to diversity. This molecular basis has enabled applications like monoclonal antibodies.
Role of copper in our body
Copper is an essential nutrient that plays many roles in our body. The document outlines dietary reference intakes for copper, lists the top 10 foods highest in copper content, provides an example of average daily copper intake, describes clinical effects of copper deficiency, and notes factors like zinc, iron, and fructose that can affect copper absorption. Osteoporosis may be linked to subclinical deficiencies in minerals like copper as levels tend to be lower in those with osteoporosis compared to those with normal bone density.
Superoxide Dismutase (Group 13)
1. Superoxide dismutase is an enzyme that catalyzes the dismutation of superoxide into oxygen and hydrogen peroxide. There are four main types of SOD enzymes, including copper/zinc SOD, manganese SOD, iron SOD, and nickel SOD.
2. Iron SOD is found in prokaryotes like bacteria and chloroplasts. It is thought to be the most primitive form due to its presence in anaerobic bacteria. Thermophilic, mesophilic, and psychrophilic forms of iron SOD show adaptations in structure to thrive at different temperatures.
3. Multiple sequence alignment of iron SOD from different organisms shows conserved residues and regions
Copper in proteins and enzymes
The document discusses several copper-containing proteins including plastocyanin, copper amine oxidase, hemocyanin, cytochrome c oxidase, tyrosinase, and superoxide dismutase. It describes their structures, catalytic functions, and roles in electron transfer reactions and oxidation processes in photosynthesis, respiration, and melanin production. Deficiencies and disorders related to defects in these copper proteins are also mentioned.
Free radicals in human diseases and the role
Free radicals reactive oxygen species and reactive nitrogen species are generated by our body by various endogenous systems, exposure to different physiochemical conditions or pathological states. A balance between free radicals and antioxidants is necessary for proper physiological function. If free radicals overwhelm the body's ability to regulate them, a condition known as oxidative stress ensues. Free radicals thus adversely alter lipids, proteins, and DNA and trigger a number of human diseases. Free radicals are a main cause of cardiovascular diseases, cancer, aging and immune defense disorders. Foods like berries and carrot protect us against free radicals.
Role of ions in living organisms
Electrolytes are ions that conduct electricity in solution and are essential for life. They maintain proper blood pressure, circulate nutrients, rebuild tissues, and remove waste from the body. Electrolytes like sodium and potassium generate currents across cell membranes in muscles and neurons to activate them. Imbalances in electrolytes can cause muscles to become too weak or contractions too severe. Electrolytes are also crucial for cell and immune system health, bone growth, organ function, and maintaining the body's internal balance.
Hardik free radical
This seminar discusses oxygen free radicals and their scavengers. It defines free radicals as atoms or groups of atoms with unpaired electrons that are highly reactive. The body produces free radicals during normal processes like energy production, but they can also be generated by external factors like pollution and smoking. Free radicals can damage cells by stealing electrons from nearby molecules and initiating chain reactions. The body has antioxidant defenses against free radicals like superoxide dismutase, glutathione, and catalase that neutralize them. However, excessive free radical production or insufficient antioxidants can lead to oxidative stress and cell/tissue damage implicated in diseases.
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Antioxidants and Fertility in The Common Fruit Fly
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Therapeutic Implications of Targeting Energy Metabolism in Breast Cancer
PPARs are ligand activated transcription factors. PPARγ agonists have been reported as a new and potentially efficacious treatment of inflammation, diabetes, obesity, cancer, AD, and schizophrenia. Since cancer cells show dysregulation of glycolysis they are potentially manageable through changes in metabolic environment. Interestingly, several of the genes involved in maintaining the metabolic environment and the central energy generation pathway are regulated or predicted to be regulated by PPARγ. The use of synthetic PPARγ ligands as drugs and their recent withdrawal/restricted usage highlight the lack of understanding of the molecular basis of these drugs, their off-target effects, and their network. These data further underscores the complexity of nuclear receptor signalling mechanisms. This paper will discuss the function and role of PPARγ in energy metabolism and cancer biology in general and its emergence as a promising therapeutic target in breast cancer.
Horrix et al. - 2010
This research article investigates how plant ribosome-inactivating proteins (RIPs) induce cellular stress responses in human cancer cells. The researchers found that two human cancer cell lines exposed to three RIPs - ricin, riproximin and volkensin - activated the unfolded protein response (UPR), a stress response pathway in the endoplasmic reticulum. This suggests the UPR induction better explains the cellular effects of RIPs, as apoptosis was induced even when some protein translation was still occurring due to ribosomal damage. The study provides new insights into the molecular mechanisms by which RIPs exert their toxic effects on cells.
Keto reductases- In cancer drug resistance
Keto reductases (AKRs) are overexpressed in a large number of human tumors and mediate
resistance to cancer chemotherapeutics and antihormonal therapies. Existing drugs and new agents in development may surmount this resistance by acting as specific AKR isoforms or AKR
pan-inhibitors to improve clinical outcome.
Keto reductases- In cancer drug resistance
Keto reductases (AKRs) are overexpressed in a large number of human tumors and mediate
resistance to cancer chemotherapeutics and antihormonal therapies. Existing drugs and new
agents in development may surmount this resistance by acting as specific AKR isoforms or AKR
pan-inhibitors to improve clinical outcome.
Keto reductases- In cancer drug resistance
Keto reductases (AKRs) catalyze the NADPH-dependent reduction of carbonyl groups to
alcohols for conjugation reactions to proceed. They are implicated in resistance to cancer
chemotherapeutic agents either because they are directly involved in their metabolism or help
eradicate the cellular stress created by these agents (e.g., reactive oxygen species and lipid
peroxides). Furthermore, this cellular stress activates the nuclear factor-erythroid 2 p45-related
factor 2 (NRF2)-Kelch-like ECH-associated protein 1 pathway. As many human AKR genes are
upregulated by the NRF2 transcription factor, this leads to a feed-forward mechanism to enhance
drug resistance. Resistance to major classes of chemotherapeutic agents (anthracyclines,
mitomycin, cis-platin, antitubulin agents, vinca alkaloids, and cyclophosphamide) occurs by this
mechanism. Human AKRs also catalyze the synthesis of androgens and estrogens and the
elimination of progestogens and are involved in hormonal-dependent malignancies. They are
upregulated by antihormonal therapy providing a second mechanism for cancer drug resistance.
Inhibitors of the NRF2 system or pan-AKR1C inhibitors offer promise to surmount cancer drug
resistance and/or synergize the effects of existing drugs.
Oxidative stress 2014
Use RT2 Profiler PCR Arrays to profile gene expression of key
regulators and effectors of necrosis, apoptosis, and autophagy pathways in
cells treated with oxidative stress inducers vs untreated controls.
Compare expression profiles to identify differentially expressed genes that
may determine cell fate decision under oxidative stress.
PI3 kinase pathway
The PI3-Kinase pathway is a complex signaling pathway that regulates many important cellular processes like growth, translation, and apoptosis. Studies in simpler organisms helped illuminate the basic pathway but it is more complex in mammals. At its core, extracellular signals activate PI3K which catalyzes the formation of PIP3 from PIP2 to transmit signals by recruiting proteins to the membrane like AKT. AKT then phosphorylates many substrates to influence processes like cell growth, survival and metabolism. Deregulation of this pathway through mutations in genes like PI3K, PTEN and AKT is strongly implicated in cancer development.
Stress oxidative and cochlea
Says about most important free radicals and main physiologic roles of free radicals(on transduction and transcriptional gene factors), about stress oxidative , effects of stress oxidative on some common cochlear anthologies and its related processes
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This research article examines the role of proteasome activator proteins PA28α and PA28β in the development of microvascular injury in diabetic nephropathy and retinopathy. The researchers found that genetically deleting the PA28α and PA28β genes in mice protected against renal injury and retinal damage caused by diabetes. In cell and tissue samples from these mice, the expression of inflammatory proteins like osteopontin and MCP-1 were reduced under high glucose conditions. The findings suggest that diabetic hyperglycemia increases PA28 activity in vulnerable kidney and eye cells, leading to microvascular damage through altered proteasome function and increased inflammation. Targeting the PA28 pathway may help prevent complications from diabetic nephro
Tyrosine kinase ppt
This document discusses tyrosine kinases, which are enzymes that transfer phosphate groups and act as on-off switches in cellular functions. Tyrosine kinases are implicated in cancer development and progression. The document describes the structural classification, general characteristics, and mechanism of action of tyrosine kinases. It also discusses kinetic studies of tyrosine kinases like Bruton's tyrosine kinase and applications of tyrosine kinase inhibitors in cancer therapy and other diseases.
acs.jmedchem.5b00495
A team of scientists developed an optimized peptide toxin derived from ShK, a peptide from sea anemone venom, for potential treatment of autoimmune diseases. They used a systematic approach called MAPS (Multi Attribute Positional Scan) analoging to chemically synthesize 132 variants of ShK with single amino acid substitutions throughout the peptide. These variants were tested for their ability to inhibit the Kv1.3 potassium ion channel while sparing the closely related Kv1.1 channel. Two lead variants showed improved selectivity for Kv1.3 over Kv1.1. One variant was further modified with a PEG polymer to improve its pharmacokinetic properties. In primate studies, the PEGylated peptide
Na f activates map ks and induces apoptosis in odontoblast-like
The study examined the effects of sodium fluoride (NaF) on odontoblast-like MDPC-23 cells. The researchers found that NaF exposure induced apoptosis in a dose-dependent manner through several markers. NaF activated the mitogen-activated protein kinases (MAPKs) JNK and p38, and induced two peaks in ERK phosphorylation. Inhibition of JNK suppressed NaF-induced apoptosis, while inhibition of p38 and ERK had lesser effects, suggesting NaF-induced apoptosis depends primarily on JNK signaling.
Arsenic and Cancer
The document examines how long-term low-dose exposure of human urothelial cells to sodium arsenite activates the lipocalin-2 (LCN2) gene via promoter hypomethylation. It finds that the LCN2 promoter in arsenic-exposed cells is hypomethylated compared to unexposed cells, leading to increased LCN2 expression. This overexpression of LCN2 enhances cellular transformation, anti-apoptotic activity, and inflammatory responses in the arsenic-exposed cells through mechanisms involving NF-κB and increased iron and reactive oxygen species levels.
Molecular Mechanisms of Radiation Damage.
Current medical management of the Acute Radiation Syndromes (ARS) does not include immune prophylaxis based on the Antiradiation Vaccine. Existing principles for the treatment of acute radiation syndromes are based on the replacement and supportive therapy. Haemotopoietic cell transplantation is recomended as an important method of treatment of a Haemopoietic form of the ARS. Though in the different hospitals and institutions, 31 pa-tients with a haemopoietic form have previously undergone transplantation with stem cells, in all cases(100%) the transplantants were rejected. Lethality rate was 87%.(N.Daniak et al. 2005).
Conclusion: Specific antibodies – possible antagonists of Toll like receptors and can inhibit massive activation of lysosomal hydrolytic enzymes and prevent radiation toxicity after high doses of Radiation.
Os saline
Transcriptional profiling of Halobacterium sp. NRC-1 showed changes in gene expression in response to changes in salinity and temperature. Growth under high salt stress resulted in modulation of genes for ion transporters like potassium and phosphate transporters. Growth at cold temperatures altered expression of genes for lipid metabolism, gas vesicles, and cold shock proteins. Heat shock induced several chaperone genes. The study provides insights into Halobacterium's responses to environmental stresses at the gene expression level.
Tissue specificity of phenyl proponoids
The document discusses phenylpropanoids (PPs), a class of plant secondary metabolites that are produced in response to stress. PPs have antioxidant and anti-inflammatory properties. They are found in many foods and medicines. The document outlines several specific PPs (resveratrol, chlorogenic acid, caffeic acid) and their roles in protecting plants from pathogens and modulating human cell and molecular processes. PPs have potential applications as antioxidants, anticancer agents, and treatments for other diseases due to these protective properties.
Analyzing oxidative stress markers
The document analyzes oxidative stress markers by discussing topics like reactive oxygen species, oxidative stress-induced diseases, antioxidants, antioxidant responsive elements, gene expression profiles related to oxidative stress, and the nuclear factor Nrf2. It provides details on how Nrf2 regulates genes involved in the oxidative stress response and its interaction with the protein Keap1 that mediates Nrf2 degradation in the cytoplasm. The key roles of cysteine residues in Keap1 and Nrf2 in regulating the retention and release of Nrf2 are also summarized.
Mitochondrial dynamics and cancer (2)
Mitochondria are double membranous organelle, the inner membrane is more larger than the outer one. For this reason the inner membrane of the mitochondria folds inside forming a special figure called creasteae. The inner mitochondrial membrane (IMM) contains the subunits for oxidative phosphorylation (OXPHOS). And this inner mitochondrial membrane coverd by a second membrane called the outer mitochondrial membrane (OMM). We called mitochondria as a power house of cell not only they generates ATP via oxidative phosphorylation they also take part in various biochemical pathways such as- pyrimidine and purine biosynthesis, heme biosynthesis, the regulation of N2 balance in urea cycle, gluconeogenesis, keton body production and fatty acid degradation and elongation. They also take part in cell signalling via regulating the protein-protein interaction or by regulating the cellular concentration of calcium ion(Ca2+) and reactive oxygen species(ROS).
During various biological diseasesmitochondrial morphology altered, as in the case when there is lack of nutrient in our body mitochondria combine together to share their nutrient and alo their DNA and ETC components to maintain their OXPHOS. But in case of high energy demand of a part of body mitochondria undergo division or called fission because they move rapidly than lager one (Zhao et al., 2013). Fission also occur in mitotic cell to share equal amount of mitochondria to the daughter cells. Many questions arise in mitochondrial dinamics but here I am going to answer a most doubtful question- Is mitochondrial dynamics play any role in tumorigenic process? Is any oncogenic signalling play crucial role in morphological alteration of mitochondria?
International Journal of Proteomics & Bioinformatics
This document discusses proteomic methodologies for studying protein phosphorylation. It begins with an introduction to protein phosphorylation and its importance in regulating cellular processes. It then describes the workflow for analyzing phosphorylation through proteomics, including isolating phosphoproteins, identifying phosphorylation sites via mass spectrometry, and comparing normal and treated phosphoproteomes. Key methods discussed are 2D gel electrophoresis, phosphoprotein staining, silver staining, spot excision, in-gel digestion, and liquid chromatography-tandem mass spectrometry for identifying phosphorylation sites. The document emphasizes that proteomic analysis is needed to fully understand phosphorylation dynamics and signaling pathways.
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Therapeutic Implications of Targeting Energy Metabolism in Breast Cancer
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Candidate young stellar objects in the S-cluster: Kinematic analysis of a sub...
Context. The observation of several L-band emission sources in the S cluster has led to a rich discussion of their nature. However, a definitive answer to the classification of the dusty objects requires an explanation for the detection of compact Doppler-shifted Brγ emission. The ionized hydrogen in combination with the observation of mid-infrared L-band continuum emission suggests that most of these sources are embedded in a dusty envelope. These embedded sources are part of the S-cluster, and their relationship to the S-stars is still under debate. To date, the question of the origin of these two populations has been vague, although all explanations favor migration processes for the individual cluster members. Aims. This work revisits the S-cluster and its dusty members orbiting the supermassive black hole SgrA* on bound Keplerian orbits from a kinematic perspective. The aim is to explore the Keplerian parameters for patterns that might imply a nonrandom distribution of the sample. Additionally, various analytical aspects are considered to address the nature of the dusty sources. Methods. Based on the photometric analysis, we estimated the individual H−K and K−L colors for the source sample and compared the results to known cluster members. The classification revealed a noticeable contrast between the S-stars and the dusty sources. To fit the flux-density distribution, we utilized the radiative transfer code HYPERION and implemented a young stellar object Class I model. We obtained the position angle from the Keplerian fit results; additionally, we analyzed the distribution of the inclinations and the longitudes of the ascending node. Results. The colors of the dusty sources suggest a stellar nature consistent with the spectral energy distribution in the near and midinfrared domains. Furthermore, the evaporation timescales of dusty and gaseous clumps in the vicinity of SgrA* are much shorter ( 2yr) than the epochs covered by the observations (≈15yr). In addition to the strong evidence for the stellar classification of the D-sources, we also find a clear disk-like pattern following the arrangements of S-stars proposed in the literature. Furthermore, we find a global intrinsic inclination for all dusty sources of 60 ± 20◦, implying a common formation process. Conclusions. The pattern of the dusty sources manifested in the distribution of the position angles, inclinations, and longitudes of the ascending node strongly suggests two different scenarios: the main-sequence stars and the dusty stellar S-cluster sources share a common formation history or migrated with a similar formation channel in the vicinity of SgrA*. Alternatively, the gravitational influence of SgrA* in combination with a massive perturber, such as a putative intermediate mass black hole in the IRS 13 cluster, forces the dusty objects and S-stars to follow a particular orbital arrangement. Key words. stars: black holes– stars: formation– Galaxy: center– galaxies: star formation
MICROBIAL INTERACTION PPT/ MICROBIAL INTERACTION AND THEIR TYPES // PLANT MIC...
MICROBIAL INTERACTION PPT/ MICROBIAL INTERACTION AND THEIR TYPES // PLANT MIC...ABHISHEK SONI NIMT INSTITUTE OF MEDICAL AND PARAMEDCIAL SCIENCES , GOVT PG COLLEGE NOIDA
Microbial interaction
Microorganisms interacts with each other and can be physically associated with another organisms in a variety of ways.
One organism can be located on the surface of another organism as an ectobiont or located within another organism as endobiont.
Microbial interaction may be positive such as mutualism, proto-cooperation, commensalism or may be negative such as parasitism, predation or competition
Types of microbial interaction
Positive interaction: mutualism, proto-cooperation, commensalism
Negative interaction: Ammensalism (antagonism), parasitism, predation, competition
I. Mutualism:
It is defined as the relationship in which each organism in interaction gets benefits from association. It is an obligatory relationship in which mutualist and host are metabolically dependent on each other.
Mutualistic relationship is very specific where one member of association cannot be replaced by another species.
Mutualism require close physical contact between interacting organisms.
Relationship of mutualism allows organisms to exist in habitat that could not occupied by either species alone.
Mutualistic relationship between organisms allows them to act as a single organism.
Examples of mutualism:
i. Lichens:
Lichens are excellent example of mutualism.
They are the association of specific fungi and certain genus of algae. In lichen, fungal partner is called mycobiont and algal partner is called
II. Syntrophism:
It is an association in which the growth of one organism either depends on or improved by the substrate provided by another organism.
In syntrophism both organism in association gets benefits.
Compound A
Utilized by population 1
Compound B
Utilized by population 2
Compound C
utilized by both Population 1+2
Products
In this theoretical example of syntrophism, population 1 is able to utilize and metabolize compound A, forming compound B but cannot metabolize beyond compound B without co-operation of population 2. Population 2is unable to utilize compound A but it can metabolize compound B forming compound C. Then both population 1 and 2 are able to carry out metabolic reaction which leads to formation of end product that neither population could produce alone.
Examples of syntrophism:
i. Methanogenic ecosystem in sludge digester
Methane produced by methanogenic bacteria depends upon interspecies hydrogen transfer by other fermentative bacteria.
Anaerobic fermentative bacteria generate CO2 and H2 utilizing carbohydrates which is then utilized by methanogenic bacteria (Methanobacter) to produce methane.
ii. Lactobacillus arobinosus and Enterococcus faecalis:
In the minimal media, Lactobacillus arobinosus and Enterococcus faecalis are able to grow together but not alone.
The synergistic relationship between E. faecalis and L. arobinosus occurs in which E. faecalis require folic acid
Pests of Storage_Identification_Dr.UPR.pdf
InIndia-post-harvestlosses-unscientificstorage,insects,rodents,micro-organismsetc.,accountforabout10percentoftotalfoodgrains
Graininfestation
Directdamage
Indirectly
•theexuviae,skin,deadinsects
•theirexcretawhichmakefoodunfitforhumanconsumption
About600speciesofinsectshavebeenassociatedwithstoredgrainproducts
100speciesofinsectpestsofstoredproductscauseeconomiclosses
CLASS 12th CHEMISTRY SOLID STATE ppt (Animated)
Description:
Dive into the fascinating realm of solid-state physics with our meticulously crafted online PowerPoint presentation. This immersive educational resource offers a comprehensive exploration of the fundamental concepts, theories, and applications within the realm of solid-state physics.
From crystalline structures to semiconductor devices, this presentation delves into the intricate principles governing the behavior of solids, providing clear explanations and illustrative examples to enhance understanding. Whether you're a student delving into the subject for the first time or a seasoned researcher seeking to deepen your knowledge, our presentation offers valuable insights and in-depth analyses to cater to various levels of expertise.
Key topics covered include:
Crystal Structures: Unravel the mysteries of crystalline arrangements and their significance in determining material properties.
Band Theory: Explore the electronic band structure of solids and understand how it influences their conductive properties.
Semiconductor Physics: Delve into the behavior of semiconductors, including doping, carrier transport, and device applications.
Magnetic Properties: Investigate the magnetic behavior of solids, including ferromagnetism, antiferromagnetism, and ferrimagnetism.
Optical Properties: Examine the interaction of light with solids, including absorption, reflection, and transmission phenomena.
With visually engaging slides, informative content, and interactive elements, our online PowerPoint presentation serves as a valuable resource for students, educators, and enthusiasts alike, facilitating a deeper understanding of the captivating world of solid-state physics. Explore the intricacies of solid-state materials and unlock the secrets behind their remarkable properties with our comprehensive presentation.
快速办理(UAM毕业证书)马德里自治大学毕业证学位证一模一样
学校原件一模一样【微信：741003700 】《(UAM毕业证书)马德里自治大学毕业证学位证》【微信：741003700 】学位证，留信认证（真实可查，永久存档）原件一模一样纸张工艺/offer、雅思、外壳等材料/诚信可靠,可直接看成品样本，帮您解决无法毕业带来的各种难题！外壳，原版制作，诚信可靠，可直接看成品样本。行业标杆！精益求精，诚心合作，真诚制作！多年品质 ,按需精细制作，24小时接单,全套进口原装设备。十五年致力于帮助留学生解决难题，包您满意。
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Methods of grain storage Structures in India.pdf
•Post-harvestlossesaccountforabout10%oftotalfoodgrainsduetounscientificstorage,insects,rodents,micro-organismsetc.,
•Totalfoodgrainproductioninindiais311milliontonnesandstorageis145mt.InIndia,annualstoragelosseshavebeenestimated14mtworthofRs.7,000croreinwhichinsectsaloneaccountfornearlyRs.1,300crores.
•InIndiaoutofthetotalproduction,about30%ismarketablesurplus
•Remaining70%isretainedandstoredbyfarmersforconsumption,seed,feed.Hence,growerneedstoragefacilitytoholdaportionofproducetosellwhenthemarketingpriceisfavourable
•TradersandCo-operativesatmarketcentresneedstoragestructurestoholdgrainswhenthetransportfacilityisinadequate
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...
ESA/ACT Science Coffee: Diego Blas - Gravitational wave detection with orbita...Advanced-Concepts-Team
Presentation in the Science Coffee of the Advanced Concepts Team of the European Space Agency on the 07.06.2024.
Speaker: Diego Blas (IFAE/ICREA)
Title: Gravitational wave detection with orbital motion of Moon and artificial
Abstract:
In this talk I will describe some recent ideas to find gravitational waves from supermassive black holes or of primordial origin by studying their secular effect on the orbital motion of the Moon or satellites that are laser ranged.EWOCS-I: The catalog of X-ray sources in Westerlund 1 from the Extended Weste...
Context. With a mass exceeding several 104 M⊙ and a rich and dense population of massive stars, supermassive young star clusters
represent the most massive star-forming environment that is dominated by the feedback from massive stars and gravitational interactions
among stars.
Aims. In this paper we present the Extended Westerlund 1 and 2 Open Clusters Survey (EWOCS) project, which aims to investigate
the influence of the starburst environment on the formation of stars and planets, and on the evolution of both low and high mass stars.
The primary targets of this project are Westerlund 1 and 2, the closest supermassive star clusters to the Sun.
Methods. The project is based primarily on recent observations conducted with the Chandra and JWST observatories. Specifically,
the Chandra survey of Westerlund 1 consists of 36 new ACIS-I observations, nearly co-pointed, for a total exposure time of 1 Msec.
Additionally, we included 8 archival Chandra/ACIS-S observations. This paper presents the resulting catalog of X-ray sources within
and around Westerlund 1. Sources were detected by combining various existing methods, and photon extraction and source validation
were carried out using the ACIS-Extract software.
Results. The EWOCS X-ray catalog comprises 5963 validated sources out of the 9420 initially provided to ACIS-Extract, reaching a
photon flux threshold of approximately 2 × 10−8 photons cm−2
s
−1
. The X-ray sources exhibit a highly concentrated spatial distribution,
with 1075 sources located within the central 1 arcmin. We have successfully detected X-ray emissions from 126 out of the 166 known
massive stars of the cluster, and we have collected over 71 000 photons from the magnetar CXO J164710.20-455217.
The debris of the ‘last major merger’ is dynamically young
The Milky Way’s (MW) inner stellar halo contains an [Fe/H]-rich component with highly eccentric orbits, often referred to as the
‘last major merger.’ Hypotheses for the origin of this component include Gaia-Sausage/Enceladus (GSE), where the progenitor
collided with the MW proto-disc 8–11 Gyr ago, and the Virgo Radial Merger (VRM), where the progenitor collided with the
MW disc within the last 3 Gyr. These two scenarios make different predictions about observable structure in local phase space,
because the morphology of debris depends on how long it has had to phase mix. The recently identified phase-space folds in Gaia
DR3 have positive caustic velocities, making them fundamentally different than the phase-mixed chevrons found in simulations
at late times. Roughly 20 per cent of the stars in the prograde local stellar halo are associated with the observed caustics. Based
on a simple phase-mixing model, the observed number of caustics are consistent with a merger that occurred 1–2 Gyr ago.
We also compare the observed phase-space distribution to FIRE-2 Latte simulations of GSE-like mergers, using a quantitative
measurement of phase mixing (2D causticality). The observed local phase-space distribution best matches the simulated data
1–2 Gyr after collision, and certainly not later than 3 Gyr. This is further evidence that the progenitor of the ‘last major merger’
did not collide with the MW proto-disc at early times, as is thought for the GSE, but instead collided with the MW disc within
the last few Gyr, consistent with the body of work surrounding the VRM.
JAMES WEBB STUDY THE MASSIVE BLACK HOLE SEEDS
The pathway(s) to seeding the massive black holes (MBHs) that exist at the heart of galaxies in the present and distant Universe remains an unsolved problem. Here we categorise, describe and quantitatively discuss the formation pathways of both light and heavy seeds. We emphasise that the most recent computational models suggest that rather than a bimodal-like mass spectrum between light and heavy seeds with light at one end and heavy at the other that instead a continuum exists. Light seeds being more ubiquitous and the heavier seeds becoming less and less abundant due the rarer environmental conditions required for their formation. We therefore examine the different mechanisms that give rise to different seed mass spectrums. We show how and why the mechanisms that produce the heaviest seeds are also among the rarest events in the Universe and are hence extremely unlikely to be the seeds for the vast majority of the MBH population. We quantify, within the limits of the current large uncertainties in the seeding processes, the expected number densities of the seed mass spectrum. We argue that light seeds must be at least 103 to 105 times more numerous than heavy seeds to explain the MBH population as a whole. Based on our current understanding of the seed population this makes heavy seeds (Mseed > 103 M⊙) a significantly more likely pathway given that heavy seeds have an abundance pattern than is close to and likely in excess of 10−4 compared to light seeds. Finally, we examine the current state-of-the-art in numerical calculations and recent observations and plot a path forward for near-future advances in both domains.
Summary Of transcription and Translation.pdf
Hello Everyone Here We are Sharing You with The process of protien Synthesis in very short points you will be Able to understand It Very well
Farming systems analysis: what have we learnt?.pptx
Presentation given at the official farewell of Prof Ken Gillet at Wageningen on 13 June 2024
Discovery of An Apparent Red, High-Velocity Type Ia Supernova at 𝐳 = 2.9 wi...
We present the JWST discovery of SN 2023adsy, a transient object located in a host galaxy JADES-GS
+
53.13485
−
27.82088
with a host spectroscopic redshift of
2.903
±
0.007
. The transient was identified in deep James Webb Space Telescope (JWST)/NIRCam imaging from the JWST Advanced Deep Extragalactic Survey (JADES) program. Photometric and spectroscopic followup with NIRCam and NIRSpec, respectively, confirm the redshift and yield UV-NIR light-curve, NIR color, and spectroscopic information all consistent with a Type Ia classification. Despite its classification as a likely SN Ia, SN 2023adsy is both fairly red (
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(
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−
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)
∼
0.9
) despite a host galaxy with low-extinction and has a high Ca II velocity (
19
,
000
±
2
,
000
km/s) compared to the general population of SNe Ia. While these characteristics are consistent with some Ca-rich SNe Ia, particularly SN 2016hnk, SN 2023adsy is intrinsically brighter than the low-
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Ca-rich population. Although such an object is too red for any low-
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cosmological sample, we apply a fiducial standardization approach to SN 2023adsy and find that the SN 2023adsy luminosity distance measurement is in excellent agreement (
≲
1
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) with
Λ
CDM. Therefore unlike low-
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Ca-rich SNe Ia, SN 2023adsy is standardizable and gives no indication that SN Ia standardized luminosities change significantly with redshift. A larger sample of distant SNe Ia is required to determine if SN Ia population characteristics at high-
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truly diverge from their low-
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counterparts, and to confirm that standardized luminosities nevertheless remain constant with redshift.
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The debris of the ‘last major merger’ is dynamically young
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Reactive Oxygen Species in Signal Transduction and its applications
- 1. Reactive Oxygen Species in Signal Transduction and its applications Supervised by: Prof. Hesham Saeed Dr. Amira Embaby Dr. Nermine Moussa By: Mostafa Gamal Saadeldin Mohamed Alexandria University Institute of Graduate Studies and Researches
- 2. Content Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling Regulation of MAPK signaling pathways Regulation of PI3K signaling pathways Regulation of Nrf2 Applications for Drugs Targeted to Increase ROS in Cancer Treatment. Miltirone, Curcumin Longikaurin, Apigenin Brusatol
- 3. Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling by ROS Regulation of MAPK signaling pathways Regulation of Nrf2 Regulation of PI3K signaling pathways
- 4. 1-Regulation of MAPK signaling pathways by ROS 3-Response 2- Transduction 1-Reception
- 5. Transduction
- 8. 2-Inhibition of MAPK phosphatases
- 9. Activation of Apoptosis signal- regulated kinase 1 (ASK1) Inhibition of MAPK phosphatases Regulation & Activation of MAPK pathway
- 10. 2-Regulation of PI3K signaling pathways by ROS
- 12. 3-Nrf2 mediated redox cellular signaling Nrf2 Transcription factor Expression of antioxidant enzymes Decrease ROS level in stress conditions
- 14. Applications for Drugs Targeted to Increase ROS in Cancer Treatment.
- 16. Miltirone & Curcumin in MAPK signaling pathways Longikaurin E as PI3K signaling pathways inhibitor Apigenin, & Brusatol as Nrf2 inhibitors Applications for Drugs Targeted to Increase ROS in Cancer Treatment.
- 17. Miltirone
- 18. Effects of Miltirone on: human leukemia cell lines primary leukemia cells nude mice U937 xenograft RESULTS: 1. ROS plays an important role in miltirone-induced apoptosis 2. Miltirone induces cytotoxicity and apoptosis in human leukemia cells 3. Miltirone exhibits anticancer activity and low toxicity in U937 xenograft model 4. Miltirone has a potential of antitumor effect and low toxicity in vivo. 5. Miltirone triggers ROS generation 6. Miltirone induces the ER stress response of human leukemia cells 7. Miltirone triggers apoptosis through the mitochondrial dysfunction pathway
- 19. Western blot analysis Miltirone induced a robust and sustained activation of JNK ROS plays an important role in miltirone-induced apoptosis
- 20. Curcumin
- 21. Western blot was used to assess the expression of antibodies: p- ASK1, p-MKK4, p-JNK, total ASK1, total MKK4 and total 1. Curcumin Induced Oxidative Stress in BGC-823 Cells 2. Curcumin-Triggered Apoptosis in BGC-823 Cells Was Related with the ROS Production in BGC-823 Cells 3. Curcumin Activated ROS-Mediated JNK Cascade in BGC-823 Cells
- 22. Longikaurin E Western blotting assay Longikaurin E increased the phosphorylation of p38 but decreased the phosphorylation of PI3K/AKT in treated cells after 24 h
- 23. Apigenin
- 25. Nrf2 Transcription factor Expression of antioxidant enzymes Decrease ROS level in stress conditions ROS level Apigenin Or Brusatol Chemotherapy Enhanced Cytotoxicity of anticancer drugs
- 26. Thank you
- 27. References • “Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling” Cellular Signaling Volume 24, Issue 5, May 2012, Pages 981–990 • Zhou, L. et al. Miltirone exhibits ant leukemic activity by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction pathways. Sci. Rep. 6, 20585; doi: 10.1038/srep20585 (2016). • “Longikaurin E induces apoptosis of pancreatic cancer cells via modulation of the p38 and PI3K/AKT pathways by ROS” DOI 10.1007/s00210-015-1107-4 • Lun Zhang, Jiahui Li, Liang Zong, et al., “Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer, "Oxidative Medicine and Cellular Longevity, vol. 2016, Article ID 1616781, 9 pages, 2016. doi:10.1155/2016/1616781 • Carcinogenesis vol.34 no.8 pp.1806–1814, 2013 doi:10.1093/carcin/bgt108 “Apigenin sensitizes doxorubicin-resistant hepatocellular carcinoma BEL-7402/ADM cells to doxorubicin via inhibiting PI3K/Akt/Nrf2 pathway” • Free Radical Biology and Medicine Volume 78, January 2015, Pages 202–212 “Brusatol provokes a rapid and transient inhibition of Nrf2 signaling and sensitizes mammalian cells to chemical toxicity—implications for therapeutic targeting of Nrf2” • Int. J. Mol. Sci. 2014, 15, 15754-15765; doi:10.3390/ijms150915754 ’’Curcumin Induced Human Gastric Cancer BGC-823 Cells Apoptosis by ROS-Mediated ASK1-MKK4-JNK Stress Signaling Pathway” • “Redox Regulation of Cell Survival” ANTIOXIDANTS & REDOX SIGNALING Volume 10, Number 8, 2008 DOI: 10.1089/ars.2007.1957 • http://www.nature.com/onc/journal/v27/n41/fig_tab/onc2008246f1.html
Editor's Notes
- FROM: MAPK signal pathways in the regulation of cell proliferation in mammalian cells Wei ZHANG and Hui Tu LIU
- From: Targeting the AKT protein kinase for cancer chemoprevention doi: 10.1158/1535-7163.MCT-07-0120Mol Cancer Ther August 2007 6;2139
- http://www.nature.com/nri/journal/v13/n7/fig_tab/nri3470_F1.html
- Pathania, Divia. "Design and discovery of novel quinazolinedione-based redox modulators as therapies for pancreatic cancer." Biochimica et Biophysica Acta, 2014: 332-343.
- FROM: Drug discovery approaches targeting the PI3K/Akt pathway in cancer C Garcia-Echeverria and W R Sellers