Antioxidants.pptx
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Free radicals are molecules with unpaired electrons that can damage cells. They are generated through normal cell processes but also environmental exposures. Antioxidants protect against free radical damage by neutralizing them. There are two main classes of antioxidants - enzymatic and non-enzymatic. Enzymatic antioxidants include superoxide dismutase and catalase while non-enzymatic antioxidants include vitamins C and E, carotenoids, and polyphenols. These antioxidants help prevent chronic diseases associated with oxidative stress and aging.
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Antioxidants
The document discusses reactive oxygen species (ROS) and antioxidants. ROS such as superoxide, hydrogen peroxide, and hydroxyl radicals are produced through normal cellular processes but can cause tissue damage if levels become too high. Antioxidants help prevent this damage by neutralizing ROS. The document outlines various antioxidants like vitamins C and E, carotenoids, polyphenols, glutathione, and superoxide dismutase. It also describes how ROS can damage proteins, lipids, and DNA and discusses the role of antioxidants and ROS in periodontal disease pathogenesis.
Free radicals & Antioxidants
This document discusses free radicals and antioxidants. It defines free radicals as molecules with unpaired electrons that are highly reactive. Free radicals are produced through normal cell metabolism but can damage cells. Antioxidants help prevent this damage by neutralizing free radicals. The document outlines the major sources of free radicals in the body and environment, the types of tissue damage they can cause, and examples of antioxidant enzymes and foods that help reduce oxidative stress.
Role of antioxidant in health and disease
This document discusses the role of antioxidants in health and disease. It defines free radicals and describes how they are produced endogenously through metabolism and exogenously through environmental factors. Free radicals can cause oxidative damage but are balanced by the body's antioxidant defense system, which includes antioxidant enzymes like catalase and glutathione peroxidase, chain breaking antioxidants like vitamin E and beta-carotene, and transition metal binding proteins. The document outlines the sources and roles of various reactive oxygen species and antioxidants in the body.
Free Radicals and Vitamin E
Free radicals are molecules with unpaired electrons that can damage cells. Vitamin E is a powerful antioxidant that protects cells from free radical damage. The document defines free radicals and describes how they are normally produced and how they can damage lipids, proteins, and DNA. It then explains the systems cells use to prevent and intercept free radicals, including enzymes like superoxide dismutase and antioxidants like vitamin E. Vitamin E acts as a chain-breaking antioxidant that stops the chain reactions of lipid peroxidation caused by free radicals. A deficiency of vitamin E can occur if one cannot absorb dietary fat or in premature infants, but it is generally uncommon as it is found in many foods.
FREE RADICALS 1 biochemistry mbbs 2.pptx
Free radicals are highly reactive molecules with unpaired electrons that can cause cell damage. The body produces free radicals during normal metabolic processes and as a defense against pathogens. However, excessive free radical production can lead to oxidative stress and damage to proteins, lipids, and DNA. The body has antioxidant defenses like superoxide dismutase, glutathione peroxidase, and catalase that neutralize free radicals and prevent oxidative damage. However, when free radical production overwhelms these defenses, it can contribute to diseases like atherosclerosis, cancer, diabetes, and neurological disorders. Antioxidant nutrients from foods help reduce oxidative stress by donating electrons to free radicals and halting radical chain reactions before damage occurs.
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This document discusses antioxidants in dermatology. It defines antioxidants as molecules that mitigate oxidative stress. Reactive oxygen species like superoxide can damage cells and tissues, but antioxidants balance this through several mechanisms. The document outlines major antioxidants like ascorbic acid, alpha-tocopherol, carotenoids, polyphenols, uric acid, glutathione, and superoxide dismutase. It describes their sources, mechanisms of action, limitations, and roles in reducing inflammation and protecting lipids, DNA, and proteins from free radical damage.
Cigarette smoke and oxidative stress
The document discusses the harmful effects of cigarette smoke. It begins by defining cigarette smoke as a complex mixture of over 4000 chemicals, including nicotine, carbon monoxide, arsenic, formaldehyde, lead and other toxins. The document then discusses how these chemicals can cause cancer, heart disease, lung disease and other serious illnesses. For example, it notes that cigarette smoking causes over 3 million deaths annually worldwide. The document also examines how cigarette smoke promotes oxidative stress and lipid peroxidation, damaging cells. Finally, it summarizes a case study that found higher oxidative stress biomarkers and lower antioxidant levels in smokers compared to non-smokers.
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.
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This document discusses the role of antioxidants in health and disease. It defines free radicals and describes how they are produced endogenously through metabolism and exogenously through environmental factors. Free radicals can cause oxidative damage but are balanced by the body's antioxidant defense system, which includes antioxidant enzymes like catalase and glutathione peroxidase, chain breaking antioxidants like vitamin E and beta-carotene, and transition metal binding proteins. The document outlines the sources and roles of various reactive oxygen species and antioxidants in the body.
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Free radicals are molecules with unpaired electrons that can damage cells. Vitamin E is a powerful antioxidant that protects cells from free radical damage. The document defines free radicals and describes how they are normally produced and how they can damage lipids, proteins, and DNA. It then explains the systems cells use to prevent and intercept free radicals, including enzymes like superoxide dismutase and antioxidants like vitamin E. Vitamin E acts as a chain-breaking antioxidant that stops the chain reactions of lipid peroxidation caused by free radicals. A deficiency of vitamin E can occur if one cannot absorb dietary fat or in premature infants, but it is generally uncommon as it is found in many foods.
FREE RADICALS 1 biochemistry mbbs 2.pptx
Free radicals are highly reactive molecules with unpaired electrons that can cause cell damage. The body produces free radicals during normal metabolic processes and as a defense against pathogens. However, excessive free radical production can lead to oxidative stress and damage to proteins, lipids, and DNA. The body has antioxidant defenses like superoxide dismutase, glutathione peroxidase, and catalase that neutralize free radicals and prevent oxidative damage. However, when free radical production overwhelms these defenses, it can contribute to diseases like atherosclerosis, cancer, diabetes, and neurological disorders. Antioxidant nutrients from foods help reduce oxidative stress by donating electrons to free radicals and halting radical chain reactions before damage occurs.
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This document discusses antioxidants in dermatology. It defines antioxidants as molecules that mitigate oxidative stress. Reactive oxygen species like superoxide can damage cells and tissues, but antioxidants balance this through several mechanisms. The document outlines major antioxidants like ascorbic acid, alpha-tocopherol, carotenoids, polyphenols, uric acid, glutathione, and superoxide dismutase. It describes their sources, mechanisms of action, limitations, and roles in reducing inflammation and protecting lipids, DNA, and proteins from free radical damage.
Cigarette smoke and oxidative stress
The document discusses the harmful effects of cigarette smoke. It begins by defining cigarette smoke as a complex mixture of over 4000 chemicals, including nicotine, carbon monoxide, arsenic, formaldehyde, lead and other toxins. The document then discusses how these chemicals can cause cancer, heart disease, lung disease and other serious illnesses. For example, it notes that cigarette smoking causes over 3 million deaths annually worldwide. The document also examines how cigarette smoke promotes oxidative stress and lipid peroxidation, damaging cells. Finally, it summarizes a case study that found higher oxidative stress biomarkers and lower antioxidant levels in smokers compared to non-smokers.
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.
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.
Oxidative stress and antioxidants
Oxidative stress occurs due to an imbalance between free radicals and antioxidants in the body. Free radicals like reactive oxygen species (ROS) and reactive nitrogen species (RNS) can be generated endogenously through normal metabolism or exogenously through environmental exposures. They damage cells and tissues through lipid peroxidation and reactions with DNA, proteins, and other molecules. Antioxidants help reduce oxidative stress by scavenging or preventing the formation of free radicals. Common antioxidants include enzymes like superoxide dismutase, catalase, and glutathione peroxidase as well as vitamins C and E. However, antioxidants can also act as pro-oxidants in high amounts or conditions of high oxygen pressure.
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Oxidative stress is the main metabolic process that causes mitochondrial dysfunction. In this presentation we show different oxidative stress pathways and the main solutions to prevent mitochondrial damage by using non enzymatic antioxidants and boosting antioxidant enzymatic systems.
Antioxidants
Free radicals are unstable molecules with unpaired electrons that can cause oxidative damage. They are produced during normal metabolism but also due to environmental toxins and radiation. Antioxidants help stabilize free radicals and prevent cellular damage. The body has endogenous antioxidants like glutathione, vitamin C and E, and antioxidant enzymes. Exogenous antioxidants from foods and supplements can further support the antioxidant defense system. Oxidative stress occurs when there is an imbalance between free radicals and antioxidants leading to diseases. Maintaining adequate antioxidant levels through diet and lifestyle can help reduce oxidative damage and disease risk.
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This document discusses lipid oxidation and peroxidation. It defines fatty acids and the difference between saturated and unsaturated fatty acids. It also defines oxidation, free radicals, and explains why fatty acids are prone to oxidation. The document outlines the mechanism of peroxidation including initiation, propagation, and termination. It discusses the impact of fatty acid oxidation and the types of oxidation that can occur. Factors that affect fatty acid oxidation both in vitro and in vivo are also summarized along with the harmful effects of lipid peroxidation and ways to prevent it.
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Free radicals are unstable chemical species that can damage cells. They are normally produced during cellular metabolism but can increase during oxidative stress, leading to cell injury. Free radicals react with proteins, lipids, carbohydrates and nucleic acids, causing damage through lipid peroxidation, protein oxidation and DNA lesions. Cells have antioxidant defenses and scavenging systems like catalase, superoxide dismutase and glutathione peroxidase to remove free radicals, but excessive free radicals overwhelm these systems and cause pathological effects that contribute to conditions like cancer, aging and neurodegenerative diseases.
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Oxidative stress occurs when there is an imbalance between reactive oxygen species (ROS) and antioxidants, leading to cellular damage. ROS are generated through normal metabolic processes and environmental exposures like cigarette smoke and air pollution. They play roles in signaling but can cause harm in excess. Antioxidants like superoxide dismutase and glutathione normally counteract ROS. In respiratory diseases like asthma, emphysema, and pulmonary fibrosis, oxidative stress is elevated due to increased ROS and/or depleted antioxidants, contributing to airway inflammation and tissue injury. This oxidative damage may be a therapeutic target through antioxidants or reducing environmental oxidant exposures.
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The document discusses antioxidants and their role in human health. It defines antioxidants as molecules that inhibit the oxidation of other molecules and prevent free radical damage. Free radicals are unstable molecules that can damage cells, but antioxidant enzymes work to stabilize free radicals. Many health conditions are linked to oxidative stress caused by free radicals, including aging, cancer, diabetes and neurodegenerative diseases. The body has both endogenous and dietary antioxidant systems to protect against free radical damage through catalytic removal of radicals and protection of macromolecules.
Antioxident
This document discusses antioxidants and their role in reducing oxidative stress and free radical damage in the body. It provides information on sources of antioxidants such as fruits and vegetables, and how different cooking methods can affect the antioxidant levels in foods. Some key points include:
- Antioxidants help neutralize free radicals and reduce oxidative stress, which is associated with diseases like cancer and heart disease. Major sources of antioxidants are fruits and vegetables.
- Cooking methods like boiling, baking, and frying can impact the antioxidant levels in foods, with some methods causing greater losses than others. Proper cooking is important to maximize antioxidant retention.
- The document outlines various assays used to measure antioxidant capacity and free radical
ROS and redox regulation
The document discusses oxidative stress and redox regulation. It defines oxidative stress as an imbalance between reactive oxygen species and antioxidants in cells. Reactive oxygen species are formed through normal metabolism but also during environmental stress. They can damage biomolecules and lead to diseases. Antioxidants help neutralize reactive oxygen species and may help prevent certain diseases. Redox regulation involves electron transfer processes like oxidation, which is the loss of electrons, and reduction, which is the gain of electrons. An example of redox regulation is the mitogen-activated protein kinase pathway, which is involved in cell survival signaling and can be activated under oxidative stress conditions through redox modification.
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 CHEMISTRY presentation ppt
Free radicals are molecules with unpaired electrons that can cause damage by reacting with other molecules to steal electrons. They are produced endogenously through metabolism but also come from exogenous sources like pollution, radiation, and cigarettes. Free radical damage at the cellular and molecular level can lead to health issues including cancer and aging. The impact of free radicals can be reduced by decreasing exposure to sources, exercising to boost antioxidant defenses, eating antioxidant-rich foods, and taking antioxidant supplements.
free radical
This document summarizes the pharmacology of free radicals and their role in various diseases. It discusses how free radicals are generated and the types of free radicals. It then describes how free radicals cause oxidative damage and lead to disorders like diabetes, neurological diseases, cancer, and rheumatoid arthritis. The document also outlines various antioxidants that can protect against free radical damage.
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.
Oxidative stress and the eye
Every component of the eye is vulnerable to damage from ROI, particularly retina. There are several reasons for the vulnerability of the retina, including high concentrations of polyunsaturated fatty acid (PUFA), constant exposure to visible light, high consumption of oxygen, an abundance of photosensitisers in the neurosensory retina and the RPE, the process of phagocytosis by the RPE which is known to generate hydrogen peroxide.
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.
oxidative stress
Oxidative stress occurs when there is an imbalance between free radicals and antioxidants in cells, leading to molecular and cellular damage. Free radicals are highly reactive chemical species with unpaired electrons that form as a natural byproduct of oxygen metabolism and can have beneficial roles but also cause oxidative damage. Antioxidants help neutralize free radicals to prevent oxidative stress and diseases like cancer and cardiovascular disease. Measurement of oxidative stress markers and use of antioxidant defenses help counter the effects of free radical damage in cells.
ROS ANTIOXIDENTS
Aerobic organisms continuously produce reactive free radicals through respiration, metabolism and phagocytosis. Approximately 1-2% of oxygen consumed is converted into superoxide radicals by the respiratory chain, one of the main sources of free radicals in cells. While oxygen is necessary for life, its partial reduction can produce reactive oxygen species (ROS) that damage living systems. The body has multiple antioxidant defenses to combat ROS, including superoxide dismutase, catalase, glutathione peroxidase and vitamin C, which help convert ROS into less reactive species and protect biomolecules from oxidative damage.
Free radical and antioxidants
This document discusses free radicals and antioxidants. It defines free radicals as unstable atoms or molecules with unpaired electrons that can damage cells. Free radicals are generated through normal cell processes but can also come from external sources like pollution. They can cause oxidative stress by damaging biomolecules, cells, and tissues. Antioxidants help counter the harmful effects of free radicals by donating electrons to stabilize them. Examples of antioxidants include vitamins C and E, minerals, and enzymes. Oxidative stress left unchecked can contribute to many health conditions.
Reactive oxygen species and its role in periodontal
This document summarizes reactive oxygen species (ROS) and their role in periodontal diseases. It discusses the origin of ROS and free radicals from neutrophils and their tissue-damaging effects through lipid peroxidation, protein and DNA damage. Biomarkers of ROS-mediated tissue destruction include MDA, isoprostanes for lipid damage and 8-OHdG for DNA damage. The body's antioxidant defense system works to reduce ROS, but studies show lower antioxidant levels and higher ROS biomarkers in the serum, saliva and gingival crevicular fluid of periodontitis patients, providing evidence of ROS-mediated tissue destruction in periodontal disease.
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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.
Oxidative stress and antioxidants
Oxidative stress occurs due to an imbalance between free radicals and antioxidants in the body. Free radicals like reactive oxygen species (ROS) and reactive nitrogen species (RNS) can be generated endogenously through normal metabolism or exogenously through environmental exposures. They damage cells and tissues through lipid peroxidation and reactions with DNA, proteins, and other molecules. Antioxidants help reduce oxidative stress by scavenging or preventing the formation of free radicals. Common antioxidants include enzymes like superoxide dismutase, catalase, and glutathione peroxidase as well as vitamins C and E. However, antioxidants can also act as pro-oxidants in high amounts or conditions of high oxygen pressure.
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Oxidative stress is the main metabolic process that causes mitochondrial dysfunction. In this presentation we show different oxidative stress pathways and the main solutions to prevent mitochondrial damage by using non enzymatic antioxidants and boosting antioxidant enzymatic systems.
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Free radicals are unstable molecules with unpaired electrons that can cause oxidative damage. They are produced during normal metabolism but also due to environmental toxins and radiation. Antioxidants help stabilize free radicals and prevent cellular damage. The body has endogenous antioxidants like glutathione, vitamin C and E, and antioxidant enzymes. Exogenous antioxidants from foods and supplements can further support the antioxidant defense system. Oxidative stress occurs when there is an imbalance between free radicals and antioxidants leading to diseases. Maintaining adequate antioxidant levels through diet and lifestyle can help reduce oxidative damage and disease risk.
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This document discusses lipid oxidation and peroxidation. It defines fatty acids and the difference between saturated and unsaturated fatty acids. It also defines oxidation, free radicals, and explains why fatty acids are prone to oxidation. The document outlines the mechanism of peroxidation including initiation, propagation, and termination. It discusses the impact of fatty acid oxidation and the types of oxidation that can occur. Factors that affect fatty acid oxidation both in vitro and in vivo are also summarized along with the harmful effects of lipid peroxidation and ways to prevent it.
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Free radicals are unstable chemical species that can damage cells. They are normally produced during cellular metabolism but can increase during oxidative stress, leading to cell injury. Free radicals react with proteins, lipids, carbohydrates and nucleic acids, causing damage through lipid peroxidation, protein oxidation and DNA lesions. Cells have antioxidant defenses and scavenging systems like catalase, superoxide dismutase and glutathione peroxidase to remove free radicals, but excessive free radicals overwhelm these systems and cause pathological effects that contribute to conditions like cancer, aging and neurodegenerative diseases.
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Oxidative stress occurs when there is an imbalance between reactive oxygen species (ROS) and antioxidants, leading to cellular damage. ROS are generated through normal metabolic processes and environmental exposures like cigarette smoke and air pollution. They play roles in signaling but can cause harm in excess. Antioxidants like superoxide dismutase and glutathione normally counteract ROS. In respiratory diseases like asthma, emphysema, and pulmonary fibrosis, oxidative stress is elevated due to increased ROS and/or depleted antioxidants, contributing to airway inflammation and tissue injury. This oxidative damage may be a therapeutic target through antioxidants or reducing environmental oxidant exposures.
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The document discusses antioxidants and their role in human health. It defines antioxidants as molecules that inhibit the oxidation of other molecules and prevent free radical damage. Free radicals are unstable molecules that can damage cells, but antioxidant enzymes work to stabilize free radicals. Many health conditions are linked to oxidative stress caused by free radicals, including aging, cancer, diabetes and neurodegenerative diseases. The body has both endogenous and dietary antioxidant systems to protect against free radical damage through catalytic removal of radicals and protection of macromolecules.
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This document discusses antioxidants and their role in reducing oxidative stress and free radical damage in the body. It provides information on sources of antioxidants such as fruits and vegetables, and how different cooking methods can affect the antioxidant levels in foods. Some key points include:
- Antioxidants help neutralize free radicals and reduce oxidative stress, which is associated with diseases like cancer and heart disease. Major sources of antioxidants are fruits and vegetables.
- Cooking methods like boiling, baking, and frying can impact the antioxidant levels in foods, with some methods causing greater losses than others. Proper cooking is important to maximize antioxidant retention.
- The document outlines various assays used to measure antioxidant capacity and free radical
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The document discusses oxidative stress and redox regulation. It defines oxidative stress as an imbalance between reactive oxygen species and antioxidants in cells. Reactive oxygen species are formed through normal metabolism but also during environmental stress. They can damage biomolecules and lead to diseases. Antioxidants help neutralize reactive oxygen species and may help prevent certain diseases. Redox regulation involves electron transfer processes like oxidation, which is the loss of electrons, and reduction, which is the gain of electrons. An example of redox regulation is the mitogen-activated protein kinase pathway, which is involved in cell survival signaling and can be activated under oxidative stress conditions through redox modification.
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.
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Free radicals are molecules with unpaired electrons that can cause damage by reacting with other molecules to steal electrons. They are produced endogenously through metabolism but also come from exogenous sources like pollution, radiation, and cigarettes. Free radical damage at the cellular and molecular level can lead to health issues including cancer and aging. The impact of free radicals can be reduced by decreasing exposure to sources, exercising to boost antioxidant defenses, eating antioxidant-rich foods, and taking antioxidant supplements.
free radical
This document summarizes the pharmacology of free radicals and their role in various diseases. It discusses how free radicals are generated and the types of free radicals. It then describes how free radicals cause oxidative damage and lead to disorders like diabetes, neurological diseases, cancer, and rheumatoid arthritis. The document also outlines various antioxidants that can protect against free radical damage.
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.
Oxidative stress and the eye
Every component of the eye is vulnerable to damage from ROI, particularly retina. There are several reasons for the vulnerability of the retina, including high concentrations of polyunsaturated fatty acid (PUFA), constant exposure to visible light, high consumption of oxygen, an abundance of photosensitisers in the neurosensory retina and the RPE, the process of phagocytosis by the RPE which is known to generate hydrogen peroxide.
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.
oxidative stress
Oxidative stress occurs when there is an imbalance between free radicals and antioxidants in cells, leading to molecular and cellular damage. Free radicals are highly reactive chemical species with unpaired electrons that form as a natural byproduct of oxygen metabolism and can have beneficial roles but also cause oxidative damage. Antioxidants help neutralize free radicals to prevent oxidative stress and diseases like cancer and cardiovascular disease. Measurement of oxidative stress markers and use of antioxidant defenses help counter the effects of free radical damage in cells.
ROS ANTIOXIDENTS
Aerobic organisms continuously produce reactive free radicals through respiration, metabolism and phagocytosis. Approximately 1-2% of oxygen consumed is converted into superoxide radicals by the respiratory chain, one of the main sources of free radicals in cells. While oxygen is necessary for life, its partial reduction can produce reactive oxygen species (ROS) that damage living systems. The body has multiple antioxidant defenses to combat ROS, including superoxide dismutase, catalase, glutathione peroxidase and vitamin C, which help convert ROS into less reactive species and protect biomolecules from oxidative damage.
Free radical and antioxidants
This document discusses free radicals and antioxidants. It defines free radicals as unstable atoms or molecules with unpaired electrons that can damage cells. Free radicals are generated through normal cell processes but can also come from external sources like pollution. They can cause oxidative stress by damaging biomolecules, cells, and tissues. Antioxidants help counter the harmful effects of free radicals by donating electrons to stabilize them. Examples of antioxidants include vitamins C and E, minerals, and enzymes. Oxidative stress left unchecked can contribute to many health conditions.
Reactive oxygen species and its role in periodontal
This document summarizes reactive oxygen species (ROS) and their role in periodontal diseases. It discusses the origin of ROS and free radicals from neutrophils and their tissue-damaging effects through lipid peroxidation, protein and DNA damage. Biomarkers of ROS-mediated tissue destruction include MDA, isoprostanes for lipid damage and 8-OHdG for DNA damage. The body's antioxidant defense system works to reduce ROS, but studies show lower antioxidant levels and higher ROS biomarkers in the serum, saliva and gingival crevicular fluid of periodontitis patients, providing evidence of ROS-mediated tissue destruction in periodontal disease.
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acid base homeostasis MBBS.pptx
The document discusses acid-base homeostasis and disorders, describing how the body maintains pH between 7.35-7.45 through buffer systems like bicarbonate that are regulated by respiration and the kidneys; it examines types of acid-base imbalances like metabolic acidosis and alkalosis, their causes, features, and treatment; and covers respiratory acidosis which results from excess carbon dioxide due to hypoventilation.
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Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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A Classical Text Review on Basavarajeeyam
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Role of Mukta Pishti in the Management of Hyperthyroidism
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The Electrocardiogram - Physiologic Principles
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Osteoporosis is an increasing cause of morbidity among the elderly.
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Antioxidants.pptx
- 2. Oxidants and antioxidants •Free radicals: free radical is a molecule or molecular fragment that contain one or more unpaired electrons in the outer orbital •They are also known as reactive oxygen species ( ROS) •Examples are: superoxide, singlet oxygen, H2O2, peroxynitrite, NO, OH, ROO
- 3. Generation of free radicals •Leakage from mitochondrial electron transport: mitochondria is the major site for production of superoxide ions. •Mitochondria also has high levels of GPx and GSH •Xanthine oxidase: in the metabolism of purine •NADPH oxidase: in inflammatory cells like neutrophils, macrophages, on phagocytosis, there is respiratory burst.
- 5. •Superoxide ions are produced due to respiratory burst: it is then converted to H2O2 and hypochlorous acid which kill the bacteria • This mechanism is deficient in chronic granulomatous disease
- 6. •Nitric oxide synthase: from arginine NO is produced •Lipooxygenase: for synthesis of leukotrienes Physical agents: •UV rays •Ionising radiation •Cigarette smoke •Air pollutants
- 7. Clinical significance •Chronic inflammation: ROS is associated with tissue damage and implicated in pathogenesis of chronic ulcerative colitis and chronic glomerulonephritis •Acute inflammation: activated macrophages produce free radicals •Respiratory diseases: Adult respiratory distress syndrome, bronchopulmonary dysplasia •Eye: retrolental fibroplasia, cataract
- 8. •Reperfusion injuries •Atherosclerosis and myocardial infarction: oxidation of LDL: formation of foam cells •Skin diseases: psoriasis •Cancers due to mutation •Ageing.
- 11. Free radical scavenger system Antioxidants: These are compounds that protect the cells from the damaging effects of free radicals
- 14. 2. According to the mode of action
- 19. Vitamin C ( ascorbic acid) •Scavenges water soluble peroxyl and perhydroxyl , superoxide, hypochlorous acid and singlet oxygen •Prevents fenton reactions : decreases heme breakdown •Re forms alpha tocopherol •Protects against ROS from cigarette smoke
- 21. Alpha Tocopherol •Lipid soluble antioxidant •Protects the cell membrane ( membrane integrity) •Requires coenzyme Q10 for regeneration •Antioxidant and anti inflammatory •Prevents release of NO from vascular endothelium •Prevents platelet aggregation •Prevents relase of superoxide radicals form macrophages
- 22. Carotenoids •These are available in deep orange red colour vegetables and fruits like carrot, tomatoes, water melon ,red grapes etc •These are also known as tetraterpines •600 variants are known •Beta carotene, alpha carotene, lycopene, retinol etc •Lycopenes are twice as effective as beta carotene •They protect against lung, stomach and prostate cancers
- 23. Polyphenols •Dietary polyphenols are found in fruits, tea, chocolates. •They contain flavones, isoflavones, flavonols, catechins and phenolic acids •They have anti oxidant, anti apoptotic, antiaging, anti inflammatory anti carcinogenic properties. •They are protective against cardiovascular diseases.