Seminario Biología Molecular
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This document discusses apoptosis in cardiomyocytes and the roles of sulfur dioxide (SO2) and cyclophilin D (CypD) in regulating apoptosis. It aims to study the effects of SO2 and isoproterenol (ISO) treatment on apoptosis in cardiomyocytes. The results found that SO2 treatment alone significantly decreased apoptosis in cardiomyocytes and caspase 9 expression. ISO treatment increased apoptosis but to a lesser extent than when combined with SO2. The conclusions discuss how increasing endogenous SO2 production in cardiomyocytes could help prevent apoptosis and cardiac output decline with age, but this would require further molecular biology studies to understand the mechanisms and inhibit apoptosis without side effects.
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Mechanisms of cellular injuries
This document discusses the mechanisms of cellular injury and death. It explains that cells can either adapt to injury, experience reversible injury, or die. Common causes of injury include hypoxia, chemicals, physical trauma, nutritional imbalances, genetics, infections, and immunological factors. Four intracellular systems are particularly vulnerable: aerobic respiration, cell membrane integrity, protein synthesis, and the genetic apparatus. Five biochemical systems mediate injury or death: ATP depletion, oxidative stress from reactive oxygen species, loss of calcium homeostasis, defects in membrane permeability, and irreversible mitochondrial damage. Reversible and irreversible injury processes are outlined for ischemia-reperfusion and from free radicals generated by radiation, enzymes, normal respiration, and transition metals.
Biochemistry of nitric oxide
Nitric oxide is formed in the body from L-arginine and can have both protective and tumor-promoting effects. It reacts with superoxide to form peroxynitrite, a reactive molecule that can damage biomolecules. Excess nitric oxide production can be inhibited by nitric oxide synthase inhibitors. Nitric oxide has direct effects through reactions with metals and inhibition of mitochondrial respiration, and indirect effects through peroxynitrite formation leading to oxidative stress.
Nitric oxide synthases sajal sen
Nitric oxide synthases (NOS) are a family of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. There are three main types of NOS - neuronal NOS, inducible NOS, and endothelial NOS - located in different tissues and performing different functions. NOS is a heme-containing dimerized protein that uses NADPH, FAD, FMN, tetrahydrobiopterin, and heme as cofactors. It converts L-arginine to citrulline and NO in a two-domain reaction involving the transfer of electrons from the reductase domain to the oxygenase domain. NOS and NO play important roles in many physiological processes and human diseases
Nitric oxide
Nitric oxide (NO) is synthesized from arginine by nitric oxide synthase (NOS). There are three isoforms of NOS - neuronal NOS (nNOS), macrophage NOS (iNOS), and endothelial NOS (eNOS). NO functions as a vasodilator, inhibits platelet adhesion, and acts as a neurotransmitter in the gastrointestinal tract and urinary tract. Diseases associated with NO include angina pectoris, pulmonary hypertension, and impotence. NO production can be inhibited by compounds such as N-Mono methyl arginine (NMMA) and asymmetric dimethyl arginine (ADMA).
Nitric oxide
Nitric oxide (NO) is a gas that acts as a signaling molecule in various physiological processes. It is produced by nitric oxide synthase enzymes from arginine and oxygen. NO signals the dilation of blood vessels by diffusing into endothelial cells and increasing cGMP levels, which leads to smooth muscle relaxation. It also prevents platelet aggregation, acts as a neurotransmitter, and is involved in the immune response by assisting macrophages in killing bacteria. While NO is important for many functions, too much or too little production can be harmful and lead to conditions like hypertension or infection.
cell 3
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use as energy. It requires a continuous oxygen supply. The air we breathe is 21% oxygen, which enters our bodies through inhalation and transfers into blood to reach cells. Low oxygen levels cause hypoxia and anaerobic respiration, generating lactic acid waste. Breathing is vital, as stopping it lowers pH and oxygen while raising carbon dioxide levels, potentially leading to cell death.
NO homeostasis_Hannibal_CAR 2016 (1)
This document discusses nitric oxide homeostasis and its role in neurodegenerative diseases such as Alzheimer's and Parkinson's. It begins by introducing nitric oxide biosynthesis by nitric oxide synthases and how their expression is altered in Alzheimer's. It then discusses factors that control nitric oxide levels, including endogenous inhibitors, tetrahydrobiopterin levels, and nitric oxide reactivity with superoxide to form peroxynitrite. Overall, the document analyzes how imbalances in nitric oxide signaling can contribute to neurodegeneration through oxidative stress and damage.
talk1
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use as energy. It requires a continuous oxygen supply. The air we breathe is 21% oxygen, which enters our bodies through inhalation and transfers into blood to oxygenate tissues. Low oxygen levels cause hypoxia and anaerobic respiration, generating lactic acid waste. Breathing controls pH, PCO2, and PO2 levels in the blood.
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Mechanisms of cellular injuries
This document discusses the mechanisms of cellular injury and death. It explains that cells can either adapt to injury, experience reversible injury, or die. Common causes of injury include hypoxia, chemicals, physical trauma, nutritional imbalances, genetics, infections, and immunological factors. Four intracellular systems are particularly vulnerable: aerobic respiration, cell membrane integrity, protein synthesis, and the genetic apparatus. Five biochemical systems mediate injury or death: ATP depletion, oxidative stress from reactive oxygen species, loss of calcium homeostasis, defects in membrane permeability, and irreversible mitochondrial damage. Reversible and irreversible injury processes are outlined for ischemia-reperfusion and from free radicals generated by radiation, enzymes, normal respiration, and transition metals.
Biochemistry of nitric oxide
Nitric oxide is formed in the body from L-arginine and can have both protective and tumor-promoting effects. It reacts with superoxide to form peroxynitrite, a reactive molecule that can damage biomolecules. Excess nitric oxide production can be inhibited by nitric oxide synthase inhibitors. Nitric oxide has direct effects through reactions with metals and inhibition of mitochondrial respiration, and indirect effects through peroxynitrite formation leading to oxidative stress.
Nitric oxide synthases sajal sen
Nitric oxide synthases (NOS) are a family of enzymes that catalyze the production of nitric oxide (NO) from L-arginine. There are three main types of NOS - neuronal NOS, inducible NOS, and endothelial NOS - located in different tissues and performing different functions. NOS is a heme-containing dimerized protein that uses NADPH, FAD, FMN, tetrahydrobiopterin, and heme as cofactors. It converts L-arginine to citrulline and NO in a two-domain reaction involving the transfer of electrons from the reductase domain to the oxygenase domain. NOS and NO play important roles in many physiological processes and human diseases
Nitric oxide
Nitric oxide (NO) is synthesized from arginine by nitric oxide synthase (NOS). There are three isoforms of NOS - neuronal NOS (nNOS), macrophage NOS (iNOS), and endothelial NOS (eNOS). NO functions as a vasodilator, inhibits platelet adhesion, and acts as a neurotransmitter in the gastrointestinal tract and urinary tract. Diseases associated with NO include angina pectoris, pulmonary hypertension, and impotence. NO production can be inhibited by compounds such as N-Mono methyl arginine (NMMA) and asymmetric dimethyl arginine (ADMA).
Nitric oxide
Nitric oxide (NO) is a gas that acts as a signaling molecule in various physiological processes. It is produced by nitric oxide synthase enzymes from arginine and oxygen. NO signals the dilation of blood vessels by diffusing into endothelial cells and increasing cGMP levels, which leads to smooth muscle relaxation. It also prevents platelet aggregation, acts as a neurotransmitter, and is involved in the immune response by assisting macrophages in killing bacteria. While NO is important for many functions, too much or too little production can be harmful and lead to conditions like hypertension or infection.
cell 3
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use as energy. It requires a continuous oxygen supply. The air we breathe is 21% oxygen, which enters our bodies through inhalation and transfers into blood to reach cells. Low oxygen levels cause hypoxia and anaerobic respiration, generating lactic acid waste. Breathing is vital, as stopping it lowers pH and oxygen while raising carbon dioxide levels, potentially leading to cell death.
NO homeostasis_Hannibal_CAR 2016 (1)
This document discusses nitric oxide homeostasis and its role in neurodegenerative diseases such as Alzheimer's and Parkinson's. It begins by introducing nitric oxide biosynthesis by nitric oxide synthases and how their expression is altered in Alzheimer's. It then discusses factors that control nitric oxide levels, including endogenous inhibitors, tetrahydrobiopterin levels, and nitric oxide reactivity with superoxide to form peroxynitrite. Overall, the document analyzes how imbalances in nitric oxide signaling can contribute to neurodegeneration through oxidative stress and damage.
talk1
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use as energy. It requires a continuous oxygen supply. The air we breathe is 21% oxygen, which enters our bodies through inhalation and transfers into blood to oxygenate tissues. Low oxygen levels cause hypoxia and anaerobic respiration, generating lactic acid waste. Breathing controls pH, PCO2, and PO2 levels in the blood.
Nitric Oxide and its utility
Nitric oxide (NO) is an endogenous signaling molecule generated from L-arginine by nitric oxide synthase. It is a key signaling molecule in the cardiovascular, nervous, and immune systems. NO activates guanylate cyclase, increasing cyclic GMP levels to cause smooth muscle relaxation and inhibit platelet aggregation. The physiological role of NO was discovered in the vasculature, where it was shown that endothelium-derived relaxing factor causing vasodilation was NO. NO has diverse functions and is involved in processes like neurotransmission, host defense, and inflammation.
talk1
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use for energy. It requires a continuous oxygen supply. Oxygen enters the body through breathing and reaches cells via blood, allowing aerobic respiration. Without enough oxygen, anaerobic respiration generates lactic acid waste. Prolonged low oxygen can cause metabolic acidosis and cell death. Normal breathing maintains pH, PCO2, and PO2 levels in a narrow range important for cellular function.
Nitric oxide
Nitric oxide (NO) is a unique signalling molecule that diffuses freely and acts as an intracellular and intercellular messenger. NO was discovered in the late 1970s and plays many important physiological roles such as acting as a neurotransmitter, mediating cellular defense, and regulating vascular tone. It is produced from L-arginine by the enzyme nitric oxide synthase (NOS) which exists in three isoforms. NO has various effects in different organ systems such as the cardiovascular, nervous, immune, and reproductive systems. Therapeutic uses of NO include treatment of pulmonary hypertension and angina. Recent research is focused on developing NO-releasing drugs for various conditions.
nitric oxide
Nitric oxide is produced by endothelial cells and is important for regulating blood flow. It acts as a vasodilator to relax smooth muscle cells in blood vessels. The three main types of nitric oxide synthase produce nitric oxide, which has many roles in the body like supporting circulation, immune function, and reproduction. It is involved in processes like maintaining blood pressure and facilitating penile erection. Foods like peppers and dark chocolate contain compounds that can boost nitric oxide levels.
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Gaso-transmitters in aird
This document provides an overview of gasotransmitters and their role in autoimmune and inflammatory rheumatic diseases (AIRD). It discusses the history and discovery of nitric oxide, carbon monoxide, and hydrogen sulfide as endogenous gas signaling molecules. Specifically regarding carbon monoxide, it describes its production via heme oxygenase enzymes, mechanisms of action through binding metalloproteins like soluble guanylate cyclase, and anti-inflammatory effects in macrophages, dendritic cells, and T-cells by inhibiting maturation and reducing proinflammatory cytokine production while increasing anti-inflammatory IL-10. The document suggests carbon monoxide may downregulate immune responses and thus play a role in preventing autoimmunity.
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The document discusses key terms related to cellular respiration, including glycolysis, aerobic respiration, anaerobic respiration, ATP, ATPase, phosphorylation, and defines the differences between aerobic and anaerobic respiration. Aerobic respiration uses oxygen and occurs in mitochondria, producing a large amount of ATP. Anaerobic respiration does not use oxygen, and pyruvate is converted to lactate in humans or ethanol in yeast, producing no ATP. The document also notes that cellular respiration is not the same as breathing.
March 1st, 2011
The document discusses topics for an essay on the film Forensics 1, including ethical issues with genetic engineering of offspring, benefits and drawbacks of genetic engineering, accuracy of crime scene investigation techniques shown in the film, and how genetic engineering influences forensic science in the film. It also provides biology homework questions about cellular respiration processes like the electron transport chain and chemiosmosis. Students are asked to describe, diagram, define, and explain topics relating to how cells generate energy through cellular respiration.
Pathogenesis of cell injury By Rohit Kumar Trivedi
Pathogenesis of Cell Injury
Pathophysiology Google Classroom Code: vbwvno4
Google Classrom Link: https://classroom.google.com/c/MzM1NjcyOTIxMjgy?cjc=vbwvno4
FACEBOOK: https://www.facebook.com/rohitkrtrivedi
INSTAGRAM: https://www.instagram.com/rohit_kumar_trivedi
SLIDESHARE: https://www.slideshare.net/Rohittrivedi321
#RohitKumarTrivedi
Pathophysiology B Pharm 2nd Semester
CONTENTS:
1. Mitochondrial damage
2. Cell membrane damage
3. Ribosome damage
4. Nuclear damage
Nitric oxide
This document discusses the endothelium and nitric oxide (NO). It begins by defining the endothelium as the thin layer of cells lining blood vessels. Endothelial cells release substances that modulate vessel tone by causing contraction or relaxation. Studies in the 1980s identified endothelium-derived relaxing factor (EDRF), which was later determined to be NO. NO is synthesized from L-arginine by nitric oxide synthase (NOS). There are three main types of NOS - neuronal (nNOS), inducible (iNOS), and endothelial (eNOS). NO signals smooth muscle relaxation through a cGMP pathway. NO has many roles in the nervous, circulatory, immune, and other body systems. The mechanisms and functions of NO are
D. H. Nagore Antioxidant Ppt
The document discusses antioxidants and various screening models used to assess antioxidant potential. It describes how free radicals can cause oxidative stress and damage to cells, leading to diseases. Various in vitro screening models are described to test scavenging of reactive oxygen and nitrogen species, including hydroxyl, superoxide, nitric oxide, and peroxyl radicals. Natural antioxidants from plants are also discussed, highlighting their importance as dietary sources of antioxidants.
Dheeraj Antioxidant Seminar
The document discusses various aspects of antioxidants and screening models used to evaluate antioxidant potential. It introduces free radicals and their sources, types including superoxide, hydroxyl and nitric oxide radicals. Various diseases associated with oxidative stress are mentioned. Different in vitro screening models to test antioxidant capacity against reactive oxygen and nitrogen species are described, including DPPH, ABTS, FRAP, ORAC assays. Natural sources of antioxidants from plants used in Ayurveda and their potential is highlighted.
Seminar0
Nitric oxide (NO) is involved in many physiological processes as a signaling molecule. It is synthesized endogenously through nitric oxide synthase enzymes and was named "Molecule of the Year" in 1992. NO regulates processes in the cardiovascular, respiratory, nervous, reproductive, immune, muscular and digestive systems. It acts as a vasodilator, neurotransmitter, and promotes smooth muscle relaxation. While NO has many beneficial functions, excessive amounts can also be toxic.
Role of nitric oxide in cell signaling
Nitric oxide (NO) is produced in the body by nitric oxide synthase (NOS) enzymes from the amino acid L-arginine. NO acts as both an intracellular and extracellular signaling molecule and is involved in many physiological processes like neurotransmission and smooth muscle relaxation. There are three isoforms of NOS - neuronal NOS, inducible NOS, and endothelial NOS. NO stimulates soluble guanylate cyclase which increases cyclic GMP levels and triggers smooth muscle relaxation. In addition to cGMP signaling, NO can also signal through S-nitrosylation of proteins or by forming nitrite and nitrate storage pools.
Mustard gas poisoning .By- Dr mohammadullah totakhil
Mustard gas poisoning:
Question :
Should drugs to elevate the WBC and RBC level be used for mustard gas poisoning? Why??
Nitric oxide
The document discusses the endothelium and the role of nitric oxide (NO) in the body. It defines the endothelium as the thin layer of cells lining blood vessels and lymphatic vessels. Endothelial cells release NO, previously called endothelium-derived relaxing factor (EDRF), which modulates blood vessel tone. NO is a gaseous signaling molecule synthesized from L-arginine by nitric oxide synthase (NOS). NO has many roles, including regulating circulation and the nervous, immune, digestive, and reproductive systems. It acts as a vasodilator, neurotransmitter, and plays roles in wound healing and apoptosis.
Role of nitric oxide in pathology
Nitric oxide plays an important role in both normal physiology and the pathology of many diseases. It is involved in processes in the nervous, circulatory, muscular, immune, and digestive systems. Reduced nitric oxide bioavailability contributes to the progression of cardiovascular diseases like atherosclerosis and hypertension by reducing its protective effects on platelets, leukocytes, and smooth muscle cells. Nitric oxide also has roles in diabetes, septic shock, and neurological disorders like Alzheimer's, Parkinson's, and ALS.
Pharmacology of Nitric oxide
The endothelium is the thin layer of cells that lines the interior surface of blood vessels. Endothelial cells release nitric oxide (NO), which acts as a vasodilator and modulates vessel tone. NO is synthesized from L-arginine by the enzyme nitric oxide synthase. It binds to guanylate cyclase, increasing cGMP levels and causing smooth muscle relaxation through various mechanisms. NO has many roles in the nervous, circulatory, immune and other body systems. It is involved in processes like vasodilation, neurotransmission, and host defense. NO synthesis can be inhibited by L-arginine analogs, while NO donors are used therapeutically to elicit smooth muscle relaxation.
Neuroprotection in stroke
Edaravone is a novel antioxidant that scavenges reactive oxygen species (ROS) and inhibits pro-inflammatory responses after brain ischemia. It has emerged as an ideal neuroprotective agent for acute ischemic stroke. Edaravone minimizes ischemic damage by trapping free radicals, preventing oxidative injury to brain cells, and limiting the downstream consequences of excitotoxicity such as mitochondrial disruption and DNA damage. Its neuroprotective effects help preserve viable brain cells in the ischemic penumbra.
Nitric oxide .pdfckjgcgchfcfhxcfhcfhchfch
Nitric oxide (NO) is a small molecule that plays a big role in physiological regulation. It is produced by nitric oxide synthase (NOS) from the amino acid arginine. NO signals through cGMP-dependent and independent pathways in cardiomyocytes. It causes vasodilation by relaxing smooth muscle and inhibits processes like platelet activation, leukocyte adhesion and myocardial contractility. Prolonged high levels of NO can be cytotoxic through formation of peroxynitrite. NO signaling is important for cardiovascular homeostasis.
OXIDATIVE STRESS AND NITRIC OXIDE: A SIGNIFICANT MARKER IN CORONARY ARTERY DI...
OXIDATIVE STRESS AND NITRIC OXIDE: A SIGNIFICANT MARKER IN CORONARY ARTERY DI...International Journal of Technical Research & Application
— Oxidative stress is well known to be involved in the
pathogenesis of lifestyle-related diseases, including, hypertension,
diabetes mellitus, coronary artery diseases, and malignancies.
However, oxidative stress also has a useful role in physiologic
adaptation and in the regulation of intracellular signal
transduction. Therefore, a significant description of oxidative
stress may be “a condition where oxidative forces go beyond the
antioxidant systems due to loss of the equilibrium between them”.
Significant Nitric Oxide (NO) confirmed as a envoy of
vasodilatation, derivative from the endothelium. Coronary artery
disease also defined as atherosclerotic heart diseases are the
outcome of the growth of antheromatous plaques (made up of
fats, cholesterol etc) within the walls of the coronary arteries that
provide the myocardium with oxygen and nutrients. The evidence
of the plaque in the lumen (free space in the artery for the flow of
nutrients, oxygen etc.) of an artery causes tapering of lumen of
the artery by declining its diameter. NO levels show a significant
relation with higher BMI and hypertension in coronary artery
disease. Many research have shown that adipose tissue contains
NO synthetase enzyme, and is thus an impending NO source.
Biological activity of Nitric Oxide provides clinicians with
additional therapeutic options in the treatment of cardiovascular
disease which will subordinate oxidative stress, a process which is
becoming gradually more standard as critical in the
pathophysiology of vascular disease.
Reactive Oxygen Species,Reactive Nitrogen Species and Redox Signaling
This document discusses reactive oxygen species, reactive nitrogen species, and redox signaling. It covers the following key points:
- Nitric oxide is an important signaling molecule produced through the oxidation of L-arginine by nitric oxide synthase. There are three NOS isoforms.
- Reactive oxygen species include superoxide and hydrogen peroxide. Superoxide is produced by NADPH oxidase and can be converted to hydrogen peroxide. These molecules are involved in cell signaling but can also cause damage.
- Hydrogen sulfide is another gasotransmitter that regulates various physiological processes through protein persulfidation.
- Reactive species can modify protein cysteine residues through oxidation
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Nitric Oxide and its utility
Nitric oxide (NO) is an endogenous signaling molecule generated from L-arginine by nitric oxide synthase. It is a key signaling molecule in the cardiovascular, nervous, and immune systems. NO activates guanylate cyclase, increasing cyclic GMP levels to cause smooth muscle relaxation and inhibit platelet aggregation. The physiological role of NO was discovered in the vasculature, where it was shown that endothelium-derived relaxing factor causing vasodilation was NO. NO has diverse functions and is involved in processes like neurotransmission, host defense, and inflammation.
talk1
Cellular respiration harvests electrons from organic compounds like glucose to produce ATP, which cells use for energy. It requires a continuous oxygen supply. Oxygen enters the body through breathing and reaches cells via blood, allowing aerobic respiration. Without enough oxygen, anaerobic respiration generates lactic acid waste. Prolonged low oxygen can cause metabolic acidosis and cell death. Normal breathing maintains pH, PCO2, and PO2 levels in a narrow range important for cellular function.
Nitric oxide
Nitric oxide (NO) is a unique signalling molecule that diffuses freely and acts as an intracellular and intercellular messenger. NO was discovered in the late 1970s and plays many important physiological roles such as acting as a neurotransmitter, mediating cellular defense, and regulating vascular tone. It is produced from L-arginine by the enzyme nitric oxide synthase (NOS) which exists in three isoforms. NO has various effects in different organ systems such as the cardiovascular, nervous, immune, and reproductive systems. Therapeutic uses of NO include treatment of pulmonary hypertension and angina. Recent research is focused on developing NO-releasing drugs for various conditions.
nitric oxide
Nitric oxide is produced by endothelial cells and is important for regulating blood flow. It acts as a vasodilator to relax smooth muscle cells in blood vessels. The three main types of nitric oxide synthase produce nitric oxide, which has many roles in the body like supporting circulation, immune function, and reproduction. It is involved in processes like maintaining blood pressure and facilitating penile erection. Foods like peppers and dark chocolate contain compounds that can boost nitric oxide levels.
Biochemistry quick quiz MIJ ACADEMY
The document contains 4 multiple choice questions about biological concepts. The first question asks about the complex in the electron transport chain that copper is associated with. The second question asks about the class of enzyme that acetaldehyde dehydrogenase belongs to. The third question asks about forms of physiological regulation of enzyme activity except one listed. The fourth questions presents a reaction sequence and asks which step would be best to control the production of compound F.
Gaso-transmitters in aird
This document provides an overview of gasotransmitters and their role in autoimmune and inflammatory rheumatic diseases (AIRD). It discusses the history and discovery of nitric oxide, carbon monoxide, and hydrogen sulfide as endogenous gas signaling molecules. Specifically regarding carbon monoxide, it describes its production via heme oxygenase enzymes, mechanisms of action through binding metalloproteins like soluble guanylate cyclase, and anti-inflammatory effects in macrophages, dendritic cells, and T-cells by inhibiting maturation and reducing proinflammatory cytokine production while increasing anti-inflammatory IL-10. The document suggests carbon monoxide may downregulate immune responses and thus play a role in preventing autoimmunity.
3 7 cell respiration
The document discusses key terms related to cellular respiration, including glycolysis, aerobic respiration, anaerobic respiration, ATP, ATPase, phosphorylation, and defines the differences between aerobic and anaerobic respiration. Aerobic respiration uses oxygen and occurs in mitochondria, producing a large amount of ATP. Anaerobic respiration does not use oxygen, and pyruvate is converted to lactate in humans or ethanol in yeast, producing no ATP. The document also notes that cellular respiration is not the same as breathing.
March 1st, 2011
The document discusses topics for an essay on the film Forensics 1, including ethical issues with genetic engineering of offspring, benefits and drawbacks of genetic engineering, accuracy of crime scene investigation techniques shown in the film, and how genetic engineering influences forensic science in the film. It also provides biology homework questions about cellular respiration processes like the electron transport chain and chemiosmosis. Students are asked to describe, diagram, define, and explain topics relating to how cells generate energy through cellular respiration.
Pathogenesis of cell injury By Rohit Kumar Trivedi
Pathogenesis of Cell Injury
Pathophysiology Google Classroom Code: vbwvno4
Google Classrom Link: https://classroom.google.com/c/MzM1NjcyOTIxMjgy?cjc=vbwvno4
FACEBOOK: https://www.facebook.com/rohitkrtrivedi
INSTAGRAM: https://www.instagram.com/rohit_kumar_trivedi
SLIDESHARE: https://www.slideshare.net/Rohittrivedi321
#RohitKumarTrivedi
Pathophysiology B Pharm 2nd Semester
CONTENTS:
1. Mitochondrial damage
2. Cell membrane damage
3. Ribosome damage
4. Nuclear damage
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Pathogenesis of cell injury By Rohit Kumar Trivedi
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Nitric oxide
This document discusses the endothelium and nitric oxide (NO). It begins by defining the endothelium as the thin layer of cells lining blood vessels. Endothelial cells release substances that modulate vessel tone by causing contraction or relaxation. Studies in the 1980s identified endothelium-derived relaxing factor (EDRF), which was later determined to be NO. NO is synthesized from L-arginine by nitric oxide synthase (NOS). There are three main types of NOS - neuronal (nNOS), inducible (iNOS), and endothelial (eNOS). NO signals smooth muscle relaxation through a cGMP pathway. NO has many roles in the nervous, circulatory, immune, and other body systems. The mechanisms and functions of NO are
D. H. Nagore Antioxidant Ppt
The document discusses antioxidants and various screening models used to assess antioxidant potential. It describes how free radicals can cause oxidative stress and damage to cells, leading to diseases. Various in vitro screening models are described to test scavenging of reactive oxygen and nitrogen species, including hydroxyl, superoxide, nitric oxide, and peroxyl radicals. Natural antioxidants from plants are also discussed, highlighting their importance as dietary sources of antioxidants.
Dheeraj Antioxidant Seminar
The document discusses various aspects of antioxidants and screening models used to evaluate antioxidant potential. It introduces free radicals and their sources, types including superoxide, hydroxyl and nitric oxide radicals. Various diseases associated with oxidative stress are mentioned. Different in vitro screening models to test antioxidant capacity against reactive oxygen and nitrogen species are described, including DPPH, ABTS, FRAP, ORAC assays. Natural sources of antioxidants from plants used in Ayurveda and their potential is highlighted.
Seminar0
Nitric oxide (NO) is involved in many physiological processes as a signaling molecule. It is synthesized endogenously through nitric oxide synthase enzymes and was named "Molecule of the Year" in 1992. NO regulates processes in the cardiovascular, respiratory, nervous, reproductive, immune, muscular and digestive systems. It acts as a vasodilator, neurotransmitter, and promotes smooth muscle relaxation. While NO has many beneficial functions, excessive amounts can also be toxic.
Role of nitric oxide in cell signaling
Nitric oxide (NO) is produced in the body by nitric oxide synthase (NOS) enzymes from the amino acid L-arginine. NO acts as both an intracellular and extracellular signaling molecule and is involved in many physiological processes like neurotransmission and smooth muscle relaxation. There are three isoforms of NOS - neuronal NOS, inducible NOS, and endothelial NOS. NO stimulates soluble guanylate cyclase which increases cyclic GMP levels and triggers smooth muscle relaxation. In addition to cGMP signaling, NO can also signal through S-nitrosylation of proteins or by forming nitrite and nitrate storage pools.
Mustard gas poisoning .By- Dr mohammadullah totakhil
Mustard gas poisoning:
Question :
Should drugs to elevate the WBC and RBC level be used for mustard gas poisoning? Why??
Nitric oxide
The document discusses the endothelium and the role of nitric oxide (NO) in the body. It defines the endothelium as the thin layer of cells lining blood vessels and lymphatic vessels. Endothelial cells release NO, previously called endothelium-derived relaxing factor (EDRF), which modulates blood vessel tone. NO is a gaseous signaling molecule synthesized from L-arginine by nitric oxide synthase (NOS). NO has many roles, including regulating circulation and the nervous, immune, digestive, and reproductive systems. It acts as a vasodilator, neurotransmitter, and plays roles in wound healing and apoptosis.
Role of nitric oxide in pathology
Nitric oxide plays an important role in both normal physiology and the pathology of many diseases. It is involved in processes in the nervous, circulatory, muscular, immune, and digestive systems. Reduced nitric oxide bioavailability contributes to the progression of cardiovascular diseases like atherosclerosis and hypertension by reducing its protective effects on platelets, leukocytes, and smooth muscle cells. Nitric oxide also has roles in diabetes, septic shock, and neurological disorders like Alzheimer's, Parkinson's, and ALS.
Pharmacology of Nitric oxide
The endothelium is the thin layer of cells that lines the interior surface of blood vessels. Endothelial cells release nitric oxide (NO), which acts as a vasodilator and modulates vessel tone. NO is synthesized from L-arginine by the enzyme nitric oxide synthase. It binds to guanylate cyclase, increasing cGMP levels and causing smooth muscle relaxation through various mechanisms. NO has many roles in the nervous, circulatory, immune and other body systems. It is involved in processes like vasodilation, neurotransmission, and host defense. NO synthesis can be inhibited by L-arginine analogs, while NO donors are used therapeutically to elicit smooth muscle relaxation.
Neuroprotection in stroke
Edaravone is a novel antioxidant that scavenges reactive oxygen species (ROS) and inhibits pro-inflammatory responses after brain ischemia. It has emerged as an ideal neuroprotective agent for acute ischemic stroke. Edaravone minimizes ischemic damage by trapping free radicals, preventing oxidative injury to brain cells, and limiting the downstream consequences of excitotoxicity such as mitochondrial disruption and DNA damage. Its neuroprotective effects help preserve viable brain cells in the ischemic penumbra.
Nitric oxide .pdfckjgcgchfcfhxcfhcfhchfch
Nitric oxide (NO) is a small molecule that plays a big role in physiological regulation. It is produced by nitric oxide synthase (NOS) from the amino acid arginine. NO signals through cGMP-dependent and independent pathways in cardiomyocytes. It causes vasodilation by relaxing smooth muscle and inhibits processes like platelet activation, leukocyte adhesion and myocardial contractility. Prolonged high levels of NO can be cytotoxic through formation of peroxynitrite. NO signaling is important for cardiovascular homeostasis.
OXIDATIVE STRESS AND NITRIC OXIDE: A SIGNIFICANT MARKER IN CORONARY ARTERY DI...
OXIDATIVE STRESS AND NITRIC OXIDE: A SIGNIFICANT MARKER IN CORONARY ARTERY DI...International Journal of Technical Research & Application
— Oxidative stress is well known to be involved in the
pathogenesis of lifestyle-related diseases, including, hypertension,
diabetes mellitus, coronary artery diseases, and malignancies.
However, oxidative stress also has a useful role in physiologic
adaptation and in the regulation of intracellular signal
transduction. Therefore, a significant description of oxidative
stress may be “a condition where oxidative forces go beyond the
antioxidant systems due to loss of the equilibrium between them”.
Significant Nitric Oxide (NO) confirmed as a envoy of
vasodilatation, derivative from the endothelium. Coronary artery
disease also defined as atherosclerotic heart diseases are the
outcome of the growth of antheromatous plaques (made up of
fats, cholesterol etc) within the walls of the coronary arteries that
provide the myocardium with oxygen and nutrients. The evidence
of the plaque in the lumen (free space in the artery for the flow of
nutrients, oxygen etc.) of an artery causes tapering of lumen of
the artery by declining its diameter. NO levels show a significant
relation with higher BMI and hypertension in coronary artery
disease. Many research have shown that adipose tissue contains
NO synthetase enzyme, and is thus an impending NO source.
Biological activity of Nitric Oxide provides clinicians with
additional therapeutic options in the treatment of cardiovascular
disease which will subordinate oxidative stress, a process which is
becoming gradually more standard as critical in the
pathophysiology of vascular disease.
Reactive Oxygen Species,Reactive Nitrogen Species and Redox Signaling
This document discusses reactive oxygen species, reactive nitrogen species, and redox signaling. It covers the following key points:
- Nitric oxide is an important signaling molecule produced through the oxidation of L-arginine by nitric oxide synthase. There are three NOS isoforms.
- Reactive oxygen species include superoxide and hydrogen peroxide. Superoxide is produced by NADPH oxidase and can be converted to hydrogen peroxide. These molecules are involved in cell signaling but can also cause damage.
- Hydrogen sulfide is another gasotransmitter that regulates various physiological processes through protein persulfidation.
- Reactive species can modify protein cysteine residues through oxidation
Mechanisms of nitric oxide synthase
"Mechanisms of nitric oxide synthase uncoupling in endotoxin-induced acute lung injury: role of asymmetric dimethylarginine" appeared in a 2010 issue of Vascular Pharmacology and summarized Stephen M. Black's research into acute lung injury/sepsis.
Role of nitric oxide in body
This document provides an overview of the role of nitric oxide (NO) in the body. It discusses NO's structure as a lipid-soluble gas that is synthesized from L-arginine by nitric oxide synthase (NOS) enzymes. The three main types of NOS - neuronal, endothelial, and inducible - are described. The roles of NO in various body systems like the nervous, circulatory, immune and digestive systems are summarized. NO functions as a neurotransmitter, vasodilator, and plays roles in platelet inhibition and host defense. Abnormal NO production can contribute to conditions like hypertension. NO donors and inhibitors that are used experimentally are also listed.
Neurobiological aspects-of-alzheimers-disease
Neurobiology of Alzheimer’s disease
Role of Acetyl choline
Amyloid-beta-mediated neurodegeneration
Amyloid beta accumulation
Amyloid cascade hypothesis
Microtubule-associated protein tau
Oxidative stress
ROS-mediated neuronal damage
The evolution of molecular hydrogen - A summary
Hydrogen shows potential as a novel medical therapy due to its antioxidant and anti-inflammatory properties. It can easily diffuse into tissues and organelles like mitochondria and nuclei. Studies show hydrogen reduces oxidative stress and improves conditions like diabetes, Alzheimer's, stroke, lung and heart disease. More research is still needed but hydrogen appears to be a promising and safe therapeutic approach for many human diseases involving oxidative stress.
Lesion por oxigeno
Perioperative Oxygen Toxicity
1) While oxygen is essential for life, in high concentrations it can produce reactive oxygen species that damage cells.
2) Hyperoxia (100% oxygen) is commonly used perioperatively to prolong the time to hypoxemia if apnea occurs, but can also cause atelectasis and impair lung function.
3) The optimal oxygen concentration balances the benefits of prolonging apnea time against the risks of oxygen toxicity and atelectasis, and 100% oxygen may not be necessary or beneficial in many cases.
Neurodegeneration: Factors Involved and Therapeutic Strategies
Neurodegenerative disorders are disorders of the nervous system which are characterized by a loss of neuronal structure and function. These changes lead to a loss of several abilities that include cognition and movement as observed in Alzheimer’s and Parkinson’s. Several factors like oxidative stress and protein misfolding have been found to play a vital role in the etiology of common neurological disorders. Whether these factors contribute to the progression of the disorders or are a consequence still remains elusive. Inspite of attempts to elucidate the molecular and pathological mechanisms of these pathways, many aspects still remain unclear. However, newer areas of therapeutic interventions like stem cell therapy and anti-oxidant therapy are now being explored as potential treatments. The aim of this review is to study the various factors that are associated with neurodegeneration along with recent therapeutic strategies that are being employed in an attempt to treat neurodegenerative disorders.
Talk 2008-meeting about NAD
NAD+ and NADH play roles in many important biological processes such as energy metabolism, mitochondrial function, calcium homeostasis, and gene expression. They have emerged as one of the most influential couples in life. Poly (ADP-ribose) polymerase 1 (PARP1) activation leads to NAD+ depletion, which mediates cell death. Intranasal administration of NAD+ can decrease ischemic brain injury by reducing PARP1-induced cell death and is a potential treatment for diseases involving PARP1.
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Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
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Seminario Biología Molecular
- 1. Jose David Rodriguez Henao Third semester Universidad Pontificia Polivariana
- 2. INTRODUCTION APOPTOSIS ● Programed death cell ● Damaged cells ● Need to keep sane the body https://concepto.de/apoptosis/
- 3. INTRODUCTION CypD cyclophilin d ● protein that binds ciclosporins ● located in the mitochondrial matrix ● acts as an important regulator of switching the mPTP opening
- 5. METHODS ● Transcription ● Cell culture
- 6. METHODS the basis and why they do this ● Western blot ● Immunofluorescence
- 8. RESULTADOS
- 9. DISCUSSIONS AUTHOR Huang et al WHAT AUTHOR SAYS “Previously, SO2 was considered to be a toxic gas and environmental pollutant. In recent years, it is shown that the SO2 can be endogenously synthesized by an enzymatic reaction catalyzed by AAT in cardiovascular tissues” ARE THE WRITER AGREE? - Endogenous SO2 exerts important cardiovascular effects. For example, the reduction of endogenous SO2 promotes the proliferation and migration of cardiac fibroblasts (Zhang et al., 2018). - Endogenous SO2 alleviates angiotensin II-induced myocardial hypertrophy and cardiomyocyte autophagy (Chen et al., 2016). - It was reported that the downregulated endogenous SO2/AAT pathway might be involved in the possible mechanisms underlying the myocardial injury. Liang et al found that the in vivo protective effect of SO2 on the myocardial injury was related to the increased myocardial antioxidant capacity (Liang et al., 2011).
- 10. 2 1 CONCLUSIONS SO2 and cardiomyocyte If we can go up the endogen production of SO2 in the cardiomyocytes we could prevent apoptosis and fall down the cardiac output that Is produced by the years, but we only do this with the implement of molecular biology to study and know the function of the mechanism and how to inhibit it without causing malformations Caspase 9 and apoptosis The inhibition of caspase 9 and CYPD its fundamental to reduces de apoptosis in cardiomyocytes and the only way to inhibit the caspase 9 is using models of molecular biology
- 11. APOPTOSIS IN CARDIOMYOCYTES USING SO2 USING ISO USING SO2 + ISO A big decrease of apoptosis in cardiomyocytes Apoptosis decrease but not much compared with only SO2 The apoptosis in cardiomyocytes increase plus the expression of caspase 9 The apoptosis in cardiomyocytes increase plus the expression of caspase 9