Lipid per oxidation and reactive oxygen species, antioxidants
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Lipid peroxidation is an auto-oxidation process that causes the production of reactive oxygen species and short-chain fatty acids from polyunsaturated fatty acids, leading to aging, atherosclerosis, inflammation, and cancer. Reactive oxygen species like hydrogen peroxide, hydroxyl radicals, and peroxyl radicals can damage cell membranes and mitochondria, causing fluidity changes in membranes and mitochondrial apoptosis. Both synthetic and natural antioxidants can prevent lipid peroxidation, with natural antioxidants including vitamin C, vitamin E, SOD, selenium, glutathione peroxidase, and catalase that act as chain-breaking or preventive antioxidants.
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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.
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Free radicals
Free radicals, especially reactive oxygen species like superoxide, hydroxyl, and perhydroxyl, can damage DNA, lipids, and proteins. This radical damage can lead to inheritable mutations, cancer, autoimmune diseases, and atherosclerosis. Sources of free radicals include ionizing radiation, transition metal ions, nitric oxide, the respiratory burst in immune cells, and mitochondrial electron transport. However, the body protects itself against radical damage through antioxidants like superoxide dismutase, catalase, glutathione peroxidase, vitamins C and E, and polyphenols; these antioxidants trap radicals in a stable form. At high concentrations, some antioxidants like vitamin C, vitamin E, and beta-carotene can also act
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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.
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Rajkumar new 2013 norma lpptm.0pdf
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Oxidative stress and periodontal disease- Dr Harshavardhan Patwal
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Free radicals are molecules with unpaired electrons that are highly reactive. They are produced through normal cellular metabolism and environmental exposures. Reactive oxygen species (ROS) include superoxide, hydrogen peroxide, and hydroxyl radicals. Lipid peroxidation occurs in three phases - initiation, propagation, and termination. ROS can damage lipids, proteins, carbohydrates, and nucleic acids. This contributes to diseases like cancer, cardiovascular disease, diabetes, and neurological disorders. Antioxidants help prevent and limit oxidative damage from free radicals. Enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase neutralize ROS.
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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.
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Oxidative stress occurs when there is an imbalance between free radicals and antioxidants in the body. Free radicals are highly reactive molecules that can damage cells by stealing electrons from them. Antioxidants help prevent this damage by donating electrons to free radicals without becoming destabilized themselves. Oxidative stress leads to many health issues like neurodegenerative diseases, cancer, heart disease, and inflammation. It can be reduced by avoiding unnecessary oxidative sources and increasing antioxidant intake through foods, supplements, and lifestyle habits.
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The document describes a study that exposed atherosclerosis-prone mice to different components of ambient ultrafine particles (UFP) near a freeway to determine if removing semi-volatile organic compounds from UFP would alter oxidative stress responses. Mice were exposed for 8 weeks to total UFP, denuded UFP, or particle-free organics. Oxidative stress biomarkers were then measured in serum. Results showed higher levels of lipid peroxidation in mice exposed to total UFP and particle-free organics, suggesting lipid modification due to semi-volatile organic compounds. This matched trends in plaque accumulation, indicating lipid modification by these compounds may accelerate plaque buildup by generating oxidized lipids that promote foam cell formation early in
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1. The document examines whether nitric oxide (NO) acts as an endogenous neurotoxin in the brain.
2. Experiments show that NMDA-induced neurotoxicity in hippocampal slice cultures is independent of NO, and that concentrations of 10 μM NO are required for toxicity - much higher than levels released by the slices.
3. NO is rapidly inactivated by cerebellar cells and brain homogenates in vitro, likely through reaction with lipid peroxides, preventing it from reaching toxic levels. Lipid peroxidation may influence physiologically relevant NO levels in vivo.
Oxidative stress and lipid peroxidation may be risk factors for metabolic car...
Metabolic cardiovascular syndrome is a combination of factors that augment a person's risk
for heart disease, diabetes and stroke. Features of which are obesity, insulin resistance, dyslipidemia [including
increased triglycerides and decreased HDL], impaired glucose tolerance, and hypertension. Obesity has the
central role in this syndrome. The prevalence of obesity in children has increased dramatically over the last 20
years, leading to higher health risk associated with complications such as type 2 diabetes, high blood pressure
and cardiovascular disease.
Aim: The aim of this study is to search for a possible relationship between oxidative stress (as interpreted by
lipid peroxidation) and risk factors for metabolic cardiovascular syndrome in obese prepubertal children, in an
attempt to overcome the increased health risk associated with obesity in children.
Subjects and methods: Eighty prepubertal children aged (5-11) years were enrolled in this study. According to
their body mass index (BMI) they were divided into two groups:
1. Obese group of which 50 subjects were selected
2. Lean group consisted 30 aged matched subjects.
Random cholesterol, high density lipoproteins (HDL) and malondialdehyde were measured in sera
spectrophotometricaly
Results: Both cholesterol and MDA serum concentrations were significantly higher in obese children than leans
( P < 0.000 ). However HDL was lower in obese children and no significant value was found when compared to
leans.
Conclusion: Obese children exhibited hypercholesterolemia and increased lipid peroxidation. This might be a
potential risk of hypertension and cardiovascular diseases especially when HDL decreases as was found. These
findings might shed a light on a possible relationship between oxidative stress metabolic cardiovascular
syndrome. A case where interventional measures might be necessary to prevent excessive weight gain during
childhood.
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Antioxidant potentials of tannic acid on lipid peroxidation induced by severa...
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Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them. ROS play a role in many chronic diseases including Alzheimer's disease (AD). The document discusses the sources and reactivity of oxygen free radicals like superoxide, hydrogen peroxide, and hydroxyl radicals that are generated in cells. It also describes how cells protect themselves against oxidants through enzymatic antioxidants like superoxide dismutase, catalase, and glutathione peroxidase. The document then focuses on AD, stating that oxidative stress is thought to play a central role in its pathogenesis by leading to neuronal dysfunction and cell death. Elevated peripheral markers of oxidative stress in AD
Hypoxic regulation of lipid metabolism
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Oxidative stress and lipid peroxidation may be risk factors for metabolic car...
Oxidative stress and lipid peroxidation may be risk factors for metabolic car...
Dr. Jerry Shurson - Assessing Lipid Quality And Effects On Swine Health And P...
Dr. Jerry Shurson - Assessing Lipid Quality And Effects On Swine Health And P...
Antioxidant potentials of tannic acid on lipid peroxidation induced by severa...
Antioxidant potentials of tannic acid on lipid peroxidation induced by severa...
Reactive Oxygen Species (ROS) an Activator of Apoptosis and Autophagy
Reactive Oxygen Species (ROS) an Activator of Apoptosis and Autophagy
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- 1. Lipid peroxidation 717 harper Fenton771… Haber Respiratory burst
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