Free Radical (molecules that have an unpaired electron in its outer shell unstable and highly reactive molecule) and Reactive Oxygen Species (produced as a normal byproduct of ATP production in the mitochondria--ROS) Excess ROS and calcium overload of the mitochondria is also caused by cardiac ischemia and reperfusion injury ROS is also produced by the absorption of high energy sources such as radiation or UV light. ROS have a role in the development of heart disease, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Antioxidants= bodies’ defense against ROS, by providing the missing electron. Can be exogenous Unstable and highly reactive molecule that has an unpaired electron in its outer shell. In attempts to stabilize itself it will steal an electron from another molecule or give up an electron to another molecule, creating other free radicals that can cause cellular injury and eventual death. ROS free radical that
6 or endogenous. overwhelm the mitochondria and exhaust intracellular antioxidants, causing cellular injury, aging and disease. ROS can cause destruction of lipids causing cell membrane damage and increased permeability of cell membrane, damage proteins which maintain ion pumps and cellular transport, fragment DNA and causes less protein synthesis, cause chromatin destruction, and damage mitochondria. Ethanol Metabolized to acetaldehyde in cytoplasm of the cell Increases the NADH/NAD+ ration in the liver which cause… Pyruvate to be changed to lactic acid and causes lactic acidosis Oxaloacetate to be converted to malate prevents gluconeogenesis and leads to fasting hypoglycemia Glyceraldehyde-3-phosphate (used in glycolysis) is converted to glycerol 3- phosphate which combines with fatty acids and forms triglycerides, that leads to elevated triglyceride levels and deposition of triglycerides in the liver known as hepatosteatosis Decrease the citric acid cycle production of NADH which leads to the utilization of Acetyl-CoA for ketogenesis (causing Ketoacidosis) and lipogenesis (causing hepatosteatosis) Ethanol is a commonly abused substance which ahs adverse effects on the liver and causes nutritional disorders. Ethanol is a CNS depressant and therefore acutely depresses motor and intellectual abilities. Acute effects on the liver include: inflammation, fatty infiltration, hepatomegaly, acute liver necrosis and suppressed fatty acid oxidation. Pathological effects of chronic ethanol use are seen mainly in the liver and stomach and are thought to be due to the generation of free radicals. Liver failure is the irreversible effect of chronic ethanol abuse. c. Evaluate the process of necrosis, infarct, and apoptosis and describe the implications for clinical practice.
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- Fall '15
- Apoptosis, Module 1, cells, cellular injury