Written Paper. Beyer, A. Erdmann, R. Lookup at Google Scholar. Peroxisomal multifunctional beta-oxidation protein of Saccharomyces cerevisiae: molecular analysis of the fox2 gene and gene product. Hiltunen, J.

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Hepatocyte oxidant stress and alcoholic liver disease. Conde de la Rosa, H. Moshage 1 y N. Palabras clave: Apoptosis. Muerte celular. Acute and chronic alcohol consumption increases the production of reactive oxygen species ROS , and enhances lipid peroxidation of lipids, proteins, and DNA. The mechanism by which alcohol causes cell injury is still not clear but a major role for ROS and lipid peroxidation-end products is considered.

Many pathways have been suggested to play a role on how ethanol induces a state of "oxidative stress", including redox-state changes, acetaldehyde production, damage to mitochondria, membrane injury, apoptosis, ethanol-induced hypoxia, effects on the immune system and altered cytokine production, increased endotoxin levels and activation of Kupffer cells, mobilization of iron, modulation of the antioxidant defense, particularly mitochondrial glutathione GSH , one electron oxidation of ethanol to 1-hydroxy-ethyl radical, and induction of CYP2E1.

These pathways are not exclusive of one another and it is likely that several, indeed many, systems contribute to the ability of ethanol to induce a state of oxidative stress. Key words: Apoptosis. Cell death. Alcoholic liver disease. Reactive oxygen species. Algunas de estas especies por ejemplo, O 2. En condiciones normales, el O 2. Genera O 2. Las tres isoformas dismutan el O 2. Los hepatocitos expresan Fas CD95 pero no ligando Fas.

La familia de la PI3-cinasa es una superfamilia que comprende tres clases distintas de enzimas vinculadas con la supervivencia celular. Se han descrito tres isoformas distintas de la HO Tumour necrosis factor related apoptosis inducing ligand TRAIL induces hepatic steatosis in viral hepatitis and after alcohol intake.

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Diphenyleneiodonium sulfate, an NADPH oxidase inhibitor, prevents early alcohol-induced liver injury in the rat. Free Radic Biol Med ; 33 3 : Marked differences in the efficacy of post-insult gene therapy with catalase versus glutathione peroxidase. Brain Res ; 1 : Hepatic mitochondrial glutathione: Transport and role in disease and toxicity. Toxicol Appl Pharmacol ; 3 : Nieto N.


Beta oxidation

In biochemistry and metabolism , beta-oxidation is the catabolic process by which fatty acid molecules are broken down [1] in the cytosol in prokaryotes and in the mitochondria in eukaryotes to generate acetyl-CoA , which enters the citric acid cycle , and NADH and FADH 2 , which are co-enzymes used in the electron transport chain. It is named as such because the beta carbon of the fatty acid undergoes oxidation to a carbonyl group. Beta-oxidation is primarily facilitated by the mitochondrial trifunctional protein , an enzyme complex associated with the inner mitochondrial membrane , although very long chain fatty acids are oxidized in peroxisomes. Free fatty acids cannot penetrate any biological membrane due to their negative charge. Free fatty acids must cross the cell membrane through specific transport proteins , such as the SLC27 family fatty acid transport protein. Once the fatty acid is inside the mitochondrial matrix , beta-oxidation occurs by cleaving two carbons every cycle to form acetyl-CoA. The process consists of 4 steps.





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