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Role of free Radicals

Liver Diseases

The liver is the largest organ in the body and has may different functions. The liver receives, processes and stores materials absorbed from the digestive tract, e.g. amino acids, carbohydrates, and fatty acids. They were also releases the metabolites on demand. It synthesizes a number of compounds including albumin, globulin, clotting factors, transport proteins and bile and is involved in the detoxification of compounds and catabolism of hormones. The liver has a diverse range of important functions which can cause major physiological imbalance in the body, resulting in different pathological conditions. Liver disease has long been associated with alcoholics as it is the major organ concerned with the removal of excess ethanol. Elevated levels of short-chain fatty acids, increased iron uptake by the hepatocytes, increased production of hydrogen peroxide and free radicals, all contribute to the increased per-oxidation of lipids in alcoholic liver. This can lead to liver dysfunction and further complications. Hepatic failure is characterized by an increase in the production of ammonia, glutamine and alpha-ketoglutarate in the brain and CSF. Altered drug metabolism can cause production of hepatotoxic components during liver damage, which may lead to many nutritional and metabolic disorders. Hypoalbuminemia has been reported in many liver disease patients, which serves to reduce the overall antioxidant protection against disease development. Liver disease can also result in ineffective bile production resulting in impaired absorption of fatty acids, which can lead to a deficiency of vitamins A, D, E and K. Metabolism of ethanol in the liver results in the production of acetaldehyde which can cause hyperlactacidemia, hyperuricemia, ketosis and purine degradation. Ethanol toxicity has been associated with increased production of free ROS and free radicals and a reduction in a number of dietary antioxidants.

References
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  2. Yabe Y. Kobayashi N. Nishihashi T. Takahashi R. Nishikawa M. Takakura Y. Hashida M. Prevention of neutrophil-mediated hepatic ischemia/reperfusion injury by superoxide dismutase and catalase derivatives. Journal of Pharmacology & Experimental Therapeutics. 298(3):894-9, 2001.

  3. Trotti R. Carratelli M. Barbieri M. Micieli G. Bosone D. Rondanelli M. Bo P. Oxidative stress and a thrombophilic condition in alcoholics without severe liver disease. Haematologica. 86(1):85-91, 2001.

  4. Gutierrez-Ruiz MC. Gomez Quiroz LE. Hernandez E. Bucio L. Souza V. Llorente L. Kershenobich D. Cytokine response and oxidative stress produced by ethanol, acetaldehyde and endotoxin treatment in HepG2 cells. Israel Medical Association Journal: Imaj. 3(2):131-6, 2001.

  5. Degoul F. Sutton A. Mansouri A. Cepanec C. Degott C. Fromenty B. Beaugrand M. Valla D. Pessayre D. Homozygosity for alanine in the mitochondrial targeting sequence of superoxide dismutase and risk for severe alcoholic liver disease. Gastroenterology. 120(6):1468-74, 2001.

  6. Alric L. Orfila C. Carrere N. Beraud M. Carrera G. Lepert JC. Duffaut M. Pipy B. Vinel JP. Reactive oxygen intermediates and eicosanoid production by kupffer cells and infiltrated macrophages in acute and chronic liver injury induced in rats by CCl4. Inflammation Research. 49(12):700-7, 2000.

  7. Valgimigli L. Valgimigli M. Gaiani S. Pedulli GF. Bolondi L. Measurement of oxidative stress in human liver by EPR spin-probe technique. Free Radical Research. 33(2):167-78, 2000.

  8. Kono H. Rusyn I. Yin M. Gabele E. Yamashina S. Dikalova A. Kadiiska MB. Connor HD. Mason RP. Segal BH. Bradford BU. Holland SM. Thurman RG. NADPH oxidase-derived free radicals are key oxidants in alcohol-induced liver disease. Journal of Clinical Investigation. 106(7):867-72, 2000.

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