Microsomal Fatty Acid Composition and Ca2+ Uptake Modifications Induced by Sod Depletion in Rat Liver
The hepatic metabolism of certain substances may result in the release of reactive free radicals capable, among other damaging effects, of initiating lipid peroxidation in biological membranes. This effect, in turn, can modify different cell functions.1,2 Animal cells have developed several defense mechanisms against oxygen toxicity, both enzymatic and non-enzymatic. Superoxide dismutase, catalase and glutathione peroxidase scavenge initiating reactive species of oxygen; glutathione, α-tocopherol, and ascorbic acid represent species of endogenous antioxidants. The impairment of defense systems should result in the increase of endogenous lipid peroxidation, as in the case of vitamin E and selenium deficiency.3,4 Moreover elevation of intracellular superoxide dismutase correlates with increased resistence toward oxygen toxicity,5 while SOD diminution6 favours the increase of intra-cellular-O2 - production. The aim of this work is to investigate if a diminution of SOD induces an oxidative stress and influences lipid composition and function of rat liver microsomal membranes. For this purpose, we have treated rats with a copper-deficient diet that inhibits Cu-Zn-SOD but does not significantly affect other important enzymes, such as the cytochrome oxidase. During the treatment we have measured hepatic SOD level, fatty acid composition, in vitro lipid peroxidation and Ca2+ uptake of endoplasmic reticulum membranes.
KeywordsGlutathione Ozone Selenium Ketone NADPH
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