Peroxidation, lipid selenium, effect

This selenium-dependent enzyme [EC 1.11.1.9] catalyzes the reaction of two molecules of glutathione with hydrogen peroxide to produce glutathione disulfide and two water molecules. Hydrogen peroxide can be replaced by steroid and lipid hydroperoxides, albeit not as effectively (nevertheless, this enzyme is not identical with phospholipid-hydroperoxide glutathione peroxidase [EC 1.11.1.12]). However, the hydroperoxy products formed by the action of lipoxygenase [EC 1.13.11.12] are not substrates. 

Hyperoxia was found to encourage the accumulation of primary and end-products of lipid peroxidation together with a significant lowering of the vitamin E content of rat brain tissue [152]. The consequence of hyperoxia was epileptiform seizures, which were prevented by vitamin E or synthetic antioxidant pre-injection. Other workers [153] have found that protection against hyperoxia is directly related to the level of vitamin E or selenium supplementation. However, some [ 154] have indicated no beneficial effects for vitamin E in reducing oxygen toxicity. 

Yin, S., Jin, Y., and Kenji, Y. 1996. Effect of dietary vitamin B6 on selenium bioavailability. IV. Effect of dietary vitamin B6 on selenium bioavailability from different chemical forms and lipid peroxidation in rats. Weishung Yanjiu 25(5), 296-300. 

More direct evidence for a role of lipid peroxidation in the development of post-traumatic spinal-cord ischemia is obtained from studies that have examined the effect of intensive antioxidant dosing on the progressive decline in SCBF after contusion injury in cats [28,29]. In one experiment, cats were pretreated daily with high oral doses of D-a-tocopherol (1000IU) and selenium (50 pg) for 5 days prior to spinal contusion injury. In untreated cats, moderately severe spinal contusion injury resulted in a progressive decrease in SCBF from near-normal levels immediately after injury to 53.5% below the pre-injury level 4 hours later. 

Saunders, R.D., Dugan, L.L., Demediuk, P., Means, E.D., Horrocks, L.A. and Anderson, D.K. (1987) Effects of methylprednisolone and the combination of alpha tocopherol and selenium on arachidonic acid metabolism and lipid peroxidation in traumatized spinal cord tissue, J. Neurochem. 49, 24-31. 

Thus, in vitamin E deficiency, selenium has a beneficial effect in lowering the concentrations of alkylperoxyl radicals, and conversely, in selenium deficiency, vitamin E has a protective effect in reducing the radicals. When selenium is adequate, but vitamin E is deficient, tissues with low activity of glutathione peroxidase [e.g., the central nervous system and (rat) placenta] are especially susceptible to lipid peroxidation, whereas tissues with high activity of glutathione peroxidase are not. Conversely, with adequate vitamin E and inadequate selenium, membrane lipid peroxidation will be inhibited, but tissues with high peroxide production and low catalase activity will still be at risk from peroxidative damage, especially to sulfhydryl proteins. 

Jamall IS, Haidar D, Wadewitz AG. 1987. Effects of dietary selenium on lipid peroxidation, mitochondrial function and protein profiles in the heart of the myopathic Syrian golden hamster (BIO 14.6). Biochem Biophys Res Commun 144 815-820. 

Due to the function of GSH peroxidase in metabolizing lipid hydroperoxides, the nutritional status of selenium may determine cellular susceptibility to the effects of peroxidized Upid administered. By feeding 7% oxidized stripped corn oil (peroxide value lOOOmequiv./kg) in a diet adequate in selenium and vitamin E to weanling rats for 14 weeks, Vilas et al. (1976) have shown an increase in specific activity of GSH peroxidase... 

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