The role of nutritional factors in the prevention of peroxidative damage to tissues.

The multi-level defence system present in vertebrate cells to protect against chain reactions initiated by free radicals (mainly toxic metabolites of oxygen) is outlined. It comprises superoxide dismutases (Cu-Zn and Mn dependent), glutathione peroxidase (Se dependent), vitamin E and glutathione S-transferase.The protective role of superoxide dismutase (SOD) was demonstrated by studies on trout (Salmo gairdneri) retina (Desrochers and Hoffert 1983). This tissue is subject to very high O2 tensions but has a high resistance to O2 toxicity that is dependent on a high dismutating capacity. The activities of both the cytosolic Cu-Zn SOD and the mitochondrial Mn SOD in the liver of rainbow trout were significantly altered in response to changes in dietary intake of these minerals.Deficiency of Se did not affect the growth rate of rainbow trout but led to greatly reduced activities of hepatic and plasma glutathione (GSH) peroxidase. There was no evidence of a Se-independent GSH peroxidase activity. In rainbow trout depleted of Se there was a compensatory increase in hepatic GSH S-transferase activity. This enzyme in conjunction with GSH has been shown to inhibit lipid peroxidation in the Festimulated microsomal systemin vitro. A dietary synergism between vitamin E and Se in rainbow trout has been demonstrated.The vitamin E requirement of rainbow trout is related to the polyunsaturated fatty acid (PUFA) content of the diet. The molar ratio PUFA: vitamin E in rainbow trout tissues is lower than that in rats. Time course studies on the uptake of orally administered vitamin E showed rapid incorporation into biomembranes; few differences between normal and vitamin E deficient fish were evident. The ester form of vitamin E was more slowly assimilated than the alcohol.