On termination of a 56-day feeding trial, the effect of dietary oxidized oil and all-rac-α-tocopheryl acetate on fatty acid and α-tocopherol status of juvenile African catfish (Clarias gariepinusj muscle and liver was investigated. Clarias of mean initial weight 15·8 (s.e. 0·29) g were given food at -proportionately 0·03 body weight per day on diets of two oxidative states (fresh or oxidized) at two levels of supplemental α-tocopheryl acetate (20 or 100 mg/kg dry matter).

As well as having a significant detrimental effect on final body weight (P < 0·001), oxidation of the dietary lipid source was responsible for decreasing muscle but not hepatic polyunsaturated fatty acids (PUTAs). Liver tissue was suspected of actively synthesizing longer chain PUT As in response to consumption of oxidized oils, as indicated by decreases in the proportions of linoleate (18:2 n-6) and linolenate (18:3 n-3) and the increased abundance of eicosatetraenoic acid (20:4 n-6, arachidonate) and docosahexaenoic acid (22: 6 n-3, DHA). This phenomenon has not been described in fish nutrition and therefore possible mechanisms are discussed. Additionally, oxidized oils in catfish diets caused significant depletion of a-tocopherol from both muscle and liver (P < 0·05).

Modulation of the effects of oxidized lipids was achieved at the higher dietary tocopherol concentration. Appearance of an unknown aliphatic compound (equivalent chain length (ECL) = 13·1), believed to be a product of lipid peroxidation, demonstrated that catfish given rancid/low-tocopherol diets had been subjected to heightened oxidative nutritional stress. Values obtained for this peak were significantly correlated with dietary regime (P < 0·02), Once more, dietary α-tocopheryl acetate moderated this effect. It was concluded that elevated inclusion of all-rac-α-tocopheryl acetate into diets for African catfish could abrogate the effects of oxidized dietary lipids on muscle and liver fatty acids and α-tocopherol.