VITAMIN-E INHIBITS FISH OIL-INDUCED HYPERLIPIDEMIA AND TISSUE LIPID-PEROXIDATION IN HAMSTERS

Previous research has linked hyperlipidemia with increased serum conce ntrations of lipid peroxidation products; however, a specific associat ion between diet-induced oxidative stress and hyperlipidemia has not b een studied. In the present study, the relationship between tissue lip id peroxidation and hyperlipidemia induced by ingestion of fish oil wa s examined. In Experiment 1, male Golden Syrian hamsters were fed semi purified diets composed of 1.6 wt% safflower oil plus 15.0 wt% of eith er butterfat (BF), safflower oil (SAFF), or high-cholesterol menhaden oil [MHO(H-CHOL)] semipurified diets for 27 d. The cholesterol content s of the diets were adjusted to 0.088%. The MHO(H-CHOL)-fed hamsters e xhibited higher serum concentrations of total cholesterol, triglycerid es, apolipoprotein B, and lipid peroxides when compared to the BF and SAFF diet groups. In a further study (Experiment 2), hamsters were fed for 27 d three dietary treatments: (i) MHO(H-CHOL) with no vitamin E content; (ii) a low-cholesterol menhaden oil containing high concentra tions of vitamin E (2.5 mg tocopherol/g oil or dietary concentrations of 375 mg/kg) [MHO(L-CHOL) + E]; and (iii) the MHO(L-CHOL + E) with ad ded cholesterol (595 mg/kg) [MHO(L-CHOL)+ CHOL + E] to match the chole sterol content of the MHO(H-CHOL). The MHO(L-CHOL) + E and MHO(L-CHOL) + CHOL + E diet groups showed lower concentrations of serum cholester ol, triglycerides, and hepatic lipid peroxides than the MHO(H-CHOL)-tr eated group. Moreover, in contrast to the hypercholesterolemia caused by the MHO(H-CHOL) feeding, the MHO(L-CHOL) + E and MHO(L-CHOL) + CHOL + E diets did not show a serum cholesterol-elevating action. This stu dy supports the hypothesis that oxidative stress in the Syrian hamster could play a causal role in dietary-induced hyperlipidemia which can be inhibited by high vitamin E intake.