Influence of dietary antioxidants on polychlorinated biphenyls (PCB)-induced hepatic lipid peroxide formation and vitamin A reduction in rats.

Abstract

This paper describes experiments designed to characterize the effect of dietary antioxidants on lipid peroxide formation and vitamin A reduction in the liver of rats fed on diets containing polychlorinated biphenyls (PCB). Rats were given 0.025% PCB diets supplemented with dietary antioxidants, for 2 weeks. The antioxidants used were as follows: 10mg% (basal and usual level), 50mg% and 100 mg% of vitamin E, and 50mg% of DPPD and tinoridine respectively. A marked liver enlargement and a significant increase of total liver lipid content were observed in the PCB-fed groups irrespective of the levels of vitamin E and kinds of antioxidants, suggesting that antioxidants were ineffective in preventing the development of fatty liver. Endogeneous lipid peroxide contents in the liver of rats receiving the diets containing 10 mg% vitamin E, DPPD, and tinoridine with PCB increased significantly, whereas no increase was found with the 50 and 100 mg % vitamin E diets with PCB. Hepatic glutathione peroxidase activity was unaffected by PCB and dietary antioxidants. No increase in hepatic vitamin E content occurred in the PCB groups with the addition of 10mg% vitamin E, DPPD, and tinoridine. However, dietary supplementation of vitamin E at higher levels caused an elevation of hepatic vitamin E content and a further increase was observed on the addition of PCB. These results suggest that a sufficiently high level of vitamin E suppresses the increment of the endogeneous lipid peroxide content in the liver of rats fed PCB. On the other hand, the administration of PCB to rats resulted in a significant decrease in hepatic vitamin A content regardless of the levels of vitamin E and kinds of dietary antioxidants. The antioxidants used in this experiment failed to suppress the hepatic vitamin A reduction caused by PCB administration. In addition, an absence of a significant difference in hepatic vitamin A contents among PCB-fed groups was observed. This suggests that the hepatic vitamin A level was independent of PCB-induced lipid peroxidation. Thus lipid peroxidation probably did not mediate the hepatic vitamin A reduction caused by PCB, especially in vivo.