Abstract
Summary
Prior administration of the lipid antioxidant, DPPD, to rats which subsequently received CC14 orally prevented the CCU-induced depression of plasma triglyc-eride concentration and maintained a normal hepatic release of triglyceride into the plasma compartment, as assessed by the post-Triton hypertriglyceridemic response. Administration of DPPD also prevented the CCl4-induced impairment in the hepatic removal of BSP. These findings, coupled with prior observation of inhibition of CCU-induced hepatic fatty infiltration, hepatic necrosis, and lethality, indicate that antioxidants can modify the degree and nature of hepatic cell injury resulting from exposure to certain toxic substances.
Get full access to this article
View all access options for this article.
