Abstract
ABSTRACT: We investigated the role of lipid peroxidation as the mechanism mediating copper toxicity in isolated rat hepatocytes and the modulating effect of vitamin E. Hepatocytes, isolated from rats fed diets containing deficient (E—), sufficient (E+), and excess (E++) amounts of vitamin E, were incubated with CuCl2 (0-2400 μM) for 150 min. Dose and time-dependent decreases in hepatocyte viability (determined by trypan blue exclusion and lactate dehydrogenase release) due to copper toxicity correlated with production of malonyldialdehyde in E - and E+ hepatocytes. However, malonyldialdehyde generation did not accompany copper toxicity in E++ cells. Copper toxicity was enhanced in E— compared to E+ and E++ hepatocytes as assessed by cell viability studies and ultrastructural plasma membrane bleb formation. In vitro vitamin E repletion of E— hepatocytes restored resistance to copper and decreased malonyldialdehyde production proportionately. Thus vitamin E deficiency appeared to increase the susceptibility of hepatocytes to copper toxicity. We conclude that lipid peroxidation may not be the mechanism by which copper is toxic to isolated hepatocytes but that the site of injury may be thiol-rich cellular proteins.
Similar content being viewed by others
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Sokol, R., Devereaux, M., Traber, M. et al. Copper Toxicity and Lipid Peroxidation in Isolated Rat Hepatocytes: Effect of Vitamin E. Pediatr Res 25, 55–62 (1989). https://doi.org/10.1203/00006450-198901000-00014
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1203/00006450-198901000-00014
This article is cited by
-
The Protective Roles of Selenium on Hepatic Tissue Ultrastructure and Mitochondrial Antioxidant Capacity in Copper-Overloaded Rats
Biological Trace Element Research (2015)
-
The Effects of Copper Sulfate on Liver Histology and Biochemical Parameters of Term Ross Broiler Chicks
Biological Trace Element Research (2010)