Tissue lipid peroxidation may be triggered by increased formation of bilirubin in vivo.

Following the administration of phenylhydrazine, cadmium chloride and ethanol to rats there was a marked increase in the concentration of liver lipid peroxides and a sharp decline in GSH levels. The oxidative stress generated by the action of these toxic compounds led to the induction of liver heme oxygenase, which exhibited a 3-fold increase in activity over the control value. Patients with various forms of liver disorders showed increased levels of plasma lipid peroxides as well as hyperbilirubinemia. In view of the known ability of bilirubin to cause lipid peroxidation in illuminated erythrocyte membranes, the results of the present paper suggest that in severely impaired liver, as in some liver diseases, lipid peroxides may be also produced by a mechanism involving heme oxygenase.