Effect of sodium copper chlorophyllin on lipid peroxidation. VI. Effect of its administration on mitochondrial and microsomal lipid peroxidation in rat liver.

Abstract

When sodium copper chlorophyllin (Cu-Chl-Na) was given i.p. to rats (2 doses of 50 or 100 mg/kg at 18 and 2 h prior to sacrifice), the ascorbic acid-dependent lipid peroxidation in both mitochondria and microsomes of the liver markedly decreased. The microsomal lipid peroxidation induced by NADPH was also depressed by the treatment with Cu-Chl-Na. In addition, the soluble fraction of liver in injected animals showed an inhibition of the ascorbic acid- and NADPH-stimulated lipid peroxidation in hepatic microsomes from untreated rats. The absorption spectrum of each subcellular fraction in liver from Cu-Chl-Na-treated rats showed a red absorption band with a peak at .apprx. 633 nm, which is characteristic of the Cu complexes of chlorophyll derivatives. The administered Cu-Chl-Na or substance(s) derived from Cu-Chl-Na is probably taken into the liver and distributed among the mitochondria, microsomes and soluble fraction in an active form functioning as an antioxidant. Subsequently, a single injection of Cu-Chl-Na was observed to prevent effectively the impairment of hepatic microsomal functions (as indicated by the depression of glucose-6-phosphatase and drug-metabolizing enzyme system) resulting from ascorbic acid-induced lipid peroxidation.