Abstract
When sodium copper chlorophyllin (Cu-Chl-Na) was given intraperitoneally to rats (two doses of 50 or 100mg/kg at 18 and 2h 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 reduced nicotinamide adenine dinucleotide phosphate (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 ca. 633nm, which is characteristic of the copper complexes of chlorophyll derivatives. These findings suggest that the administered Cu-Chl-Na or substance (s) derived from Cu-Chl-Na is 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.
