Morphometric cytochemistry of diminution of catalase-containing peroxisomes in copper-loaded liver

Abstract

The density of hepatocellular catalase-containing peroxisomes was quantified, utilizing a computer-aided image analysing technique, on 1-micron thick diaminobenzidine-stained sections. Hepatic copper accumulation following intraperitoneal injection of cupric chloride resulted in a dose-dependent reduction in the density of catalase-containing peroxisomes. A significant correlation between the density of peroxisomes and the activity of hepatic catalase indicated that computer-aided image analysis of peroxisomes stained by the diaminobenzidine technique provided a useful estimate of catalase activity in liver injured by copper. Slight treatment-related differences in the mean diameter of peroxisomes were detected in high-dose but not low-dose rats.

Inhibition of Copper-Associated Erythrocyte Ghost Membrane Lipid Peroxidation by Hepatic Cytosolic Low Molecular Weight Proteins

“…The mechanism of copper toxicity involves the formation of copper-induced organellar lesions (26), inactivation ofproteins by the binding offree copper to sulfhydryl groups (42), and copper-catalyzed formation of toxic free radicals (1,2 1 , 30,4 1 , 43). Free radical damage may occur as the result of both inactivation of proteins (20) and initiation of lipid peroxidation (9, 13, 25, 43, resulting in biomembrane damage and cell death.…”