Metabolic and morphological disorientations in the liver and skeletal muscle of mice exposed to hexavalent chromium

Abstract

Chromium exposure (10 mg/kg b.w/day for 30 days) produced hypoglycaemia in Swiss albino mice associated with increased glycogenolytic activity of hepatic and muscular tissue and suppressed glycolytic activity of the liver. Lactate dehydrogenase activity was decreased in hepatic tissue following exposure to chromium. Chromium significantly inhibited the activities of succinate dehydrogenase and NADH dehydrogenase in all the studied tissues. Moreover, suppressed malate dehydrogenase activity in chromium stressed muscle indicates less energy supply to that tissue, whereas its increased activity may aid substrates for gluconeogenesis in the liver. Chromium caused marked alteration in the liver and muscle protein contents and increased free amino acid nitrogen level. Proteolytic enzyme activities like trypsin, cathepsin and pronase were also significantly altered. Additionally, the transaminase enzyme activities were elevated in all the tissues after chromium exposure. A compensatory mechanism was initiated by inducing fatty acid synthase activity in hepatic tissue. The lipogenesis was enhanced in the liver which might involve the isocitrate dehydrogenase activity as well as overproduction of cholesterol and triglycerides. In response to these, the reverse transport of cholesterol from the blood to the liver was hampered due to less production of HDL cholesterol in chromium toxicity. Histopathological changes in the liver showed steatosis along with alteration in radiating pattern of hepatic cells in chromium treated mice. Additionally, skeletal muscle fibre degeneration was also evident. Over accumulation of chromium was noted in the studied tissues after chromium treatment at the present dose and duration. The study suggests potential threatening effect of hexavalent chromium on the liver and skeletal muscle metabolism.