AIM: The present study explored the hepatoprotective role of zinc in lithium-induced hepatotoxicity. METHODS: Rats received either lithium treatment in diet at a dose level of 1.1 g/kg diet, zinc alone at a dose level of 227 mg/L in drinking water, and combined lithium plus zinc or drinking water alone for different time durations of 1, 2 and 4 months. This study explored the hepatic marker enzymes, antioxidant status and histopathological investigations in the liver of rats following different treatments. RESULTS: The activities of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and alkaline phosphatase were found to be elevated significantly following 2 and 4 months of lithium treatment. Lithium-treated rats showed a significant increase in the levels of lipid peroxidation and superoxide dismutase and a significant inhibition in the levels of reduced glutathione, catalase and glutathione-S-transferase, following 2 and 4 months of treatment. However, zinc co-administration revealed significant improvement in the altered activities of hepatic marker and antioxidant enzymes in comparison with lithium-treated animals. Lithium-treated rats also indicated drastic alterations in hepatic histoarchitecture and zinc co-administration resulted in improvement in the structure of hepatocytes. CONCLUSION: The present study suggests the protective potential of zinc in lithium-induced hepatotoxicity.
AIM: The present study explored the hepatoprotective role of zinc in lithium-induced hepatotoxicity. METHODS:Rats received either lithium treatment in diet at a dose level of 1.1 g/kg diet, zinc alone at a dose level of 227 mg/L in drinking water, and combined lithium plus zinc or drinking water alone for different time durations of 1, 2 and 4 months. This study explored the hepatic marker enzymes, antioxidant status and histopathological investigations in the liver of rats following different treatments. RESULTS: The activities of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and alkaline phosphatase were found to be elevated significantly following 2 and 4 months of lithium treatment. Lithium-treated rats showed a significant increase in the levels of lipid peroxidation and superoxide dismutase and a significant inhibition in the levels of reduced glutathione, catalase and glutathione-S-transferase, following 2 and 4 months of treatment. However, zinc co-administration revealed significant improvement in the altered activities of hepatic marker and antioxidant enzymes in comparison with lithium-treated animals. Lithium-treated rats also indicated drastic alterations in hepatic histoarchitecture and zinc co-administration resulted in improvement in the structure of hepatocytes. CONCLUSION: The present study suggests the protective potential of zinc in lithium-induced hepatotoxicity.
Authors: Małgorzata Kiełczykowska; Joanna Kocot; Jacek Kurzepa; Anna Lewandowska; Renata Żelazowska; Irena Musik Journal: Biol Trace Elem Res Date: 2014-03-28 Impact factor: 3.738
Authors: Andrey A Skalny; Alexey A Tinkov; Yulia S Medvedeva; Irina B Alchinova; Mikhail Yu Karganov; Olga P Ajsuvakova; Anatoly V Skalny; Alexandr A Nikonorov Journal: Interdiscip Toxicol Date: 2015-09