Parisa Hasanein1, Masumeh Ghafari-Vahed1, Iraj Khodadadi2. 1. a Department of Biology , School of Basic Sciences, Bu-Ali Sina University , Hamedan , Iran. 2. b Department of Medical Biochemistry , School of Medicine, Hamedan University of Medical Sciences , Iran.
Abstract
OBJECTIVES: Liver is considered a target organ affected by lead toxicity. Oxidative stress is among the mechanisms involved in liver damage. Here we investigated the effects of the natural alkaloid berberine on oxidative stress and hepatotoxicity induced by lead in rats. METHODS: Animals received an aqueous solution of lead acetate (500 mg Pb/l in the drinking water) and/or daily oral gavage of berberine (50 mg/kg) for 8 weeks. Rats were then weighed and used for the biochemical, molecular, and histological evaluations. RESULTS: Lead-induced oxidative stress, shown by increasing lipid peroxidation along with a concomitant decrease in hepatic levels of thiol groups, total antioxidant capacity, the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, and reduced versus oxidized glutathione ratio. Berberine corrected all the disturbances in oxidative stress markers induced by lead administration. Berberine also prevented the elevated levels of enzymes (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) and the decrease in body weight and albumin. The protective effects of berberine were comparable with silymarin. Furthermore, berberine attenuated liver damage, shown by decreased necrosis and inflammatory cell infiltration. DISCUSSION: Berberine represents a potential therapeutic option against lead-induced hepatotoxicity through inhibiting lipid peroxidation and enhancing antioxidant defenses. CONCLUSION: Berberine exerted protective effects on lead-induced oxidative stress and hepatotoxicity in rats.
OBJECTIVES: Liver is considered a target organ affected by lead toxicity. Oxidative stress is among the mechanisms involved in liver damage. Here we investigated the effects of the natural alkaloidberberine on oxidative stress and hepatotoxicity induced by lead in rats. METHODS: Animals received an aqueous solution of lead acetate (500 mg Pb/l in the drinking water) and/or daily oral gavage of berberine (50 mg/kg) for 8 weeks. Rats were then weighed and used for the biochemical, molecular, and histological evaluations. RESULTS: Lead-induced oxidative stress, shown by increasing lipid peroxidation along with a concomitant decrease in hepatic levels of thiol groups, total antioxidant capacity, the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione-S-transferase, and reduced versus oxidized glutathione ratio. Berberine corrected all the disturbances in oxidative stress markers induced by lead administration. Berberine also prevented the elevated levels of enzymes (alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase) and the decrease in body weight and albumin. The protective effects of berberine were comparable with silymarin. Furthermore, berberineattenuated liver damage, shown by decreased necrosis and inflammatory cell infiltration. DISCUSSION: Berberine represents a potential therapeutic option against lead-induced hepatotoxicity through inhibiting lipid peroxidation and enhancing antioxidant defenses. CONCLUSION:Berberine exerted protective effects on lead-induced oxidative stress and hepatotoxicity in rats.
Authors: Aziza A El-Nekeety; Ahmed A El-Kady; Mahmoud S Soliman; Nabila S Hassan; Mosaad A Abdel-Wahhab Journal: Food Chem Toxicol Date: 2009-06-14 Impact factor: 6.023
Authors: Pedro Silvino Pereira; Adrielle Rodrigues Costa; Thalyta Julyanne Silva de Oliveira; Carlos Vinícius Barros Oliveira; Maria do Carmo Alves de Lima; Jamerson Ferreira de Oliveira; Bonglee Kim; Henrique D M Coutinho; Antonia Eliene Duarte; Jean Paul Kamdem; Teresinha Gonçalves da Silva Journal: Antioxidants (Basel) Date: 2022-02-18