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抗坏血酸可对抗砷诱导的小鼠肝脏氧化应激。

Ascorbic acid combats arsenic-induced oxidative stress in mice liver.

作者信息

Banerjee Pathikrit, Bhattacharyya Soumya Sundar, Bhattacharjee Nandini, Pathak Surajit, Boujedaini Naoual, Belon Philippe, Khuda-Bukhsh Anisur Rahman

机构信息

Department of Zoology, University of Kalyani, Kalyani-741235, West Bengal, India.

出版信息

Ecotoxicol Environ Saf. 2009 Feb;72(2):639-49. doi: 10.1016/j.ecoenv.2008.07.005. Epub 2008 Aug 19.

DOI:10.1016/j.ecoenv.2008.07.005
PMID:18715643
Abstract

Repeated injections of arsenic trioxide induced oxidative stress and hepatotoxicity in mice as revealed from elevated levels of glutamate oxaloacetate transaminases, glutamate pyruvate transaminases, acid and alkaline phosphatases, lipid peroxidation along with reduction of superoxide dismutase, catalase, reduced glutathione content, glutathione reductase and succinate dehydrogenase activities. The present investigation was undertaken to test whether simultaneous feeding of vitamin C can combat hepatotoxicity in arsenic intoxicated mice. Hepatoprotective potential of vitamin C was indicated by its ability to restore GSH, SOD, CAT, AcP, AlkP and GRD levels towards near normal. Electron microscopic studies further supported the biochemical findings confirming the hepatoprotective potential of ascorbic acid. Besides, cytogenetical endpoints (chromosome aberrations, micronuclei, mitotic index and sperm head anomaly) were also analyzed. Administration of vitamin C alone did not show any sign of toxicity of its own. Based on the present findings, ascorbic acid appears to have protective effects against arsenic toxicity and oxidative stress.

摘要

重复注射三氧化二砷可诱导小鼠产生氧化应激和肝毒性,这可从谷氨酸草酰乙酸转氨酶、谷氨酸丙酮酸转氨酶、酸性和碱性磷酸酶水平升高、脂质过氧化以及超氧化物歧化酶、过氧化氢酶、还原型谷胱甘肽含量、谷胱甘肽还原酶和琥珀酸脱氢酶活性降低中看出。本研究旨在测试同时投喂维生素C是否能对抗砷中毒小鼠的肝毒性。维生素C的肝保护潜力体现在其能将谷胱甘肽、超氧化物歧化酶、过氧化氢酶、酸性磷酸酶、碱性磷酸酶和谷胱甘肽还原酶水平恢复至接近正常水平的能力。电子显微镜研究进一步支持了生化研究结果,证实了抗坏血酸的肝保护潜力。此外,还分析了细胞遗传学终点(染色体畸变、微核、有丝分裂指数和精子头部异常)。单独给予维生素C未显示出其自身的任何毒性迹象。基于目前的研究结果,抗坏血酸似乎对砷毒性和氧化应激具有保护作用。

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