Department of Biomedical Laboratory Science and Management, Cellular and Molecular Toxicology Laboratory, Vidyasagar University, Midnapore, West Bengal, India.
Drug Chem Toxicol. 2012 Jan;35(1):81-8. doi: 10.3109/01480545.2011.589439. Epub 2011 Aug 17.
The present study elucidated the protective role of vitamin B(12) with folic acid against arsenic-induced hepatotoxicity in female rats. Ingestion of sodium-arsenite- contaminated water [0.4 ppm/100 g body weight (b.w.)/day] in combination with vitamin B(12) plus folic acid (0.07 and 4.0 μg, respectively/100 g b.w./day) for 24 days to Wistar rats offered a significant protection against alone arsenic-induced distorted liver function, damaged histoarchitecture, elevated oxidative stress, and DNA fragmentation of hepatic tissues. Arsenic only exposure decreased hepatic superoxide dismutase (SOD), catalase activities, and the level of nonprotein-soluble thiol (NPSH), with a concomitant increase in thiobarbituric acid reactive substances (TBARS) and conjugated dienes (CDs) in the liver. Vitamin supplementation restrained the increase of TBARS and CDs by restoring catalase, SOD, and NPSH levels. Restricted generation of free radicals may be correlated to the protection of DNA stability and hepatic morphology. This study explains the decisive role of vitamin B(12) with folic acid to ameliorate arsenic-mediated liver injuries.
本研究阐明了维生素 B(12)和叶酸对砷诱导的雌性大鼠肝毒性的保护作用。在 Wistar 大鼠中，摄入含有砷酸钠的污染水（0.4ppm/100g 体重/天），同时摄入维生素 B(12)和叶酸（分别为 0.07 和 4.0μg/100g 体重/天）24 天，可显著对抗单独砷诱导的肝功能异常、肝组织形态损伤、氧化应激升高和 DNA 片段化。单独暴露于砷会降低肝脏中超氧化物歧化酶（SOD）和过氧化氢酶的活性，以及非蛋白可溶性巯基（NPSH）的水平，同时肝脏中丙二醛（TBARS）和共轭二烯（CDs）的含量增加。维生素补充通过恢复过氧化氢酶、SOD 和 NPSH 的水平来抑制 TBARS 和 CDs 的增加。自由基的生成受到限制可能与 DNA 稳定性和肝形态的保护有关。本研究解释了维生素 B(12)和叶酸在改善砷介导的肝损伤中的决定性作用。
