Laboratory of Cell and Molecular Biology, Department of Life Science and Bioinformatics, Assam University, Silchar, Assam, India.
Environment and Human Toxicology, Department of Life Science and Bioinformatics, Assam University, Silchar, Assam, India.
J Environ Sci Health C Toxicol Carcinog. 2020;38(4):384-408. doi: 10.1080/26896583.2020.1860400.
Arsenic contamination in the groundwater of Southern Assam, India is well-documented. A specific type of smokeless tobacco (, SG) is highly prevalent among the local population. Thus, the present study is aimed to evaluate the toxicological implications of arsenic and smokeless tobacco co-exposure on the reproductive health of female mice. The estrous cycle of experimental animals was monitored for 30 days. Histopathological studies and comet assay of ovarian and uterine tissues were performed after 30 days of exposure to SG and arsenic (sodium arsenite, SA). Oxidative stress was estimated biochemically by taking tissue glutathione, lipid peroxidation (LPO), and superoxide dismutase activity as endpoints. Our findings indicated a prolonged diestrus phase in the SG + L + SA group ( < 0.001). Histopathological study revealed abnormal tissue architecture in treated groups. Comet assay study showed that SG + SA exposure significantly induced DNA damage in test animals. The elevated LPO level in the SG + SA group indicated oxidative stress generation in the reproductive tissues. The present study suggests that female reproductive organs are vulnerable to SA and SG and oxidative stress generation may be the possible mechanism behind DNA damage, impaired follicular growth, atresia, and altered estrous cycle in the mice test system.
印度阿萨姆邦南部地下水砷污染已有大量记录。当地居民非常普遍地使用一种特殊类型的无烟烟草(SG)。因此,本研究旨在评估砷和无烟烟草共同暴露对雌性小鼠生殖健康的毒理学影响。实验动物的动情周期被监测了 30 天。在暴露于 SG 和砷(亚砷酸钠,SA)30 天后,对卵巢和子宫组织进行了组织病理学研究和彗星试验。通过测定组织谷胱甘肽、脂质过氧化(LPO)和超氧化物歧化酶活性作为终点,进行了生物化学氧化应激评估。我们的研究结果表明,SG+L+SA 组的动情周期延长(<0.001)。组织病理学研究显示处理组的组织结构异常。彗星试验研究表明,SG+SA 暴露显著诱导了试验动物的 DNA 损伤。SG+SA 组中升高的 LPO 水平表明生殖组织中产生了氧化应激。本研究表明,雌性生殖器官容易受到 SA 和 SG 的影响,氧化应激的产生可能是 DNA 损伤、卵泡生长受损、闭锁和发情周期改变的可能机制。