Environmental pollution due to arsenic is associated with several adverse health effects including neurotoxicity in animals and humans. Selenium is a nutritionally essential trace metalloid well documented to elicit compelling pharmacological activities in vitro and in vivo. Report on the influence of selenium on arsenic-mediated behavioral derangement is lacking in literature. Hence, to fill this knowledge gap, rats were either exposed to arsenic per se in drinking water at 60 μg AsO2Na/L or co-administered with inorganic selenium at 0.25 mg/kg or organic selenium diphenyl diselenide (DPDS) at 2.5 mg/kg body weight for 45 successive days. Neurobehavioural data from rats in a new environment using video-tracking software evinced that inorganic and organic forms of selenium significantly (p < 0.05) abrogated arsenic-induced motor and locomotor insufficiencies such as increased negative geotaxis and fecal pellets numbers as well as the diminution in grip strength, body rotation, maximum speed, absolute turn angle and total distance travelled. The augmentation in the behavioral activities in rats co-administered with arsenic and both forms of selenium was substantiated using track and occupancy plots analyses. Selenium mitigated arsenic-induced decreases in glutathione level and acetylcholinesterase activity as well as the increase in oxidative stress and reactive oxygen and nitrogen species. Moreover, selenium diminished inflammatory parameters (myeloperoxidase activity, nitric oxide, tumour necrosis factor alpha and interleukin-1 beta levels), caspase-3 activity and ameliorated histological lesions in the cerebellum, cerebrum and liver of the rats. Collectively, selenium abated arsenic-induced behavioral derangements via anti-inflammation, antioxidant and anti-apoptotic mechanisms in rats.

中文翻译：

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硒对大鼠砷诱导的行为障碍的神经保护机制。

砷引起的环境污染与多种不良健康影响相关，包括对动物和人类的神经毒性。硒是营养必不可少的微量准金属，据文献记载，硒在体外和体内均可引起令人信服的药理活性。缺乏关于硒对砷介导的行为失调影响的报道。因此，为了填补这一知识空白，大鼠要么在饮用水中以60μgAsO2Na / L的砷本身暴露，要么与0.25 mg / kg的无机硒或2.5 mg / kg的有机硒二苯基二硒化物（DPDS）共同施用体重连续45天。在新环境中使用视频跟踪软件从大鼠获得的神经行为数据表明，硒的无机和有机形式显着（p <0。05）消除了由砷引起的运动和运动功能不足，例如增加的负地轴和粪便颗粒数量以及握力，身体旋转，最大速度，绝对转弯角和总行驶距离的减少。使用轨迹图和占用图分析证实了与砷和两种形式的硒合用的大鼠行为活动的增强。硒减轻了砷引起的谷胱甘肽水平和乙酰胆碱酯酶活性的下降，以及氧化应激和活性氧和氮物种的增加。此外，硒减少了炎症参数（髓过氧化物酶活性，一氧化氮，肿瘤坏死因子α和白介素1β的水平），胱天蛋白酶3活性和小脑组织病变的减轻，大鼠的大脑和肝脏。硒通过大鼠的抗发炎，抗氧化和抗凋亡机制共同减轻了砷引起的行为异常。