Public Health, Operation Unit, Hydrocarbon Pollution Remediation Project, Aba - Port Harcourt Expressway, Port Harcourt, 350, Rivers State, Nigeria.
Department of Pharmacy, University of Port Harcourt Teaching Hospital, Choba, Port Harcourt, Rivers State, Nigeria.
Psychopharmacology (Berl). 2022 Feb;239(2):399-412. doi: 10.1007/s00213-021-06010-7. Epub 2021 Oct 29.
Excessive exposure to manganese (Mn) is associated with neurotoxicity characterized by oxidative stress, inflammation, and apoptosis induction. Selenium (Se) has been shown to possess antioxidant, anti-inflammatory, and anti-apoptotic properties in humans and animals. The present study investigated the neuroprotective mechanism of Se in rats sub-chronically treated with Mn at 30 mg/kg body weight or orally co-treated with Se at 0.2 and 0.4 mg/kg body weight for 35 consecutive days. Locomotive and exploratory profiles were recorded and computed with the aid of ANY-Maze (a video-tracking software) for 5-min trial, in a novel apparatus. The ANY-Maze analysis showed that Se significantly (p < 0.05) abated Mn-induced locomotive impairment evidenced by increased in maximum speed, total time traveled, absolute turn angle, number of line crossing, rotation and forelimb grip and decreased total time immobile, grooming, and negative geotaxis as verified by the enhanced track plot density. Furthermore, the striatum and hippocampus of the rats were excised and the levels of Mn and Se, oxidative stress markers, proinflammatory cytokines including acetylcholinesterase and caspase-3 activities were assayed. The result shows that Se abates Mn-mediated accumulation of Mn. Also, Se ameliorated Mn-induced decrease in antioxidant enzymes as well as glutathione level and increase in acetylcholinesterase activity, lipid peroxidation, proinflammatory cytokines (i.e., interleukin (IL)-6, IL-1β, tumor necrosis factor alpha), and caspase-3 activation in the striatum and hippocampus of the rats. Collectively, Se abated Mn-induced striatal and hippocampal toxicity via abrogation of neurobehavioral deficits, biometal accumulation, oxidative stress, inflammation, and caspase-3 activation in rats. Se may serve as a neuroprotective agent against Mn-mediated neurotoxicity.
过量接触锰（Mn）与氧化应激、炎症和细胞凋亡诱导有关的神经毒性有关。硒（Se）已被证明在人类和动物中具有抗氧化、抗炎和抗凋亡作用。本研究调查了硒在 30mg/kg 体重的 Mn 亚慢性处理或 0.2 和 0.4mg/kg 体重的 Se 口服共同处理的大鼠中的神经保护机制，连续 35 天。使用 ANY-Maze（视频跟踪软件）在新装置中记录和计算了 5 分钟试验的运动和探索性图谱。ANY-Maze 分析表明，Se 显著（p<0.05）减轻了 Mn 诱导的运动障碍，表现为最大速度、总行程、绝对转角、线交叉次数、旋转和前肢抓地力增加，总不动时间、梳理和负趋地性减少，轨迹图密度增强得到证实。此外，切除大鼠纹状体和海马，测定 Mn 和 Se 水平、氧化应激标志物、促炎细胞因子（包括乙酰胆碱酯酶和 caspase-3 活性）。结果表明，Se 减轻了 Mn 介导的 Mn 积累。此外，Se 改善了 Mn 诱导的抗氧化酶、谷胱甘肽水平降低以及乙酰胆碱酯酶活性、脂质过氧化、促炎细胞因子（即白细胞介素 (IL)-6、IL-1β、肿瘤坏死因子 α）和 caspase-3 激活增加。大鼠纹状体和海马中的激活。总之，Se 通过减轻神经行为缺陷、生物金属积累、氧化应激、炎症和 caspase-3 激活，减轻了 Mn 诱导的纹状体和海马毒性。Se 可能是一种针对 Mn 介导的神经毒性的神经保护剂。
