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评价锰亚急性暴露后暴露期大鼠的神经行为和神经炎症终点。

Evaluation of neurobehavioral and neuroinflammatory end-points in the post-exposure period in rats sub-acutely exposed to manganese.

出版信息

Toxicology. 2013 Dec 6;314(1):95-9. doi: 10.1016/j.tox.2013.09.008. Epub 2013 Sep 20.

Abstract

Manganese (Mn) can cause manganism, a neurological disorder similar to Parkinson' Disease (PD). The neurobehavioral and neuroinflammatory end-points in the Mn post exposure period have not been studied yet. Rats were injected on alternate days with 8 doses of MnCl2 (25mg/kg) or saline, then euthanized 1, 10, 30 or 70 days following the last dose. Whole-blood (WB) (p<0.05), urine (p<0.05) and brain cortical (p<0.0001) Mn levels were significantly increased 24h after the last dose. Decreases in the rats' ambulation were noted 1, 10 and 30 days after the last Mn dose (p<0.001; p<0.05; p<0.001, respectively) and also in the rearing activity at the four time-points (p<0.05). Cortical glial fibrillary acid protein immunoreactivity (GFAP-ir) was significantly increased at 1, 10, 30 (p<0.0001) and 70 (p<0.001) days after the last Mn dose, as well as tumor necrosis α (TNF-α) levels (p<0.05) but just on day 1. Taken together, the results show that, during the 70-day clearance phase of Mn, the recovery is not immediate as behavioral alterations and neuroinflammation persist long after Mn is cleared from the cortical brain compartment.

摘要

锰(Mn)可导致锰中毒,这是一种类似于帕金森病(PD)的神经障碍。但目前尚未研究 Mn 暴露后的神经行为和神经炎症终点。大鼠每隔一天接受 8 次 MnCl2(25mg/kg)或生理盐水注射,然后在最后一次给药后 1、10、30 或 70 天安乐死。末次给药后 24 小时,全血(WB)(p<0.05)、尿液(p<0.05)和皮质脑(p<0.0001)Mn 水平显著升高。末次 Mn 剂量后 1、10 和 30 天,大鼠的运动减少(p<0.001;p<0.05;p<0.001),并且在四个时间点的活动增加(p<0.05)。末次 Mn 剂量后 1、10、30(p<0.0001)和 70 天(p<0.001),皮质神经胶质纤维酸性蛋白免疫反应性(GFAP-ir)显著增加,肿瘤坏死因子-α(TNF-α)水平也显著增加(p<0.05),但仅在第 1 天。综上所述,这些结果表明,在 Mn 的 70 天清除期内,行为改变和神经炎症在 Mn 从皮质脑区清除后很长时间内仍然持续,因此恢复并不是立即的。

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