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首页> 外文期刊>Toxicology: An International Journal Concerned with the Effects of Chemicals on Living Systems >Comments to the Editor concerning the cholinergic response to manganese-induced neurotoxicity, based on the paper entitled 'The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the brain' by Santos et al.
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Comments to the Editor concerning the cholinergic response to manganese-induced neurotoxicity, based on the paper entitled 'The inhibitory effect of manganese on acetylcholinesterase activity enhances oxidative stress and neuroinflammation in the brain' by Santos et al.

机译：Santos等人根据题为“锰对乙酰胆碱酯酶活性的抑制作用可增强大脑中的氧化应激和神经发炎”的论文，对编辑对锰诱导的神经毒性的胆碱能反应的评论。

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摘要

Santos et al. (2012) reported in their recent manuscript some very interesting data concerning the cholinergic response to the neurotoxicity induced by manganese (Mn), that we would like to compare with our recent findings on the topic. The authors reported that after either 4 or 8 intraperitoneal (i.p.) injections of 25 mg MnCl_2/kg/day every 48 h, the adult rat brain acetylcholinesterase (AChE) activity is significantly decreased to 60% and 55% of control levels, respectively (Santos et al., 2012). This decrease in AChE activity is reported to be accompanied by clear signs of neurobehavioral toxicity (decrease in ambulation and rearings in open-field after both 4 and 8 Mn doses, as compared to controls), and significantly increased brain F4-neuroprostane levels and brain Mn-superoxide dismutase protein expression levels (after 4 Mn doses, but not after 8 Mn doses, as compared to controls) (Santos et al., 2012). Moreover, the authors report a dose- and time-dependent increase in brain prostaglandin E_2 levels (used as a biomarker of neuroinflammation) due to Mn, that is statistically significant only in the 8 dose Mn treated group vs. the control group (Santos et al., 2012).
机译：Santos等。 （2012年）在他们的最新手稿中报道了一些非常有趣的数据，涉及对锰（Mn）引起的神经毒性的胆碱能反应，我们希望将其与我们在该主题上的最新发现进行比较。作者报告说，每48小时腹膜内（ip）注射25毫克MnCl_2 / kg /天4或8次，成年大鼠脑乙酰胆碱酯酶（AChE）活性分别显着降低至对照水平的60％和55％（ Santos等，2012）。据报道，AChE活性的这种降低伴随着明显的神经行为毒性迹象（与对照组相比，在4和8 Mn剂量后，野外活动性下降和开阔地饲养减少），并且大脑F4-神经前列腺素水平和大脑明显增加锰超氧化物歧化酶蛋白表达水平（与对照相比，在4百万剂后，但在8百万剂后没有）（Santos等人，2012）。此外，作者报告了由于锰引起的脑前列腺素E_2水平（用作神经炎症的生物标志物）的剂量和时间依赖性增加，这仅在8剂量锰治疗组与对照组之间具有统计学意义（Santos等）等人，2012年）。

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