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锰(II)对成年斑马鱼引起的组织病理学、遗传毒性和行为损伤。

Histopathological, genotoxic, and behavioral damages induced by manganese (II) in adult zebrafish.

机构信息

Post Graduation Program in Environmental Quality, Feevale University, Brazil.

Biological Science Student, Feevale University, Brazil.

出版信息

Chemosphere. 2020 Apr;244:125550. doi: 10.1016/j.chemosphere.2019.125550. Epub 2019 Dec 5.

Abstract

Manganese is a metal often found as an environmental pollutant and very associated with neurological disorders when in high concentrations. However, little is known about the effects that this contaminant can cause when in environmentally relevant concentrations and occurrence, that is, much lower than those commonly studied. So, the aim of the study was to evaluate the effects that environmentally relevant concentrations of this metal would cause in different zebrafish organs (brain, liver, and blood). Acute 96-h and chronic 30-day exposures were performed using the manganese chloride salt as a pollutant. Behavioral alterations of anxiogenic type were observed in the animals after chronic exposures to 4.0 mg L MnCl, which traveled a greater distance at the bottom of the aquarium. This may be associated with neuronal damages in the telencephalic region responsible for motor and cognitive activity of the fish, observed in animals from the same exposure. In addition, hepatic histopathological damage as vacuolization of hepatocytes and genotoxic damage, identified by comet assay and micronucleus test, was also observed after acute and chronic exposure, especially at the highest pollutant concentrations (8.0 and 16.0 mg L in acute exposure, and 4.0 mg L in chronic exposure. The study reinforces the risk that environmental pollutants pose to the ecosystem, even in low concentrations.

摘要

锰是一种金属,通常作为环境污染物存在,并且在高浓度时与神经紊乱密切相关。然而,人们对这种污染物在环境相关浓度和存在时可能造成的影响知之甚少,也就是说,其浓度要远低于通常研究的浓度。因此,本研究旨在评估环境相关浓度的这种金属对不同斑马鱼器官(大脑、肝脏和血液)的影响。使用氯化锰盐作为污染物进行了 96 小时急性暴露和 30 天慢性暴露。在慢性暴露于 4.0 mg/L MnCl 后,动物表现出焦虑型行为改变,即在鱼缸底部游动的距离更大。这可能与负责鱼类运动和认知活动的端脑区域的神经元损伤有关,在同一暴露条件下的动物中观察到了这种损伤。此外,在急性和慢性暴露后,尤其是在最高污染物浓度(急性暴露时为 8.0 和 16.0 mg/L,慢性暴露时为 4.0 mg/L)下,还观察到了肝细胞空泡化和遗传毒性损伤,这可通过彗星试验和微核试验来识别。该研究强调了环境污染物即使在低浓度下对生态系统构成的风险。

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