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镉暴露对幼年小鼠大脑皮质组织病理学的影响。

Effect of cadmium exposure on the histopathology of cerebral cortex in juvenile mice.

作者信息

Yang X F, Fan G Y, Liu D Y, Zhang H T, Xu Z Y, Ge Y M, Wang Z L

机构信息

College of Animal Science, Henan Institute of Science and Technology, Xinxiang, Henan Province, People's Republic of China, 453003,

出版信息

Biol Trace Elem Res. 2015 Jun;165(2):167-72. doi: 10.1007/s12011-015-0246-2. Epub 2015 Feb 3.

Abstract

Cadmium, a heavy metal, is a toxic environmental and industrial pollutant. Exposure to cadmium can lead to the toxic effects in a variety of tissues, also including the brain. The present study investigated the effect of cadmium exposure on the histopathology of cerebral cortex in juvenile mice. Juvenile mice were randomly divided into control, low (1.87 mg/kg), medium (3.74 mg/kg), and high (7.48 mg/kg) dose groups. After cadmium exposure by drinking water for 10 days, the cerebral cortex was obtained for histopathology studies. The medium and high dose of cadmium, rather than low dose, could induce the histopathology alterations of cerebral cortex in a dose-dependent manner. In the high-dose group, microstructure significantly showed pia mater encephali divorcing from cerebral cortex layer, serious hyperemia of blood capillary in pia mater encephali and cerebral cortex, broadening vessel peripheral clearance, a large number of eosinophil leukocyte infiltrating around blood vessel, vacuolar degeneration in part granule cells, and obviously increasing apoptotic cells. Ultrastructure obviously displayed marginalized heterochromatin, incomplete or fused nuclear membranes, broadened perinuclear space, ambiguous mitochondria cristae, decreased synaptic cleft, and fused presynaptic and postsynaptic membrane. Our results revealed that cadmium at the middle and high dose could induce obvious microstructure and ultrastructure alterations of cerebral cortex in juvenile mice, which may be one important mechanism of cadmium neurotoxicity.

摘要

镉作为一种重金属,是一种有毒的环境和工业污染物。接触镉会对包括大脑在内的多种组织产生毒性作用。本研究调查了镉暴露对幼年小鼠大脑皮质组织病理学的影响。将幼年小鼠随机分为对照组、低剂量(1.87毫克/千克)、中剂量(3.74毫克/千克)和高剂量(7.48毫克/千克)组。通过饮水方式让小鼠暴露于镉10天后,获取大脑皮质进行组织病理学研究。中、高剂量的镉而非低剂量镉,能够以剂量依赖的方式诱导大脑皮质的组织病理学改变。在高剂量组中,显微结构显著显示软脑膜与大脑皮质层分离,软脑膜和大脑皮质中的毛细血管严重充血,血管周围间隙增宽,血管周围有大量嗜酸性粒细胞浸润,部分颗粒细胞出现空泡变性,凋亡细胞明显增多。超微结构明显显示异染色质边缘化、核膜不完整或融合、核周间隙增宽、线粒体嵴模糊、突触间隙变窄以及突触前膜和突触后膜融合。我们的结果表明,中、高剂量的镉可诱导幼年小鼠大脑皮质明显的显微结构和超微结构改变,这可能是镉神经毒性的一个重要机制。

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