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氯化铈致小鼠海马细胞凋亡及认知功能障碍的信号通路

Signal pathway of hippocampal apoptosis and cognitive impairment of mice caused by cerium chloride.

机构信息

Medical College, Soochow University, Suzhou 215123, People's Republic of China.

出版信息

Environ Toxicol. 2012 Dec;27(12):707-18. doi: 10.1002/tox.20696. Epub 2011 Mar 7.

Abstract

Experimental studies have demonstrated that lanthanides could impair cognitive functions of children and animals, but very little is known about the hippocampal apoptosis and its molecular mechanism. The study investigated the signal pathway of hippocampal apoptosis induced by intragastric administration of CeCl(3) for 60 consecutive days. It showed that cerium had been significantly accumulated in the mouse hippocampus, and CeCl(3) caused hippocampal apoptosis and impairment of spatial recognition memory of mice. CeCl(3) effectively activated caspase-3 and -9, inhibited Bcl-2, and increased the levels of Bax and cytochrome c, promoted accumulation of reactive oxygen species in the mouse hippocampus. It implied that CeCl(3)-induced apoptosis in the mouse hippocampus could be triggered via mitochondrion-mediated pathway. Our findings suggest the need for great caution to handle the lanthanides for workers and consumers.

摘要

实验研究表明,镧系元素可能会损害儿童和动物的认知功能,但对于其诱导海马体细胞凋亡的分子机制却知之甚少。本研究通过灌胃给予氯化铈连续 60 天,探讨了其诱导海马体细胞凋亡的信号通路。结果表明,铈在小鼠海马体中明显蓄积,氯化铈可引起海马体细胞凋亡和小鼠空间识别记忆损伤。氯化铈可有效激活半胱氨酸天冬氨酸蛋白酶-3 和 -9,抑制 Bcl-2,增加 Bax 和细胞色素 c 的水平,促进小鼠海马体中活性氧的积累。这提示我们,氯化铈诱导的小鼠海马体细胞凋亡可能是通过线粒体介导的途径触发的。这些发现提示我们,工人和消费者在处理镧系元素时应格外小心。

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