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美洲大蠊体外和体内杀虫剂处理后中枢神经系统的细胞损伤。I. 神经细胞体和神经纤维网。

Cellular lesions in the central nervous system of Periplaneta americana following insecticide treatment in vitro and in vivo. I. Nerve cell bodies and the neuropile.

作者信息

Singh G J, Singh B

出版信息

Neurobehav Toxicol Teratol. 1984 May-Jun;6(3):201-13.

PMID:6493424
Abstract

Cellular lesions in the metathoracic ganglion of P. americana following insecticide treatment have been examined. Treatment of the isolated ganglia with dieldrin (10 microM) and bioresmethrin (5 microM) induced mitochondrial damage in the neuropile and nerve cell bodies. The mitochondria in treated nerve cells were swollen with broken cristae and devoid of normal morphological appearance. Following in vivo treatment of cockroaches with these insecticides, this type of mitochondrial damage was observed even at the onset of poisoning. In the prostrate cockroaches, however, the mitochondrial swelling was accompanied by the accumulation of electron dense granules. In addition, the neuropiles of insecticide-treated ganglia contained secondary lysosomes which increased in size and number with the progress of poisoning and showed signs of depletion of synaptic vesicles. The action of dieldrin upon the ultrastructure was completely abolished by pretreatment of ganglia with 10 mM Mg2+. On the other hand, pretreatment of ganglia with tetrodotoxin and pentobarbital-sodium had very little effect on the action of dieldrin though these compounds blocked the action of bioresmethrin. The results of this study suggest that cellular lesions in the insect CNS, caused by dieldrin, are due to an enhanced uptake of calcium into nerve terminals which may occur independent of membrane depolarization. The effects of bioresmethrin upon the ultrastructure of the CNS are apparently mediated by nerve excitation and membrane depolarization. It is concluded that treatment of intact cockroaches with dieldrin and bioresmethrin initiates catabolic processes in the nerve cells leading to cellular lesions which are indicative of neuronal degeneration.

摘要

已对经杀虫剂处理的美洲大蠊后胸神经节中的细胞损伤进行了研究。用狄氏剂(10微摩尔)和生物苄呋菊酯(5微摩尔)处理分离的神经节,会导致神经纤维网和神经细胞体中的线粒体损伤。经处理的神经细胞中的线粒体肿胀,嵴断裂,失去正常形态。用这些杀虫剂对蟑螂进行体内处理后,即使在中毒初期也观察到了这种类型的线粒体损伤。然而,在瘫倒的蟑螂中,线粒体肿胀伴随着电子致密颗粒的积累。此外,经杀虫剂处理的神经节的神经纤维网含有次级溶酶体,其大小和数量随着中毒进程而增加,并显示出突触小泡耗尽的迹象。用10毫摩尔镁离子预处理神经节可完全消除狄氏剂对超微结构的作用。另一方面,用河豚毒素和戊巴比妥钠预处理神经节对狄氏剂的作用影响很小,尽管这些化合物会阻断生物苄呋菊酯的作用。这项研究的结果表明,狄氏剂引起的昆虫中枢神经系统中的细胞损伤是由于钙进入神经末梢的摄取增加,这可能独立于膜去极化而发生。生物苄呋菊酯对中枢神经系统超微结构的影响显然是由神经兴奋和膜去极化介导的。得出的结论是,用狄氏剂和生物苄呋菊酯处理完整的蟑螂会引发神经细胞中的分解代谢过程,导致细胞损伤,这表明神经元发生了退化。

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