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四种拟除虫菊酯中毒未显示大鼠神经肌肉功能障碍与神经生化异常之间存在任何关联。

Intoxication with four synthetic pyrethroids fails to show any correlation between neuromuscular dysfunction and neurobiochemical abnormalities in rats.

作者信息

Rose G P, Dewar A J

出版信息

Arch Toxicol. 1983 Aug;53(4):297-316. doi: 10.1007/BF00294995.

Abstract

The neurological effects of four synthetic pyrethroids resmethrin, permethrin, cypermethrin, and deltamethrin have been investigated in the rat to establish whether there is a correlation between the clinical-functional status of the animal and peripheral nerve damage as measured biochemically. Neuromuscular dysfunction was assessed by means of the inclined plane test and peripheral nerve damage by reference to beta-glucuronidase and beta-galactosidase activity increases in nerve tissue homogenates from treated and control animals. A transient functional impairment was found in animals treated with any one of the four pyrethroids tested and in all cases this was maximal at the end of the 7 day subacute dosing regimen. Significant increases in beta-glucuronidase and beta-galactosidase were found 3-4 weeks after the start of dosing in the distal portion of the sciatic/posterior tibial nerves from permethrin, cypermethrin, and deltamethrin treated animal; but no changes were found in remesthrin-dosed animals. It is concluded therefore, that there is no direct correlation between the time-course of the neuromuscular dysfunction and the neurobiochemical changes. This suggests that these pyrethroids have at least two distinct actions--a short-term pharmacological effect and at near-lethal dose levels a more chronic neurotoxic effect that results in sparse axonal nerve damage.

摘要

研究了四种合成拟除虫菊酯(苄呋菊酯、氯菊酯、氯氰菊酯和溴氰菊酯)对大鼠的神经学影响,以确定动物的临床功能状态与通过生化方法测定的周围神经损伤之间是否存在相关性。通过斜面试验评估神经肌肉功能障碍,并参照处理组和对照组动物神经组织匀浆中β-葡萄糖醛酸酶和β-半乳糖苷酶活性的增加来评估周围神经损伤。在用四种测试拟除虫菊酯中的任何一种处理的动物中发现了短暂的功能损害,并且在所有情况下,这种损害在7天亚急性给药方案结束时最大。在氯菊酯、氯氰菊酯和溴氰菊酯处理的动物坐骨神经/胫后神经远端,给药开始3-4周后,β-葡萄糖醛酸酶和β-半乳糖苷酶显著增加;但在苄呋菊酯给药的动物中未发现变化。因此得出结论,神经肌肉功能障碍的时间进程与神经生化变化之间没有直接相关性。这表明这些拟除虫菊酯至少有两种不同的作用——短期药理作用和在接近致死剂量水平时更慢性的神经毒性作用,后者导致稀疏的轴突神经损伤。

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