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体外甲草胺对人精子活性氧生成、运动模式及凋亡标志物的影响。

In vitro alachlor effects on reactive oxygen species generation, motility patterns and apoptosis markers in human spermatozoa.

作者信息

Grizard Geneviève, Ouchchane Lemlih, Roddier Héléne, Artonne Christine, Sion Benoît, Vasson Marie-Paule, Janny Laurent

机构信息

CHU Clermont-Ferrand, Service de Biologie de la Reproduction, Hôtel Dieu, F 63001 Clermont-Ferrand, France.

出版信息

Reprod Toxicol. 2007 Jan;23(1):55-62. doi: 10.1016/j.reprotox.2006.08.007. Epub 2006 Aug 30.

Abstract

Due to its extensive production and application, the toxicity of chloracetanilide herbicide alachlor[2-chloro-2',6'-diethyl-N-(methoxymethyl)-acetanilide] should be evaluated to establish minimum effects. In this study, we have examined the in vitro effects of alachlor on human sperm motion using a computer-assisted sperm analyser (CASA). An evaluation of both reactive oxygen species (ROS) and markers of apoptosis was also performed to investigate the mechanism by which alachlor modifies the sperm movement. After exposure up to 2 h to alachlor (0, 0.18, 0.37, 0.90 and 1.85 mM), the percentage of viable, motile spermatozoa and sperm velocities were concentration and/or time dependently decreased. The most sensitive parameters were progressive motility, mean average path velocity and mean straight velocity. Alachlor (1.85 mM) induced an increase in ROS production. A decrease of mitochondrial membrane potential (DeltaPsi(m)), an increase of both phosphatidylserine (PS) externalization and DNA fragmentation, which were concentration and/or time dependent, were also observed. It is possible that toxic effects of alachlor result in an oxidative stress which could act as a mediator of apoptosis. Alachlor could also contribute to some hypofertility cases.

摘要

由于氯乙酰胺类除草剂甲草胺[2-氯-2',6'-二乙基-N-(甲氧基甲基)-乙酰苯胺]的广泛生产和应用,应对其毒性进行评估以确定最小影响。在本研究中,我们使用计算机辅助精子分析仪(CASA)检测了甲草胺对人类精子运动的体外影响。还对活性氧(ROS)和凋亡标志物进行了评估,以研究甲草胺改变精子运动的机制。在暴露于甲草胺(0、0.18、0.37、0.90和1.85 mM)长达2小时后,存活、有运动能力的精子百分比和精子速度呈浓度和/或时间依赖性下降。最敏感的参数是前向运动能力、平均路径速度和平均直线速度。甲草胺(1.85 mM)诱导ROS产生增加。还观察到线粒体膜电位(ΔΨm)降低、磷脂酰丝氨酸(PS)外化和DNA片段化增加,且均呈浓度和/或时间依赖性。甲草胺的毒性作用可能导致氧化应激,而氧化应激可能是凋亡的介导因素。甲草胺也可能导致一些生育力低下的情况。

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