啶虫脒通过氧化应激损害小鼠睾丸的超微结构

Acetamiprid Impairs the Ultrastructure of Testes Via Inducing Oxidative Stress in Mice

旨在研究啶虫脒对雄性小鼠睾丸支持细胞和生精细胞的损害作用是否与氧化应激有关。将50只成年昆明雄鼠(25～30g)随机分成5组,灌喂方式给药,所有实验动物连续灌喂35d,通过电镜观察睾丸超微结构的变化,并检测一氧化氮合酶(NOS)、羟自由基、谷胱甘肽(GSH)和总抗氧化能力(T-AOC)的变化确定抗氧化能力的变化。观察睾丸的超微结构发现,啶虫脒组小鼠睾丸的支持细胞胞质中内质网扩张,溶酶体数量减少;初级精母细胞的细胞核溶解,染色质异常聚集,线粒体固缩,细胞器较少;精子细胞的核染色质异常聚集,精子细胞内出现明显染色质样小体,线粒体固缩明显。此外,啶虫脒能引起睾丸中总一氧化氮合酶(TNOS)和诱导型一氧化氮合酶(iN-OS)的活性及产生羟自由基的能力升高(P<0.05),GSH和T-AOC活性降低(P<0.05)。维生素E能够明显降低啶虫脒对睾丸超微结构的损害作用。研究结果表明啶虫脒通过诱导氧化应激对小鼠睾丸的超微结构产生损害作用。

The objective of this study was to explore whether the impairment of acetamiprid on the ultrastructure of sertoli cells and spermatogenic cells was associated with oxidative stress.Fifty adult Kunming male mice（25-30 g） were divided into five groups（n=10 per group）.All groups were treated for 35 days by gavage.The results showed that,in the acetamiprid alone group,the endoplasmic reticulum was expanded in sertoli cells,and there were numerous lysosomes.The nucleus of primary spermatocytes was dissolved and mitochondrial was pyknosised;chromatin aggregated abnormally.Furthermore,the nuclear chromatin of spermatids was aggregated abnormally,and emerged apparent chromatin-like corpuscles,while mitochondrial was pyknosised significantly.Acetamiprid increased the concentrations of total NO synthase（TNOS） and induce NO synthase（iNOS） in testes and the capability of producing hydroxyl radical（P0.05,for all）,but reduced the activity of glutathione（GSH） and total antioxygen capability（T-AOC）（P0.05,for both）.Vitamin E significantly ameliorated the impairment of acetamiprid on the ultrastructure of sertoli cells and spermatogenic cells.Therefore,acetamiprid impairs the ultrastructure of testes via inducing oxidative stress in male mice.