关键词: 啶虫脒, 小鼠, 睾丸支持细胞, 生精细胞, 超微结构, 氧化应激

Abstract: 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 (P<0.05, for all), but reduced the activity of glutathione (GSH) and total antioxygen capability (TAOC) (P<0.05, 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.

Key words: acetamiprid, mouse, sertoli cell, spermatogenic cell, ultrastructure, oxidative stress