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首页> 外文期刊>Archives of Environmental Contamination and Toxicology >The effects of di(2-ethylhexyl)phthalate exposure and selenium nutrition on sertoli cell vimentin structure and germ-cell apoptosis in rat testis.
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The effects of di(2-ethylhexyl)phthalate exposure and selenium nutrition on sertoli cell vimentin structure and germ-cell apoptosis in rat testis.

机译:邻苯二甲酸二(2-乙基己基)酯和硒营养对大鼠睾丸睾丸精子细胞波形蛋白结构和生殖细胞凋亡的影响。

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摘要

This study aimed to investigate the effects of di(2-ethylhexyl)phthalate (DEHP) on Sertoli-cell vimentin filaments and germ-cell apoptosis in testes of pubertal rats at different selenium (Se) status. Se deficiency was produced in 3-weeks old Sprague-Dawley rats by feeding them ≤ 0.05 Se mg/kg diet for 5 weeks, Se supplementation group was on 1 mg Se/kg diet, and DEHP was applied at 1000 mg/kg dose by gavage during the last 10 days of the feeding period. The diet with excess Se did not cause any appreciable alteration in vimentin staining and apoptosis of germ cells, but Se deficiency caused a mild decrease in the intensity of vimentin immunoreactivity and enhanced germ-cell apoptosis significantly (approximately 3-fold, p <0.0033). DEHP exposure caused disruption and collapse of vimentin filaments and significantly induced apoptotic death of germ cells (approximately 8-fold, p <0.0033). In DEHP-exposed Se-deficient animals, compared with the control, collapse of vimentin filaments was more prominent; there was serious damage to the seminiferous epithelium; and a high increment (approximately 25-fold, p <0.0033) in apoptotic germ cells was observed. Thus, Se deficiency exacerbated the toxicity of DEHP on Sertoli cells and spermatogenesis, whereas Se supplementation provided protection. These results put forward the critical role of Se in the modulation of redox status of testicular cells and emphasize the importance of Se status for reproductive health.
机译:本研究旨在探讨邻苯二甲酸二(2-乙基己基)酯(DEHP)对处于不同硒(Se)状态的青春期大鼠睾丸睾丸支持细胞细丝波形蛋白和生殖细胞凋亡的影响。在3周大的Sprague-Dawley大鼠中,饲喂≤0.05 Se mg / kg的饲料5周,产生了硒缺乏症; Se补充组的饮食为1 mg Se / kg的饲料; DEHP的剂量为1000 mg / kg。在喂食期的最后10天进行管饲。硒过量的饮食没有引起波形蛋白染色和生殖细胞凋亡的明显改变,但是硒缺乏引起波形蛋白免疫反应强度的轻度降低,并显着增强了生殖细胞凋亡(约3倍,p <0.0033) 。 DEHP暴露引起波形蛋白丝的破坏和瓦解,并显着诱导生殖细胞凋亡死亡(约8倍,p <0.0033)。与对照组相比,DEHP暴露的缺硒动物中,波形蛋白细丝的塌陷更为明显;曲细精上皮严重受损;并在凋亡生殖细胞中观察到高增量(约25倍,p <0.0033)。因此,硒缺乏加剧了DEHP对支持细胞和精子发生的毒性,而硒的补充则提供了保护。这些结果提出了硒在睾丸细胞氧化还原状态调节中的关键作用,并强调硒状态对生殖健康的重要性。

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