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[多氯联苯对精子发生的损害:损伤的内分泌和旁分泌机制]

[Spermatogenesis impairment by polychlorbiphenyls: endocrine and paracrine mechanisms of the damage].

作者信息

Krugovykh N F, Abdullina A Z, Galimova E F, Galimov Sh N

出版信息

Aviakosm Ekolog Med. 2004 Nov-Dec;38(6):51-6.

Abstract

Possible role of changed contents of certain cytokines in the genesis of reproductive disorders was studied in an experiment with rats intoxicated chronically by polychlorbiphenyl (PCB) ecopollutants at the total doses of 0.3 g/kg of the body weight (0.05 LD50 and 3 g/kg of the body weight (0.5 LD50). The enzyme immunodetection was used to analyze blood serum, testicle tissues and sperm for interleukin-1beta, interleukin-6, interleukin-4, tumor necrosis factor alpha, and testosterone and estradiol. The experiment showed that chronic PCB intoxication significantly increases the production of pro-inflammatory cytokines and decreases the production of anti-inflammatory cytokines on a background of a sharp testosterone reduction and inversion of the androgen-estrogen profile. Implications of these shifts to steroido- and spermatogenesis are discussed along with cell and molecular mechanisms of cytokine-mediate PCB intoxication.

摘要

在一项实验中,研究了某些细胞因子含量变化在生殖系统紊乱发生过程中的可能作用。实验用大鼠长期暴露于多氯联苯(PCB)环境污染物中,总剂量分别为0.3 g/kg体重(0.05 LD50)和3 g/kg体重(0.5 LD50)。采用酶免疫检测法分析血清、睾丸组织和精子中的白细胞介素-1β、白细胞介素-6、白细胞介素-4、肿瘤坏死因子α以及睾酮和雌二醇。实验表明,在睾酮急剧减少和雄激素 - 雌激素谱反转的背景下,慢性PCB中毒显著增加促炎细胞因子的产生,减少抗炎细胞因子的产生。讨论了这些变化对类固醇生成和精子发生的影响,以及细胞因子介导的PCB中毒的细胞和分子机制。

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