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亚慢性给予二苯基二硒化物会增强镉诱导的小鼠睾丸损伤。

Sub-chronic administration of diphenyl diselenide potentiates cadmium-induced testicular damage in mice.

作者信息

Santos Francielli W, Graça Dominguita L, Zeni Gilson, Rocha João B T, Weis Simone N, Favero Alexandre M, Nogueira Cristina W

机构信息

Departamento de Quimica, Centro de Ciencias Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria CEP 97105-900, RS, Brazil.

出版信息

Reprod Toxicol. 2006 Oct;22(3):546-50. doi: 10.1016/j.reprotox.2005.12.009. Epub 2006 Feb 10.

DOI:10.1016/j.reprotox.2005.12.009
PMID:16472969
Abstract

Sub-chronic cadmium (Cd) exposure causes testicular damage in mice. The mode of action may involve oxidative stress and especially lipid peroxidation. The present study has monitored the pathogenesis of testicular damage during sub-chronic Cd exposure and has evaluated the potential protective effect of antioxidant therapy with diphenyl diselenide (PhSe)(2). Male mice were dosed with 2.5 mg/kg CdCl(2) (2.5 mg/kg) with or without (PhSe)(2) (5 micromol/kg) at 30 min post-exposure using a model of five weekly subcutaneous injections. Histological evaluation of the testis was performed across a 4 week test period. Animals exposed to CdCl(2) and CdCl(2) plus (PhSe)(2) displayed a reduction in body weight gain and testicular weight. Progressive damage and histolopathological changes in the testis were not remedied with, but rather were potentiated by, (PhSe)(2) therapy. We conclude that (PhSe)(2) enhances testicular injury in an animal model for sub-chronic Cd exposure mice.

摘要

亚慢性镉(Cd)暴露会导致小鼠睾丸损伤。其作用方式可能涉及氧化应激,尤其是脂质过氧化。本研究监测了亚慢性镉暴露期间睾丸损伤的发病机制,并评估了二苯基二硒醚(PhSe)₂抗氧化治疗的潜在保护作用。雄性小鼠采用每周皮下注射5次的模型,在暴露后30分钟给予2.5毫克/千克氯化镉(2.5毫克/千克),同时或不给予(PhSe)₂(5微摩尔/千克)。在4周的试验期内对睾丸进行组织学评估。暴露于氯化镉和氯化镉加(PhSe)₂的动物体重增加和睾丸重量均有所下降。(PhSe)₂治疗并未修复睾丸的进行性损伤和组织病理学变化,反而使其加剧。我们得出结论,在亚慢性镉暴露小鼠的动物模型中,(PhSe)₂会加重睾丸损伤。

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