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牛磺酸可逆转成年大鼠睾丸中硫丹诱导的氧化应激和细胞凋亡。

Taurine reverses endosulfan-induced oxidative stress and apoptosis in adult rat testis.

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Al-Azhar University, Nasr City, Cairo, Egypt.

Physics Department, Girls College for Arts, Science and Education, Ain Shams University, Cairo, Egypt.

出版信息

Food Chem Toxicol. 2014 Feb;64:1-9. doi: 10.1016/j.fct.2013.11.007. Epub 2013 Nov 19.

Abstract

The present study was aimed to investigate the mechanistic aspect of endosulfan toxicity and its protection by taurine in rat testes. Pre-treatment with taurine (100 mg/kg/day) significantly reversed the decrease in testes weight, and the reduction in sperm count, motility, viability and daily sperm production in endosulfan (5 mg/kg/day)-treated rats. Sperm chromatin integrity and epididymal L-carnitine were markedly decreased by endosulfan treatment. Endosulfan significantly decreased the level of serum testosterone and testicular 3β-HSD, 17β-HSD, G6PDH and LDH-X. Sperm Δψm and mitochondrial cytochrome c content were significantly decreased after endosulfan. Testicular caspases-3, -8 and -9 activities were significantly increased but taurine showed significant protection from endosulfan-induced apoptosis. Oxidative stress was induced by endosulfan treatment as evidenced by increased H2O2 level and LPO and decreased the antioxidant enzymes SOD, CAT and GPx activities and GSH content. These alterations were effectively prevented by taurine pre-treatment. In conclusion, endosulfan decreases rat testes weight, and inhibits spermatogenesis and steroidogenesis. It induces oxidative stress and apoptosis by possible mechanisms of both mitochondria and non-mitochondria pathways. These data provide insight into the mode of action of endosulfan-induced toxicity and the beneficial role provided by taurine to counteract endosulfan-induced oxidative stress and apoptosis in rat testis.

摘要

本研究旨在探讨硫丹毒性的机制及其在大鼠睾丸中的保护作用。牛磺酸(100mg/kg/天)预处理可显著逆转硫丹(5mg/kg/天)处理大鼠睾丸重量下降、精子计数、活力、活力和每日精子产量减少的现象。精子染色质完整性和附睾 L-肉碱明显减少硫丹处理。血清睾酮和睾丸 3β-HSD、17β-HSD、G6PDH 和 LDH-X 水平显著降低。硫丹处理后精子 Δψm 和线粒体细胞色素 c 含量显著降低。睾丸 caspase-3、-8 和 -9 活性显著增加,但牛磺酸对硫丹诱导的细胞凋亡有显著保护作用。硫丹处理诱导氧化应激,表现为 H2O2 水平升高、LPO 降低、抗氧化酶 SOD、CAT 和 GPx 活性和 GSH 含量降低。这些变化可通过牛磺酸预处理有效预防。总之,硫丹降低大鼠睾丸重量,抑制精子发生和类固醇生成。它通过线粒体和非线粒体途径的可能机制诱导氧化应激和细胞凋亡。这些数据提供了对硫丹诱导毒性作用方式的深入了解,并表明牛磺酸在对抗硫丹诱导的大鼠睾丸氧化应激和细胞凋亡方面具有有益作用。

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