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作 者:于功昌[1] 谢琳[1] 刘衍忠[1] 王筱芬[1]
机构地区:[1]山东省职业卫生与职业病防治研究院毒理室,山东济南250002
出 处:《中华男科学杂志》2009年第6期505-510,共6页National Journal of Andrology
基 金:山东省科技攻关计划(2006GG2202057)~~
摘 要:目的:探讨多菌灵对雄性大鼠睾丸发育和生精功能的影响及其作用机制。方法:40只清洁级未成年Wistar雄性大鼠随机分为4组(对照组,低、中、高剂量组,每组10只),低、中、高剂量组经口灌胃不同浓度的多菌灵溶液(分别为20、100、200mg/kg体重),对照组给予吐温80溶液,1次/d,连续80d。染毒结束后,立即取睾丸和附睾,观察其形态。测定各组大鼠体重及右侧睾丸和附睾重量;取左侧附睾尾测定精子活率和精子数量;采用HE染色法、原位末端标记法(TUNEL)及免疫组化SABC法观察大鼠睾丸组织的病理学变化、细胞凋亡和Bcl-2/Bax表达情况。结果:中、高剂量组大鼠睾丸和附睾均明显萎缩、右侧睾丸和附睾重量减轻,左侧附睾尾精子活率和精子数量均低于对照组(P<0.01);中、高剂量组睾丸组织病理学检查可见明显异常;随多菌灵染毒浓度的增加,各剂量组生精细胞凋亡率逐渐升高,Bcl-2表达下降,Bax表达升高,与对照组比较差异有统计学意义(P<0.05,P<0.01)。结论:多菌灵可影响雄性大鼠的睾丸发育和生精功能,可能与下调Bcl-2和上调Bax致细胞凋亡增加有关。Objective : To explore the effects of carbendazim on the testicular development and spermatogenic function of male rats and its action mechanism. Methods: Forty clean-grade impubic male Wistar rats were equally randomized into a low-dose, a mediumdose, a high-dose and a control group, treated respectively with carbendazim at 20, 100 and 200 mg / kg (bw) and Tween-80 solution, all by oral gavage once a day for 80 days. After treatment, the rats were weighed, their testes and epididymides immediately excised, their morphological changes observed and the weights of the right testis and epididymis obtained. Sperm motility and counts in the left cauda epididymis were determined. Histopathological changes, cell apoptosis and the expression of Bcl-2/Bax in the testis were detected by HE staining, TUNEL and immunohistocbemical SABC method. Results: The medium- and high-dose groups showed obviously atrophic testes and epididymides, marked histopathological abnormality of the testis, reduced weight of the right testis and epididymis, and decreased sperm motility and counts in the left cauda epididymis (P 〈 0. 01 ). With the increasing dose of carbendazim, the apoptosis rate and Bax expression were significantly raised, while the expression of Bcl-2 significantly decreased (P 〈 0.05, P 〈 0.01 ). Conclusion: Carbendazim affects the testicular development and spermatogenic function of male rats, and the mechanism may involve cell apoptosis induced by down-regulation of Bcl-2 and up-regulation of Bax.
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