Geng Xiao, Bo Cunxiang, Han Guizhi, Shao Hua
Shandong Academy of Medical Sciences, Shandong Institute of Prevention and Control of Occupational Health and Occupational Disease, Jinan 250062, China.
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Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2015 Mar;33(3):180-5.
To investigate the effects of malathion on the testicular spermatogenic function of male rats and its working mechanism.
Forty specific pathogen-free male Wistar rats were randomly and equally divided into four groups: three exposure groups and a control group. Malathion was administered orally to male rats in the exposure groups at 33.75, 54, and 108 mg/kg (1/32 LD₅₀, 1/20 LD₅₀, and 1/10 LD₅₀) for 60 days. Rats in the control group received an equal volume of water. The body weights of rats were measured after exposure. The organ weights and coefficients of the testes and epididymes were determined as soon as rats were sacrificed. The sperm motility, counts, and malformation rates were measured in the left epididymis. Histopathological changes, cell apoptosis, and the expression levels of Bcl-2/Bax in the testes of rats were observed using HE staining, terminal deoxynucleotidyl transferase-mediated dUPT-biotin nick end labeling, and immunohistochemistry SABC method.
The body weights and the testis weights in the exposure groups were significantly lower than those in the control group (P < 0.01). The exposure groups had significantly lower sperm motility and significantly higher sperm malformation rates than the control group (P < 0.01). The sperm counts were significantly lower in the exposure groups than in the control group (P<0.01). The sperm counts and motility were negatively correlated with exposure dose (r = -0.81, P < 0.01; r = -0.51, P < 0.01), while the sperm malformation rate was positively correlated with exposure dose (r = 0.85, P 0.01). The exposure groups had significantly higher spermatogenic cell apoptosis rates than the control group (P<0.01). The expression level of Bax was significantly higher in the exposure groups than in the control group (P<0.01), while the expression level of Bcl-2 was significantly lower in the exposure groups than in the control group (P < 0.01). Histopathological examination of the testes showed degenerative changes in the seminiferous tubules at various doses along with the increase in malathion exposure dose.
Malathion affects the testicular spermatogenic function of male rats and its working mechanism may involve cell apoptosis induced by down-regulation of Bcl-2 and up-regulation of Bax.
探讨马拉硫磷对雄性大鼠睾丸生精功能的影响及其作用机制。
将40只无特定病原体雄性Wistar大鼠随机等分为四组：三个染毒组和一个对照组。染毒组雄性大鼠分别按33.75、54和108mg/kg（1/32半数致死量、1/20半数致死量和1/10半数致死量）口服给予马拉硫磷，连续60天。对照组大鼠给予等量的水。染毒后测量大鼠体重。大鼠处死后立即测定睾丸和附睾的脏器重量及脏器系数。检测左侧附睾精子活力、计数及畸形率。采用苏木精-伊红染色、末端脱氧核苷酸转移酶介导的dUTP生物素缺口末端标记法及免疫组织化学SABC法观察大鼠睾丸组织病理学变化、细胞凋亡及Bcl-2/Bax表达水平。
染毒组大鼠体重和睾丸重量均显著低于对照组（P<0.01）。染毒组精子活力显著低于对照组，精子畸形率显著高于对照组（P<0.01）。染毒组精子计数显著低于对照组（P<0.01）。精子计数和活力与染毒剂量呈负相关（r=-0.81，P<0.01；r=-0.51，P<0.01），而精子畸形率与染毒剂量呈正相关（r=0.85，P<0.01）。染毒组生精细胞凋亡率显著高于对照组（P<0.01）。染毒组Bax表达水平显著高于对照组（P<0.01），而Bcl-2表达水平显著低于对照组（P<0.01）。睾丸组织病理学检查显示，随着马拉硫磷染毒剂量增加，各剂量组生精小管均出现退行性改变。
马拉硫磷影响雄性大鼠睾丸生精功能，其作用机制可能与下调Bcl-2、上调Bax诱导细胞凋亡有关。
