阿特拉津暴露对雄性小鼠减数分裂进程及生精能力的影响

Atrazine changes meiosis and reduces spermatogenesis in male mice

目的:探讨阿特拉津暴露对成年雄性小鼠减数分裂进程及生精能力的影响。方法:将SPF级ICR成年雄鼠分成溶剂对照组和阿特拉津处理组,腹腔注射染毒,浓度为100 mg/(kg·d),共4周。统计分析小鼠体重和睾丸重量变化;利用组织化学法分析睾丸组织形态,TUNEL法检测凋亡水平变化;荧光定量PCR分析精母细胞减数分裂关键基因的表达。结果:与对照组相比,随着染毒时间延长,处理组小鼠体重增长减慢,且体重增量显著降低[(11.2±0.17)g vs(8.29±0.51)g,P<0.05];睾丸重量显著下降[(0.28±0.01)g vs(0.24±0.01)g,P<0.05];生精小管管腔变薄,排列疏松,生精细胞排列紊乱且数目减少,附睾尾中精子浓度显著减少[(2.36±0.14)×10^(6)/ml vs(0.90±0.12)×10^(6)/ml,P<0.01],且畸形率显著增加[(8.60±1.07)%vs(18.02±1.71)%,P<0.05];精母细胞凋亡水平升高;SCP1、SCP3及Rad51 mRNA的表达显著降低(P<0.05)。结论:阿特拉津通过损害睾丸形态,增加精母细胞的凋亡水平,改变减数分裂相关基因的表达,进而降低雄鼠的生精能力。

Objective:To investigate the effects of exposure to atrazine on meiosis and spermatogenesis in adult male mice.Methods:We divided 16 adult male Institute for Cancer Research(ICR)mice into a solvent control and an atrazine exposure group of an equal number and intraperitoneally injected with solvent dimethylsulfoxide(DMSO)and atrazine at 100 mg/kg/d,respectively.After 4 weeks of treatment,we obtained the body and testis weights of the mice,observed the changes in the testicular histomorphology,examined the cell apoptosis in the testis tissue,and determined the expressions of meiosis-related key genes in the spermatocytes by real-time fluorescence quantitative PCR.Results:Compared with the controls,the mice treated with atrazine showed significantly less increase in the body weight([11.2±0.17]vs[8.29±0.51]g,P<0.05)and testis weight([0.28±0.01]vs[0.24±0.01]g,P<0.05),loosely arranged and thinned lumens of seminiferous tubules,disordered arrangement and reduced number of spermatogenic cells,decreased sperm concentration([2.36±0.14]vs[0.90±0.12]×10^(6)/ml,P<0.01)and increased percentage of morphologically abnormal sperm in the epididymis tail([8.60±1.07]%vs[18.02±1.71]%,P<0.05),elevated apoptosis rate of spermatocytes,and down-regulated the expressions of SCP1,SCP3 and Rad51 mRNA in the spermatocytes(P<0.05).Conclusion:Atrazine can reduce spermatogenesis in male mice by damaging testicular morphology,increasing the apoptosis of spermatocytes and down-regulating the expressions of meiosis-related genes in the spermatocytes.