丁草胺暴露对雄性褐菖鮋精细胞发育的干扰

Exposure to Butachlor Disrupts Development of Sperm in Male Sebastiscus marmoratus

丁草胺是全球范围内使用最广泛的酰胺类除草剂之一。目前丁草胺对非目标生物的潜在毒性研究较多,但有关丁草胺对近海鱼类生殖毒性的研究鲜有报道。以近海鱼类褐菖鮋为研究对象,探讨丁草胺对海洋鱼类精细胞发育的影响及机制。以环境浓度(2、20和200 ng·L^(-1))的丁草胺对雄性褐菖鮋暴露50 d后,其精巢成熟精细胞数量下降,发育早期阶段的精原细胞与精母细胞数量上升,精巢雄激素睾酮(T)水平下降,Caspase-3活性上升,γ-谷酰胺转移酶(γ-GT)活性下降。相对荧光定量PCR分析结果显示,促卵泡激素受体基因(FSHRβ)与促黄体生成激素受体基因(LHRβ)mRNA表达量被抑制。这表明,丁草胺对雄性褐菖鮋有明显的生殖毒性,精巢支持细胞功能被抑制引起睾酮水平降低,进而导致精子发生被抑制。精巢细胞凋亡也是原因之一。

Butachlor is one of the most widely used amide herbicides in the world.There are many studies on the possible toxic effects of butachlor on non-target organisms,but few studies addressing the reproductive toxicity of butachlor on offshore fishes are available.The present study was conducted to investigate the effects of butachlor on sperm development in Sebastiscus marmoratus and to gain insight into its mechanism.After exposed to butachlor at environmental concentrations(2,20,200 ng·L^(-1))for 50 d,the development of sperm in testis was repressed in different extent,testosterone(T)was decreased in the testis,while the activities of Caspase-3 were dose-dependently increased,and the activities ofγ-GT were dose-dependently decreased.Real-time PCR showed that the expression of FSHRβand LHβwere reduced in the testis.These results indicate that butachlor can cause significant reproductive toxicity to fish.The inhibited expression of FSHRβand LHRβresulted in decreased T levels in the testis and suppressed spermatogenesis.In addition,the apoptosis of testicular cells was another reason for the inhibition of spermatogenesis.