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Epigenetic dysregulation of Mdr1b in the blood-testis barrier contributes to dyszoospermia in mice exposed to cadmium.
Ecotoxicology and Environmental Safety ( IF 6.2 ) Pub Date : 2020-01-06 , DOI: 10.1016/j.ecoenv.2019.110142 Yu Fang 1 , Ying Xiang 1 , Xing Lu 2 , Xin Dong 1 , Jiexin Zhang 1 , Shan Zhong 3
Ecotoxicology and Environmental Safety ( IF 6.2 ) Pub Date : 2020-01-06 , DOI: 10.1016/j.ecoenv.2019.110142 Yu Fang 1 , Ying Xiang 1 , Xing Lu 2 , Xin Dong 1 , Jiexin Zhang 1 , Shan Zhong 3
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Cadmium (Cd) has been reported to induce reproductive toxicity. Recent study indicated that aberrant epigenetic regulation of Multidrug resistance 1b (Mdr1b) causes xenobiotic efflux failure at the blood-testis barrier (BTB). However, whether Mdr1b dysregulation is involved in Cd-mediated dyszoospermia and the underlying mechanism remain unknown. In this study, mice were intragastrically administered 0 or 2.5 mg/kg CdCl2 every other day for 2 months to investigate changes in spermatogenesis and epigenetic regulation of Mdr1b. Mouse Leydig cells TM3 were cultured to detect Mdr1b expression localization. We found that the Cd group revealed BTB disruption concomitant with obvious sperm abnormity and dynamic impairment. Hypermethylation and decreased nuclear factor Ya (Nfya) recruitment to the Mdr1b promoter were correlated with low sperm motility in response to Cd. In conclusion, these findings provide in vivo evidence that epigenetic dysregulation of Mdr1b in the BTB is a potential cause of dyszoospermia upon Cd exposure.
中文翻译：
血液-睾丸屏障中Mdr1b的表观遗传失调会导致镉暴露小鼠的精子异常。
据报道，镉会引起生殖毒性。最近的研究表明，多重耐药性1b（Mdr1b）的异常表观遗传调控会导致血睾屏障（BTB）的异源外排失败。但是，Mdr1b失调是否参与Cd介导的性精子症及其潜在机制尚不清楚。在这项研究中，每隔一天给小鼠胃内注射0或2.5 mg / kg CdCl2，持续2个月，以研究Mdr1b精子发生和表观遗传调控的变化。培养小鼠Leydig细胞TM3，以检测Mdr1b表达定位。我们发现Cd组显示出BTB破坏，并伴有明显的精子异常和动态损伤。高甲基化和减少的核因子Ya（Nfya）募集到Mdr1b启动子与对Cd的低精子运动相关。总而言之，这些发现提供了体内证据，表明Bdr中Mdr1b的表观遗传失调是镉暴露后异精症的潜在原因。
更新日期：2020-01-06
中文翻译：
血液-睾丸屏障中Mdr1b的表观遗传失调会导致镉暴露小鼠的精子异常。
据报道，镉会引起生殖毒性。最近的研究表明，多重耐药性1b（Mdr1b）的异常表观遗传调控会导致血睾屏障（BTB）的异源外排失败。但是，Mdr1b失调是否参与Cd介导的性精子症及其潜在机制尚不清楚。在这项研究中，每隔一天给小鼠胃内注射0或2.5 mg / kg CdCl2，持续2个月，以研究Mdr1b精子发生和表观遗传调控的变化。培养小鼠Leydig细胞TM3，以检测Mdr1b表达定位。我们发现Cd组显示出BTB破坏，并伴有明显的精子异常和动态损伤。高甲基化和减少的核因子Ya（Nfya）募集到Mdr1b启动子与对Cd的低精子运动相关。总而言之，这些发现提供了体内证据，表明Bdr中Mdr1b的表观遗传失调是镉暴露后异精症的潜在原因。
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