Epigenetic dysregulation of Mdr1b in the blood-testis barrier contributes to dyszoospermia in mice exposed to cadmium
文献类型： 外文期刊
作者： Fang, Yu 1 ; Xiang, Ying 1 ; Lu, Xing 2 ; Dong, Xin 1 ; Zhang, Jiexin 1 ; Zhong, Shan 1 ;
作者机构： 1.Wuhan Univ, Dept Med Genet, Sch Basic Med Sci, Wuhan 430071, Peoples R China
2.Chinese Acad Fishery Sci, Yangtze River Fisheries Res Inst, Key Lab Freshwater Biodivers Conservat & Utilizat, Minist Agr, Wuhan 430223, Hubei, Peoples R China
3.Hubei Prov Key Lab Allergy & Immunol, Wuhan 430071, Hubei, Peoples R China
关键词： Cadmium; Blood-testis barrier; Dyszoospermia; Mdr1b; Epigenetic regulation
期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.291； 五年影响因子：6.393 ）
ISSN： 0147-6513
年卷期： 2020 年 190 卷
页码：
收录情况： SCI
摘要： 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.
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