Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China; Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, Anhui Medical University, Hefei, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Anhui Medical University, Hefei, China.
Department of Toxicology, School of Public Health, Anhui Medical University, Hefei, China; Key Laboratory of Environmental Toxicology of Anhui Higher Education Institutes, Anhui Medical University, Hefei, China; Anhui Provincial Key Laboratory of Population Health & Aristogenics, Anhui Medical University, Hefei, China.
Ecotoxicol Environ Saf. 2022 Sep 1;242:113927. doi: 10.1016/j.ecoenv.2022.113927. Epub 2022 Jul 29.
Four-week-old female ICR mice were exposed to Cd through drinking water from puberty through lactation to investigate the effects of reproductive development in female offspring. Our results showed that maternal Cd exposure from puberty to lactation induced vaginal opening delay, and disturbed estrous cycle in the offspring on postnatal day (PND) 21, without affecting the body weight at vaginal opening. The histopathology results showed the increased primordial follicles and the decreased secondary follicles, and the mRNA level of Amh increased in the offspring's ovaries upon Cd exposure, suggesting the inhibition of ovarian follicular development on PND21. Moreover, the level of serum estradiol reduced and genes associated with steroidogenesis (3β-Hsd, P450scc and P450arom) were downregulated upon Cd exposure on PND 21. Thus, Cd may inhibit the follicular development via disturbing the mRNA level of genes associated with steroidogenesis and then the synthesis of estradiol in prepuberty. Taken together, despite the lack of attention to estrous cycle at termination, maternal Cd exposure from puberty to lactation induced the adverse effects on reproductive development of female offspring, including the delay of vaginal opening, irregular estrous cycle and inhibition of follicular development, via disturbing the mRNA level of genes associated with follicular development and steroidogenesis.
四周龄雌性 ICR 小鼠从青春期到哺乳期通过饮水暴露于 Cd，以研究雌性后代生殖发育的影响。我们的结果表明，母体从青春期到哺乳期的 Cd 暴露导致阴道开口延迟，并在产后第 21 天扰乱了后代的动情周期，而不影响阴道开口时的体重。组织病理学结果显示，Cd 暴露后，后代卵巢中的原始卵泡增加，次级卵泡减少，Amh 的 mRNA 水平升高，提示卵巢卵泡发育在 PND21 时受到抑制。此外，Cd 暴露后，血清雌二醇水平降低，与类固醇生成相关的基因（3β-Hsd、P450scc 和 P450arom）的 mRNA 水平下调。因此，Cd 可能通过干扰与类固醇生成相关的基因的 mRNA 水平，进而干扰雌二醇的合成，从而抑制青春期前卵泡的发育。总之，尽管在研究结束时没有关注动情周期，但母体从青春期到哺乳期的 Cd 暴露通过干扰与卵泡发育和类固醇生成相关的基因的 mRNA 水平，对雌性后代的生殖发育产生了不良影响，包括阴道开口延迟、动情周期不规则和卵泡发育抑制。
