Maternal exposure to cadmium from puberty through lactation induces abnormal reproductive development in female offspring

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 (3 beta-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.

Automated summary

The research found that maternal cadmium exposure can result in reproductive developmental issues in female offspring on PND21, including delayed vaginal opening, irregular estrous cycle, and inhibited follicular development.