| Objective:Cadmium（Cd）,a well-known environmental pollutant,can damage the reproductive system.However,the effects of maternal Cd exposure on reproductive system of the offspring have not been clarified.In this study,female ICR mice were exposed to Cd through drinking water to investigate the effects of reproductive development in female offspring.Methods:Four-week-old female ICR mice were randomly divided into 3 groups（control,low-Cd and high-Cd group）.Each group received 0,10,or 100 mg/L Cd chloride（Cd Cl2）through drinking water,respectively.Female mice in the treatment groups were exposed to Cd through drinking water for 4 weeks,and mated with normal male mice at a ratio of 1:2.The pregnant mice were continuously exposed to Cd during gestation and lactation periods.Body weight and the time of vaginal opening of offspring were observed and recorded.The vaginal smears were made to document the stages of the estrous cycle.Sections of ovaries were stained with hematoxylin and eosin for morphological evaluation and follicular count.The level of hormone in serum was determined by ELISA kits.The quantitative real-time reverse transcription PCR was used to detect the mRNA levels of genes related to follicular development in ovaries of the offspring.Results:Maternal Cd exposure from puberty to lactation induced vaginal opening delay,and disturbed estrous cycle in the offspring.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.Conclusion: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. |
