Research has revealed that cadmium can disrupt ovarian function; however, few reports have focused on MI oocytes meiotic progression, especially the activity of maturation promoting factor (MPF) and its related genes (Cdk1, Ccnb1, and Cdc25b) expression. In this study, GV oocytes cultured in vitro for 0, 6, and 9 hours with five groups (control and doses of 0.05, 0.5, 2.5, and 5 μM Cd). At the same dose of cadmium but different exposure time: compared with 0h, Periodic changes in MPF activity were changed and continuously increased over time. The mRNA and protein expression of each MPF-related gene in different cadmium dose groups were changed compared with that of 0h. At the same exposure time but different dose of cadmium: compared with control group, MPF activity, mRNA and protein expressions of each MPF-related gene in all the cadmium exposure groups were increased at 9h after exposure. Cadmium maintains the high MPF activity in mouse MI oocytes during its meiotic process and disturbs the periodic change of MPF activity; meanwhile, cadmium exposure promotes the syntheses of MPF-related gene, which may be one of the molecular mechanisms for the maintenance of high MPF activity, and ultimately prevents the meiotic progression in oocytes.

研究表明，镉会破坏卵巢功能。但是，很少有报道关注MI卵母细胞的减数分裂进程，特别是成熟促进因子（MPF）及其相关基因（Cdk1，Ccnb1和Cdc25b）的表达。在这项研究中，GV卵母细胞与5组（对照组和0.05、0.5、2.5和5μMCd的剂量）在体外培养了0、6和9小时。在相同剂量的镉但不同的暴露时间下：与0h相比，MPF活性的周期性变化会随着时间的推移而变化并不断增加。与0h相比，不同镉剂量组各MPF相关基因的mRNA和蛋白质表达均发生变化。在相同暴露时间但镉剂量不同的情况下：与对照组相比，MPF活性，镉暴露后9h各MPF相关基因的mRNA和蛋白质表达均升高。镉在减数分裂过程中在小鼠MI卵母细胞中维持较高的MPF活性，并扰乱了MPF活性的周期性变化。同时，镉暴露促进了MPF相关基因的合成，这可能是维持高MPF活性的分子机制之一，并最终阻止了卵母细胞的减数分裂进程。