Ovarian function |
Higher doses of TCS led to ovarian oxidative damage and advanced reactive oxygen-dependent ovarian apoptosis (Guo et al., 2021). Urinary TCS concentration was also negatively correlated with sinus follicle count, negatively impacting ovarian reserve (Wang et al., 2020b). |
Steroidogenesis |
TCS could disorder energy metabolism and disrupt hormone homeostasis by dominating glucose flow to steroid hormone biosynthesis (Huang et al., 2020). |
Reproductive hormone levels |
Adult female mice exposed to TCS showed the lower serum luteinizing hormone (LH), follicle stimulating hormone (FSH), and progesterone, and gonadotropin releasing hormone (GnRH) mRNA levels (Cao et al., 2018). |
Carcinogenic effect on reproductive organs |
TCS facilitated ovarian cancer growth by regulating cell cycles and apoptosis-related genes through an ER-dependent pathway (Du et al., 2021). |
Impact on offspring |
Exposure to TCS during pregnancy and lactation could adversely influence the reproductive function and fertility in male rats of the F1 and F2 generations (Feng et al., 2016; Wang et al., 2018c), and lead to the decline of uterine weight and the occurrence of miscarriages (Patti et al., 2021). In addition, there was a significant association between prenatal TCS exposure and allergic disease in children (Lee et al., 2017). |