Thyroid hormones alter estrous cyclicity and antioxidative status in the ovaries of rats

To expand our understanding of the roles of thyroid hormones on female reproduction, we induced hypo‐ and hyper‐T rat models to investigate the roles of thyroid hormones on estrous cyclicity, as well as the antioxidative status in the ovaries of rats. In the current study, our data show that hypothyroidism (hypo‐T) and hyperthyroidism (hyper‐T) led to significantly reduced body weights and ovarain weights and delayed vaginal opening day. For hyper‐T, thyroxine (T4), tri‐iodothyronine (T3), progesterone (P4) and follicle‐stimulating hormone (FSH) were significantly increased, while estradiol (E2) and luteinizing hormone (LH) were significantly decreased. For hypo‐T rats, serum levels of total T4 and T3, E2, P4, FSH and LH were significantly increased, while concentrations of E2 and LH were significantly decreased. For ovary morphology, the numbers of secondary and antral follicles were significantly decreased with more atretic antral follicles and less corpora lutea in both hyper‐ and hypo‐T groups. Both hyper‐T and hypo‐T treatment significantly decreased the expressions of thyroid hormone receptor α1 in the ovary. Hypo‐T significantly reduced nitric oxide (NO), total NO synthase (tNOS), inducible NOS and constitutive NOS activities, but hyper‐T increased them. For antioxidative parameters, hypo‐T and hyper‐T treatment significantly increased malondialdehyde (MDA) contents. The activities of both glutathione peroxidase (GSH‐Px) and catalase (CAT) significantly decreased in the hypo‐T group but increased in the hyper‐T group. Total superoxide dismutase (T‐SOD) activity was significantly increased in the hyper‐T group. In summary, thyroid hormones alter estrous cyclicity and antioxidative status in the ovary of the rat may act through the NOS signaling pathway.