Pubertal exposure to bismerthlazol inhibits thyroid function in juvenile female rats

Abstract

Bismerthiazol, as a thiadiazole fungicide, is widely used in China. The structure of bismerthiazol shows a close relationship to N, N-methylene-bis (2-amino-1,3,4-thiadiazole) (Bis-A-TDA), which is a teratogen. A few studies have shown that this fungicide acts as an endocrine disruptor in mature rats via disturbance in thyroid hormone homeostasis at a certain dose. Little is known about the effect of pubertal exposure to bismerthiazol on the development in pubertal female rats. Based on the protocol of the 20-Day Pubertal Female Assay, postnatal days (PND) 22 old SD rats were administered with bismerthiazol daily by oral gavage at doses of 0, 10, 20 or 40 mg/kg/day for 20 days. After treatment, the rats were sacrificed for blood collection; the reproductive organs, liver, pituitary, adrenal and thyroid gland were harvested. The results indicated that changes in thyroid endpoints following bismerthiazol administration were decreased serum triiodothyronine (T 3) and thyroxine (T 4) concentrations, increased thyroid stimulating hormone (TSH) concentrations and the ratios of thyroid gland weights, and produced thyroid gland hyperplasia. No histological changes were observed in the uterus and ovaries; moreover, the age and weight at vaginal opening (VO) were unaffected by bismerthiazol in all treatment groups. These data and changes demonstrate that bismerthiazol is likely a thyroid disrupter in female rat following exposure during development, but does not affect the development of pubertal female rats. Further studies using environmentally relevant doses are needed for hazard identification.