[CAS NO. 51-52-5]  Propylthiouracil

Propylthiouracil-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism in rats, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms. Propylthiouracil-induced congenital hypothyroidism upregulates vimentin phosphorylation and depletes antioxidant defenses in immature rat testis. Propylthiouracil results in lesser concentrations of thyroxine (T4) and triiodothyronine (T3), greater concentrations of follicle stimulating hormone (FSH) and luteinizing hormone (LH) peptides, and increase in steroidogenic gene expression after 12 hours and 48 hours in zebrafish. Propylthiouracil-induced hypothyroidism is associated with increased tolerance of the isolated rat heart toischaemia-reperfusion. Propylthiouracil (PTU) dramatically reduces thyroid hormones on PND21 and produced deficits in body weight that persisted to adulthood in developing rats. Propylthiouracil inhibits both the synthesis of thyroid hormones in the thyroid gland and the conversion of T4 to its active form, T3. Propylthiouracil treatment significantly increases circulating TSH at both P3 and P7. Propylthiouracil exposure of adult rats, at a dose inducing modest reductions in circulating T4 concentrations and no significant effect on brain BDNF, significantly alteres the thyroid hormones and hippocampal BDNF levels in the offspring at 3 and 7 d after birth.