Perinatal Propylthiouracil-Induced Hypothyroidism Impaired Motor Coordination in Adult Female Offspring

Thyroid hormone (TH) play crucial roles in the growth and development of brain. Efficiency of TH during the perinatal period results in severe mental and physical retardation, known as cretinism in humans. Animal models have largely focused on mild and severe hypothyroidism associated with deficits in body weight, developmental delays, and cognitive deficits. Although various behavioral analyses have been reported, the effect of perinatal hypothyroidism in adult female mice has not been clarified. The aim of this study was to examine whether propylthiouracil (PTU)-induced hypothyroidism could impair motor coordination in female offspring. We used C57BL/6j mice and divided them into three groups based on the dose of PTU which was applied during perinatal period (embryonic day-14 to postnatal day-14); control, 5 ppm, and 50 ppm groups. We observed motor coordination function and additional nociceptive test in female offspring. We found that motor coordination and nociceptive threshold were affected in 50 ppm groups. We concluded that the moderate hypothyroidism could impair motor coordination in adult offspring.

Perinatal hypothyroidism modulates antioxidant defence status in the developing rat liver and heart

In the present study, we investigated oxidative stress parameters and antioxidant defence status in perinatal hypothyroid rat liver and heart. We found that the proteincarbonyl content did not differ significantly between the three groups both in the pup liver and in the heart. The OH˙ level was significantly decreased in the hypothyroid heart but not in the liver compared with controls. A slight but not significant decrease in SOD activity was observed in both perinatal hypothyroid liver and heart. A significantly increased activity of CAT was observed in the liver but not in the heart of hypothyroid pups. The GPx activity was considerably increased compared with controls in the perinatal hypothyroid heart and was unaltered in the liver of hypothyroid pups. We also found that vitamin E levels in the liver decreased significantly in hypothyroidism and were unaltered in the heart of perinatal hypothyroid rats. The GSH content was elevated significantly in both hypothyroid liver and heart. The total antioxidant capacity was higher in the liver of the hypothyroid group but not in the hypothyroid heart. Thyroxine replacement could not repair the above changes to normal. In conclusion, perinatal hypothyroidism modulates the oxidative stress status of the perinatal liver and heart.