Vitamin D improves oxidative stress and histopathological damage in rat ovaries caused by hyperthyroidism

The aim of this study is to investigate the histopathological and biochemical efficacy of vitamin D on oxidative damage and fibrosis in rat ovaries induced by experimental hyperthyroidism.

This study is a comparative, prospective experimental rat study. Sprague-Dawley female rats were divided into four groups. Only distilled water was given to the rats in group 1 for 25 days. In group 2, 100 μg/day L-thyroxine was given to rats for 25 days. In Group 3, 100 μg/day L-thyroxine and 200 IU/day vitamin D were given to rats for 25 days. In group 4, only 200 IU/day vitamin D was administered for 25 days.

This study is the first to demonstrate the protective effect of vitamin D against ovarian damage caused by experimental hyperthyroidism. Hyperthyroidism caused fibrotic degenerative changes in the ovaries and an increase in the fibrillin 1 score. It caused serum follicle-stimulating hormone (FSH) levels to increase and serum E2 levels to decrease. In addition, malondialdehyde (MDA) and total oxidant status (TOS) levels increased in rats with hyperthyroidism. Vitamin D decreased MDA and TOS values and increased total antioxidant status (TAS) values in rats with hyperthyroidism. It also increased TSH values by causing a decrease in TT3 and TT4 values. It decreased fibrosis, follicle degeneration, stromal degeneration, and fibrillin 1 score in ovarian tissue.

Vitamin D has positive histopathological and biochemical effects on the oxidative stress and follicle damage caused by hyperthyroidism in ovarian tissue. Human studies with larger case populations should be conducted to evaluate the effects and clinical applications of vitamin D.