Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.

Polycystic ovary syndrome is a very common cause of female infertility. This study aims to assess the prevalence of vitamin D deficiency and its association with clinical and anthropometric characteristics of Iraqi women with and without polycystic ovary syndrome. Fifty eightwomen with the disease and their matched control group were included. Their blood pressure was measured. Serum level of 25 hydroxy vitamin D of <20 ng/mL was graded as vitamin D deficiency. The polycystic ovary syndrome group had significantly lower levels of 25 hydroxy vitamin D, higher body mass index, and higher waist to hip ratio in contrast to the control group. The difference in body mass index was more significant in the obese category. Within subjects with the waist to hip ratio of  ≥0.85, who were all vitamin D deficient, vitamin D was significantly lower and waist to hip ratio was significantly higher in patients than in controls. Vitamin D levels were significantly lower in patients than in controls in the non-hypertensive category. Further studies are needed to investigate the role of vitamin D in the pathogenesis of polycystic ovary syndrome.