Specific activities of seminal vesicular phosphomonoesterases and Mg2+-,Ca2+- and Na+/K(+)-adenosine triphosphatases in hypo- and hyperthyroid albino rats.

Hypothyroidism (surgical thyroidectomy) inhibited the activities of acid phosphatase and Mg(2+)-ATPase in seminal vesicular tissue and fluid and that of Ca(2+)- and Na+/K(+)-ATPases in fluid alone, and T4 supplementation restored normalcy in all, except acid phosphatase. Hyperthyroidism (T4 25 micrograms/100g body weight/day for 60 days, im) enhanced the activities of alkaline phosphatase and ATPases in seminal vesicular tissue and fluid, and decreased acid phosphatase activity in tissue alone. Withdrawal of T4 treatment from hyperthyroid rats (after 30 days) augmented the activity of ATPases in tissue and impaired the same in fluid, while phosphomonoesterases remained at hyperthyroid level. The results suggest specific responses of various seminal vesicular phosphatases to altered thyroid hormone status. Modification in the specific threshold of androgen/estrogen action on different phosphatases in seminal vesicles appears to be the plausible mechanism underlying these changes in hypo- and hyperthyroid conditions.

Influence of prolactin on pulmonary lipids in mature male bonnet monkey, Macaca radiata.

Administration of ovine prolactin (250 micrograms/kg body weight/day) for 30 days to mature male bonnet monkeys increased the pulmonary total lipids and total phospholipids. While total cholesterol did not show any appreciable change in PRL treated monkeys, the ratio of free: esterified cholesterols was altered with perceptible decrease in free cholesterol and increase in esterified cholesterol. Pulmonary tissue total glyceride glycerol concentration was diminished as a result of decreased monoacyl, diacyl and triacyl glycerols. Among phospholipid fractions, phosphatidylcholine and phosphatidylinositol were elevated while phosphatidic acid and cardiolipin were reduced. The data suggest that hyperprolactinemia interferes with pulmonary lipid metabolism in adult monkeys and modifies the ratio of cholesterol and phospholipid composition. Further, hyperprolactinemia appears to favour esterification of cholesterol with specific changes in phospholipid fractions. Thus, the present study demonstrates that hyperprolactinemia modifies the pattern of pulmonary neutral and phospholipid fractions and thereby is likely to affect the structure and function of mature primate lungs.