Differential effect of hyperthyroidism on rat epididymal glycosidases.

The impact of hyperthyroidism on epididymal glycosidases was studied in albino rats. Hyperthyroidism was induced in Wistar rats aged 30 days by daily injection of T4 (25 microg/100 g body weight/day intramuscularly) for 30 or 60 days; control rats were injected with vehicle (alkaline saline, pH 7.8). One set of hyperthyroid rats was reverted to euthyroid status by withdrawing T4 treatment after 30 days of hyperthyroidism. To asses the direct effect of thyroid hormone on epididymal hexosaminidases, caput, corpus and cauda tissues were stimulated with 25, 50 or 100 ng/mL T3 for 24 h, after an initial culture of 24 h. The activity of beta-glucosidase decreased in caput, corpus and cauda epididymis of hyperthyroid rats. beta-Galactosidase activity increased in the caput epididymis irrespective of the duration of hyperthyroidism. While a similar decrease occurred in the corpus and cauda epididymis in the 30 day hyperthyroid group, an opposite trend was observed in 60 day hyperthyroid rats. Caput beta-N-acetylglucosaminidase activities increased at both time points, whereas activity decreased in the corpus and cauda in 30 day, but increased in 60 day hyperthyroid rats. Hyperthyroidism consistently increased caput and corpus beta-N-acetylgalactosaminidase activity irrespective of the duration. Cauda epididymal beta-N-acetylgalactosaminidase activity was decreased in 30 day and increased in 60 day hyperthyroid rats. Hyperthyroidism induced changes in caput beta-galactosidase, beta-N-acetylgalactosaminidases, corpus beta-N-acetylglucosaminidase and cauda beta-N-acetylgalactosaminidase which were irreversible while the remaining actvities were brought back to normal when T4 treatment was withdrawn. In vitro studies showed that T3 stimulates epididymal hexosaminidases (beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase) irrespective of the dose. These data suggest that thyroid hormones have a specific and direct influence on glycosidases in specific regions of the epididymis.

Thyroidectomy modulates rat prostatic monosaccharides.

Earlier studies have shown that thyroid hormones play an important role in glycoprotein metabolism in the prostate. In this paper, hypothyroidism induced changes in prostatic glycoprotein-associated monosaccharides and fructose concentrations were studied in 30-day-old peripubertal rats. Hypothyroidism was induced by total surgical thyroidectomy and confirmed by radioimmunoassay (RIA) of thyroid hormones and thyroid stimulating hormone (TSH). Animals were killed after 30 and 60 days post-thyroidectomy. To test the direct effect of thyroid hormones on prostatic monosaccharides, prostatic tissue was incubated for 24 h at 37 degrees C with 25, 50 or 100 ng/mL T3. Ventral prostatic hexosamines and sialic acid concentrations were significantly decreased in hypothyroid rats aged 30 and 60 days, whereas fucose concentration was increased at 30 days but decreased at 60 days in hypothyroid rats. In the case of the dorsolateral prostate, hypothyroidism enhanced the concentration of hexosamines but caused a decrease in levels of fucose, sialic acid and fructose, irrespective of the duration of hypothyroidism. Concentrations of fucose, fructose and hexosamines in the anterior prostate were decreased and sialic acid concentration was increased in 60-day hypothyroid rats. In in vitro studies, the concentrations of fucose, sialic acid and hexosamines were significantly increased in all three prostatic lobes irrespective of the T3 dose with which they had been incubated. A consistent increase in fructose concentration was observed in anterior and dorsolateral prostates when incubated with different doses of T3 stimulation. It is concluded that the influence of hypothyroidism on prostatic monosaccharides seems to be specific for each sugar in different lobes of the prostate. These results clearly show that thyroid hormones differentially regulate prostatic glycoprotein metabolism.

Impact of altered thyroid hormone status on prostatic glycosidases.

The impact of hyper- and hypothyroidism on prostatic glycosidases was investigated. Hyper-thyroidism was induced by administering L-thyroxine (25 micrograms/100 g body weight/day) for 60 days and hypothyroidism was induced by total thyroidectomy. To test the direct influence of thyroid hormones, prostatic lobes were incubated with different concentrations (10, 25 and 50 ng/mL) of T3 and beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase were assayed. Serum levels of thyroid hormones, oestradiol and testosterone increased in hyperthyroid, and decreased in hypothyroid rats. TSH decreased in hyperthyroid, and an opposite trend was seen in thyroidectomized, rats. Prostatic [anterior (coagulating glands), dorsolateral and ventral prostates] beta-glucosidase, beta-galactosidase, beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase activities increased uniformly in hyperthyroid, and decreased in thyroidectomized, rats. In vitro studies showed a dose-dependent stimulatory effect of T3 on beta-N-acetylglucosaminidase and beta-N-acetylgalactosaminidase in all three lobes of the prostate. From the present study, it is concluded that hyperthyroidism augments and hypothyroidism inhibits prostatic glycosidases and T3 has a direct stimulatory effect on these enzymes.

Inhibition of Leydig cell activity in vivo and in vitro in hypothyroid rats.

Leydig cell steroidogenic activity under basal and stimulated conditions was studied in hypothyroid rats. Hypothyroidism was induced at a prepubertal age (30 days postpartum) by surgical thyroidectomy, and L-thyroxine (T4) supplementation (6 micrograms/100 g body weight/day for 30 days) to hypothyroid rats was begun after 30 days. Hypothyroidism for 60 days reduced serum LH and FSH without affecting prolactin. Serum and intratesticular testosterone and the specific activity of Leydig cell 3 beta- and 17 beta-hydroxysteroid dehydrogenases diminished in hypothyroid rats. The stimulatory effect of LH on Leydig cell steroidogenic activity and cAMP was also adversely affected in hypothyroid rats. All these changes were reversed by T4 supplementation. The present results suggest that prepubertal hypothyroidism suppresses both basal and stimulated Leydig cell activity in adult rats.

Dorsolateral prostatic phosphomonoesterases and adenosine triphosphatases in hypo- and hyperthyroid rats.

Specific activities of phosphomonoesterases (acid and alkaline phosphatases) and adenosine triphosphatases (Mg2+, Ca2+ and Na+/K+ dependent ATPases) of dorsolateral prostate were studied in albino rats, under altered thyroid hormone status. Thyroidectomy induced hypothyroidism and thyroxine administered hyperthyroidism (25 micrograms/100 g body wt/day for 60 days, im) showed no impact on the activity of acid phosphatase. Three fold decrease in the activity of alkaline phosphatase was observed in hyperthyroid group. Ca2+ and Mg2+ dependent ATPases were significantly decreased in hypo- and hyperthyroid status whereas Na+/K+ ATPase was decreased in hyperthyroidism and showed an opposite trend in hypothyroid group.

Influence of thyroidectomy on seminal vesicular glycosidases of young albino rats.

Impact of thyroidectomy (hypothyroidism) on few glycosidases was studied in the seminal vesicles of young albino rats. Thyroidectomy was performed at 30 days post partum. Seminal vesicular beta-D-glucosidase, beta-D-galactosidase, and N-acetyl-beta-D-galactosaminidase exhibited a similar response of decreased activities under short- (30 days) and long-term (60 days) hypothyroid conditions. On the other hand, N-acetyl-beta-D-glucosaminidase registered a temporal biphasic response of increased and decreased activities in the seminal vesicles of rats subjected to short- and long-term hypothyroidism, respectively. The data obtained in the present study suggest that thyroid hormones have specific influences on different glycosidases in the seminal vesicles of rats and euthyroid status is essential for the maintenance of normal activities of these enzymes.

Impact of hyperprolactinaemia on testicular neutral lipids and phospholipids in mature bonnet monkeys, Macaca radiata (Geoffroy).

Impact of hyperprolactinaemia, induced by daily injection of ovine prolactin (250 micrograms/kg body weight, ip for 30 days) on testicular lipids was studied in M. radiata. Wet weights of testis and accessory sex organs decreased in hyperprolactinaemic monkeys. Even though total lipids in the testis did not show any significant change, total cholesterol and total glyceride glycerol decreased. While all fractions of testicular neutral lipids showed a perceptible decrease, phosphatidic acid, phosphatidyl ethanolamine and phosphatidyl choline increased in hyperprolactinaemic monkeys. Hyperprolactinaemia appears to influence male fertility by altering the composition of testicular neutral lipids and phospholipids.