Bromocriptine induced hypoprolactinemia and accessory reproductive glands response to testosterone in castrated male rats.

Testosterone stimulates the Accessory Reproductive Glands (ARG) and may increase the serum titres of prolactin in castrated male rats. Bromocriptine antagonizes the testosterone-induced alteration of ARG responses; the testosterone antagonistic action of bromocriptine depends on the degree of serum prolactin depletion.

Pimozide-induced chronic hyperprolactinaemia and quantitative initiation of spermatogenesis in maturing rats.

When pimozide was given to maturing rats, a rise in the level of prolactin in the serum was accompanied by a fall in LH. There was also incomplete initiation of spermatogenesis as well as simultaneous adrenal hypertrophy. Bilateral adrenalectomy failed to prevent hyperprolactinaemia-induced antispermatogenic response, while a significant ameliorating effect was observed with LH, indicating that hyperprolactinaemia influenced the quantitative initiation of spermatogenesis by affecting the secretion of LH.

Spermatogenesis in rat: effect of L-tryptophan loading.

The present experiment was designed to assess the role of enhanced central 5-HT level on testicular steroidogenesis and spermatogenesis of rat. L-tryptophan, a precursor in the synthesis of 5-HT in brain, was injected in male rats on a short-term (7-days) and a long-term (21-days) basis. The short-term treatment had no effect on the spermatogenic pattern (Stage - VII of the cycle of the seminiferous epithelium), while the long-term treatment showed a degenerative change (reduced count of the germ cells).

Effect of corticosterone on serum concentrations of alpha 2 micro-globulin and on spermatogenesis in oestrogen-treated rats.

Treatment of adult male rats with oestradiol-17 beta (50 microgram/100 g body wt per day for 7 days) resulted 14 days later in reduced levels of alpha 2 micro-globulin in serum and inhibition of spermatogenesis. Administration of corticosterone (2 mg/day) for 14 days to oestrogen-treated rats raised the concentration of alpha 2 micro-globulin in the serum and prevented spermatogenic degeneration. It is concluded that endogenous alpha 2 micro-globulin induced by corticosterone may play a role in spermatogenesis in oestrogenized rats.

Prolactin suppression and spermatogenic developments in maturing rats. A quantitative study.

Prolonged suppression of prolactin (PRL) in immature male rats inhibits the spermatocyte-spermatid conversion process, alters leydig cell morphology, decreases accessory sex organ weight and increases serum LH levels without a significant alteration in serum FSH concentration. Amelioration of these effects by exogenous PRL strongly indicates that in the absence of PRL excess titers of endogenous LH fail to exert an influence on the spermatogenic activity of maturing testes.

Urinary excretion of alpha 2 mu-globulin and albumin by adult male rats following treatment with nephrotoxic agents.

Nephrotoxic agents such as puromycin aminonucleoside (PAN) and sodium maleate (MAL) have been used to induce experimental glomerular proteinuria and tubular disease, respectively. Current studies show that PAN caused a massive loss of albumin in the urine while not affecting the excretion of the smaller, sex-dependent alpha 2 mu-globulin. On the other hand, MAL which inhibits the reabsorption of proteins, increased the loss of both alpha 2 mu and albumin.

Augmentation of luteinizing hormone action by prostaglandin E2 in the prevention of antispermatogenic effect of indomethacin. Indomethacin & spermatogenesis.

Administration of indomethacin exhibited antigonadal action by inhibiting the Leydig cells, sex-accessories and spermatocyte-spermatid conversion process. Administration of PGE2 or PGF2 alpha had no effect on Leydig cell nuclear volume or accessory organ weights, but PGE2 had a restorative effect on the efficiency of meiosis, although at a statistical non-significant level. Administration of LH to indomethacin treated rats restored the accessories fully with a non-significant effect on the yield of step-7 spermatids from meiosis.

Possible alpha-adrenergic involvement in nicotine induced alteration of spermatogenesis in rat.

Nicotine caused a fall in primary spermatocyte number together with a retardation of spermatocyte to spermatid conversions process. These effects of nicotine were possibly secondary to increased activity of adrenomedullary catecholamines, since the antispermatogenic effect of nicotine was prevented by phentolamine, a known blocker of catecholamine action at the alpha-receptor level.

Andrenogonadal interactions in nicotine-induced alteration of steroidogenesis in male rat.

Chronic nicotine administration in larger doses inhibits steroidogenesis in testis. This inhibition is possibly secondary to increased adrenomedullary norepinephrine activity, since the anti-steroidogenic effect of nicotine can be prevented by alpha-adrenergic blocker like phentolamine. In vitro incubation of testicular slices with nicotine failed to elicit any appreciable effect on delta 5-3 beta-hydroxysteroid dehydrogenase activity indicating lack of direct action of nicotine on testicular steroidogenesis.

In vitro studies on histochemical localization of testicular delta5-3beta-hydroxysteroid dehydrogenase activity from indomethacin pretreated rats--effect of prostaglandins and luteinizing hormone.

In vitro studies on the effect of LH and prostaglandins on delta5 3beta-hydroxysteroid dehydrogenase activity using indomethacin pre-treated testis as the experimental model, revealed a greater stimulation of the enzyme activity when the incubation medium contained LH and PGE2 both at a concentration of 1 microgram/ml in comparison to the effect produced by 1 microgram LH/ml alone, but the augmentory effect of PGE2 on testicular response to LH was not evidenced as the LH: PGE2 ratio became 1 : 10. Neither PGE2 nor PGF2A produced any stimulation of the enzyme activity at concentrations of 1, 10, or 20 microgram/ml in the incubating medium. PGF2A at concentrations of 1 or 10 microgram/ml did not appear to interfere with LH action on this steroidogenic enzyme.

Histochemical studies of testicular delta5-3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase after chronic indomethacin administration in rats pretreated with clomiphene-citrate.

Histochemical studies of testicular delta5-3beta-Hydroxysteroid Dehydrogenase and 17beta-Hydroxysteroid Dehydrogenase in sexually immature rats treated chronically with simultaneous Indomethacin and Clomiphene revealed greater inhibition in the enzyme activities when compared to Clomiphene treated animals alone. This suggests prostaglandin-inhibitors may be directly inhibitory to NAD-requiring enzymes involved in testicular steroid biosynthesis.