Histochemical & radioisotopic study of the effects of malonate treatment on plasmal formation in rat liver.
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Animals↗
Biomedical subjects
C Deb
Publications and source records attributed to C Deb.
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. On the contrary, prostaglandins, both PGE2 and PGF2A, at concentrations of 20 microgram/ml, antagonized LH action over testicular delta5-3beta-hydroxysteroid dehydrogenase activity. On the basis of these findings, it appears that prostaglandin E2 in some way, is necessary for manifestation of the steroidogenic action of LH in testis.
3-Hydroxysteroid Dehydrogenases↗
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.
3-Hydroxysteroid Dehydrogenases↗
Action of mitomycin C on testicular steroidogenesis and its probable mode of action in albino rats.
Testicular steroidogenesis was determined by radioimmuno assay of serum testosterone and histochemical demonstration of the key steroidogenic enzyme (delta 5 3 beta hydroxysteroid dehydrogenase) activity in the Leydig cells after treatment with mitomycin C (mc), (500 microgram/kg, Bwt). In vivo experiments showed mc treatment causes a remarkable fall of serum testosterone level along with significant reduction in the weights of testis and sex accessories. In vitro studies resulted in a diminution in the delta 5 3 beta hydroxysteroid dehydrogenase and glucose-6-phosphate dehydrogenase activity in the section of the testis after addition of mc (100, 200 microgram/ml) in the incubation medium. The consideration of the above findings coroborated to the suggestion that mc reduced testicular steroidogenesis.
3-Hydroxysteroid Dehydrogenases↗
Effect of quinalphos on testicular steroidogenesis in rats.
The effect of quinalphos (250 micrograms/kg i.p.) an organophosphorus insecticide treatment for 13 and 26-days on the testicular steroidogenic enzymes viz. 3 beta-Hydroxysteroid Dehydrogenase and 17 beta-Hydroxysteroid Dehydrogenase, as well as cholesterol content and histology of the testes of the Wistar strain rats was studied. The time duration of 13 days is approximately equivalent to one cycle of the seminiferous epithelium in Wistar strain rats. Treatment of quinalphos for 13 days failed to produce any effect on the relative weights of the testes and accessory sex glands. However, significant inhibition of 3 beta-HSD activity and increased cholesterol level in testis were observed. The rats treated for 26 days similarly showed a highly significant inhibition of the activity of both 3 beta-HSD and 17 beta-HSD. The relative weights of the testes and accessory sex glands were also significantly reduced. Histological examination of the testis revealed that quinalphos treatment produced detrimental changes in the seminiferous epithelium. Treatment with quinalphos for 13-days produced no toxic effect with the exception of a significant increase in serum alkaline phosphatase. However, after 26-days of treatment toxicity was significantly increased as reflected on serum transaminases, phosphatases and blood urea levels of rat. Present study indicated that quinalphos impairs testicular functions in rats.
17-Hydroxysteroid Dehydrogenases↗
Effect of aldrin on accessory sex glands and plasma testosterone levels in rats.
The effects of aldrin, an organochlorine insecticide, on accessory sex glands and plasma testosterone levels in rats were studied. The aldrin was administered i.p. for 13 days and 26 days at a dose of 150 micrograms/kg. Relative weights of prostate, seminal vesicles and coagulating glands were significantly decreased in the treated rats compared to those in controls. In addition, there was a significant fall in acid phosphatase activity in prostate and fructose content in accessory sex glands was also observed in treated animals. Plasma testosterone values showed a decrease with the duration of treatment. HCG supplementation with aldrin treatment prevented all those untoward effects of aldrin in experimental rats.
Acid Phosphatase↗