Biomedical subjects
Publications and source records attributed to A R Sheth.
Using indirect immuno-peroxidase staining technique, localization of immunoreactive follicle-stimulating hormone (IR-FSH) is demonstrated in the cytoplasm of the epithelial cells of normal human stomach. In view of their triangular shape and central nucleus and their predominance in the intermediate glands of the gastric mucosa, these cells are identified as parietal cells. The stromal tissue is devoid of staining reaction.
A comparative study on the localization of prostatic inhibin peptide was carried out by the immunoperoxidase technique in prostates of humans, bonnet and langur monkeys, marmosets, dogs, and rats. A positive reaction was observed in the prostatic epithelial cells of humans, in all three species of monkeys, and in the rat, while the dog prostate did not exhibit any reaction. These observations indicate a close immunological similarity among human, monkey, and rat prostatic inhibin peptides.
A synthetic C-terminal nonapeptide fragment of human seminal plasma inhibin preferentially enhances the basal release of FSH from rat pituitaries incubated in vitro, which indicates a direct action of the peptide on the pituitary. However, in the presence of LHRH, both FSH and LH release was increased particularly at higher doses of the nonapeptide. There was no change in prolactin release at 5 and 50 ng/ml but prolactin release was suppressed significantly at 500 ng/ml.
Prolactin-regulating factor (PRF) of molecular size of 25 kD has been isolated from human seminal plasma. This 25 kD factor inhibits circulating PRL levels in intact adult male rats to the extent of about 48% at dose level of 10 micrograms. Furthermore, in vitro incubation of pituitary demonstrated that PRF inhibits the release of PRL in the medium. PRF also interferes with the binding of I125 PRL to its receptors in liver, prostate, and spermatozoa. However, I125 PRF itself does not bind to these receptors. PRF seems to modulate PRL release as well as its binding to receptors. A sensitive, specific RIA was developed for PRF. Using the RIA, levels of PRF in seminal plasma were measured. PRF levels were low in vasectomized subjects as compared with controls. A negative correlation was noted with seminal plasma PRF levels and sperm count.
Age-related changes in human prostatic inhibin peptide (PIP) were carried out immunocytochemically in the prostate of various age ranges from newborn to 60 years. PIP was localized in the cytoplasm of the epithelial cells of the prostate at age 14 years and it persisted thereafter.
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Immunocytochemical study on the localization of inhibin in the testes of human, bonnet monkey, dog and rat was carried out using indirect immunoperoxidase technique, in order to investigate the cell types involved in inhibin production/storage. A positive reaction was observed in the testes of human, monkey and dog while it was negative in rat testis using specific antiserum to human testicular inhibin generated against homogeneous preparation of human testicular inhibin in our laboratory. Inhibin was found to be localized in Sertoli cells, spermatogonia and primary spermatocytes of human, monkey and dog testes. A weak positive reaction was observed in spermatids of human testis only. Interestingly, Leydig cells of human, monkey and dog testes showed positive reaction indicating presence of inhibin in these cells also.
Synthesis and biological profile of a decapeptide analogue, [Tyr85, Cys(Acm)87]85-94 of human seminal plasma inhibin (HSPI) are described. The peptide suppressed the circulatory levels of follicle stimulating hormone (FSH) in adult male rats. No change in the levels of luteinizing hormone (LH) and prolactin (Prl) was observed. Whereas the peptide suppressed the release of both FSH and LH in vitro. This decapeptide is the smallest peptide reported so far to have FSH suppressing activity.
Evidence to demonstrate suppressive effect of inhibin on prolactin has been presented. The inhibin preparations derived from human testicular tissue, human seminal plasma and porcine follicular fluid were tested and all the three preparations were found to exhibit prolactin suppressing activity.
Effects of prostatic inhibin and thyroid releasing hormone (TRH) on lipid peroxidation in rat prostate was studied in an in vitro system. It was found that both inhibited the lipid peroxidase activity thus having a protective role in the prostate.
This is a highly specific enzyme-linked immunosorbent assay (ELISA) for measuring prostatic inhibin-like peptide (PIP) in urine, in which we use penicillinase (EC 3.5.2.6) conjugated with PIP and, as solid phase, a polystyrene microtiter plate. We used this ELISA to measure PIP in 24-h urine specimens from men with prostatic cancer (PCa) and from age-matched controls. For prostatic cancer patients the mean +/- SEM urinary PIP of 36.1 +/- 5 micrograms/24 h was significantly (P less than 0.001) lower than the mean of 127.1 +/- 9 micrograms/24 h for the age-matched controls. PIP values for 30 samples measured by both ELISA and RIA correlated well (r = 0.985). We could detect as little as 1.56 ng of PIP in a sample. Analytical recovery of added PIP ranged from 91% to 104%. Mean CVs were 8.9% within-assay and 12.7% between-assay. We believe that this ELISA will be useful in assessing the status of PIP in men with normal and diseased prostates and in examining the function of the hypothalamus-pituitary-prostate axis.
The levels of immunoreactive prostatic inhibin-like peptide (PIP), having follicle-stimulating hormone suppressing properties, were estimated in the sera and urine samples of patients with benign prostatic hyperplasia (BPH) and prostatic carcinoma (PC) as compared to age-matched controls. Significantly elevated serum PIP levels in BPH (107.8 +/- 19 ng/ml) and PC (88.7 +/- 9 ng/ml) patients were observed as compared to those in control men (10.2 +/- 1 ng/ml). Unlike serum, in urine high levels of PIP in BPH (294 +/- 49 micrograms/24 h) and extremely low levels in PC (23.6 +/- 5 micrograms/24 h) patients were seen as compared to control values (137.6 +/- 10 micrograms/24 h). Furthermore, striking differences were observed between the urinary PIP levels of BPH and PC patients. The results of the present investigation thus indicate the possible use of urinary PIP as a biological marker for prostate cancer.
Immunohistological studies on the localization of inhibin in human testes were carried out to investigate the cell types involved in inhibin synthesis/storage. The paraffin embedded testicular tissues were stained by an indirect immunoperoxidase technique. Specific antiserum to human testicular inhibin generated against the homogenous preparation of human testicular inhibin at our laboratory was used as the first antibody. Inhibin was found to be localized in Sertoli cells, spermatogonia, and primary spermatocytes. A weak positive reaction was also observed in spermatids. Interestingly, Leydig cells showed positive reaction indicating presence of inhibin in these cells too.
In-vivo as well as in-vitro studies carried out demonstrate for the first time the interaction between thyroid releasing hormone (TRH) and inhibin at the pituitary, testes, prostate and spermatozoa levels. At the pituitary level both peptides act as antagonists to each other and modify the release of pituitary hormones. Further, these peptides act at the prostatic level wherein they modulate ornithine decarboxylase activity as well as 5 alpha-reductase activity. At the testicular level TRH blocks inhibin biosynthesis whereas in semen, it significantly reduces the binding of spermatozoa to specific antibodies directed against inhibin. In conclusion, although TRH and inhibin are widely different in their molecular size and chemical structure, these peptides seems to act antagonistically at multiple sites.
Forty-five men presenting with erectile dysfunction were evaluated through history and nocturnal penile tumescence, Doppler, and EMG studies. Fifteen were classified as having organic and 30 as having psychogenic impotence. Three men had mild hypergonadotropism with low testosterone levels. One had hyperprolactinemia. No case of hypogonadotropic hypogonadism was detected. Six patients who had psychogenic impotence had low levels of testosterone.
Prostatic inhibinlike peptide (PIP) was detected in the ventral but not in the dorsal lobe of rat prostate. On orchiectomy, PIP concentration in the ventral prostate increased significantly, whereas it decreased on testosterone administration and attained value comparable with that in intact control. Estradiol-17 beta treated animals exhibited high levels of PIP in absence of significant alterations in the protein content. The effect of prolactin and human chorionic gonadotropin on PIP concentration was not so prominent at the dose levels studied. The present study thus demonstrates negative regulation of PIP by testosterone and stimulatory effect of estradiol-17 beta on PIP in rat ventral prostrate.
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