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N. M. Biswas

Bio: N. M. Biswas is an academic researcher from University of Calcutta. The author has contributed to research in topics: Testosterone & Spermatogenesis. The author has an hindex of 13, co-authored 35 publications receiving 619 citations.

Papers
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Journal Article
TL;DR: Arsenite has a suppressive influence on spermatogenesis and gonadotrophin and testosterone release in rats, with significant dose-dependent decreases in the accessory sex organ weights, epididymal sperm count and plasma concentrations of LH, FSH and testosterone.
Abstract: Aim To investigate the effect of arsenic on spermatogenesis. Methods Mature (4 months old) Wistar rats were intraperitoneally administered sodium arsenite at doses of 4, 5 or 6 mg.kg(-1).day(-1) for 26 days. Different varieties of germ cells at stage VII seminiferous epithelium cycle, namely, type A spermatogonia (ASg), preleptotene spermatocytes (pLSc), midpachytene spermatocytes (mPSc) and step 7 spermatids (7Sd) were quantitatively evaluated, along with radioimmunoassay of plasma follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone and assessment of the epididymal sperm count. Results In the 5 and 6 mg/kg groups, there were significant dose-dependent decreases in the accessory sex organ weights, epididymal sperm count and plasma concentrations of LH, FSH and testosterone with massive degeneration of all the germ cells at stage VII. The changes were insignificant in the 4 mg/kg group. Conclusion Arsenite has a suppressive influence on spermatogenesis and gonadotrophin and testosterone release in rats.

204 citations

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TL;DR: It is concluded that atenolol may protect testicular androgen synthesis by inhibiting the action of noradrenaline on testicular Leydig cells and adrenocortical hyperactivity in cadmium-treated rats.

77 citations

Journal Article
TL;DR: It is suggested that copper has got a dose-dependent effect on testicular steroidogenic enzyme activity and stimulation of testicular spermatogenesis and serum testosterone and LH level in maturing male rats.
Abstract: Background: Copper is essential as a trace element for metabolic processes. Exposure to copper in industries develops toxicity among the workers. Previous findings on adverse effects of copper on male reproductive function in adult albino rats led to investigate the effects of this metal on reproductive function of maturing male rats in the present experiment. Methodology: To study these effects, immature (30 to 35 days old) Wistar strain albino rats weighing about 50-60 g were treated intraperitoneally with copper chloride at doses of 1000, 2000 and 3000 µg/kg body weight/day for 26 days. Result: Significant fall in accessory sex organ weight and inhibition of testicular 17β-hydroxysteroid dehydrogenase activity along with degeneration of testicular growing spermatogenic cells and reduction in serum testosterone, FSH and LH level were observed at the doses of 2000 and 3000µg/kg/day. On the other hand, at the dose of 1000 µg/kg/day significant increase in testicular steroidogenic enzyme activity and stimulation of testicular spermatogenesis along with rise in serum testosterone and LH level were observed, though no significant change was observed in serum FSH level. This suggests that copper has got a dose-dependent effect on testicular steroidogenesis and spermatogenesis and serum testosterone and LH level in maturing male rats.

33 citations

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TL;DR: Lithium has an adverse effect on testicular function in immature rats by reducing serum levels of FSH, LH, PRL, and testosterone and hormonal changes and altered spermatogenic activities were evident when the serum concentration of lithium was within the therapeutic range.
Abstract: The present study was performed on immature male rats aged 35 days. Subcutaneous injections of lithium chloride at a daily dose of 2.0 mg/kg for 15 days resulted in significant inhibition of spermatogenesis at stage VII of the seminiferous epithelial cycle. Spermatogonia A, preleptotene spermatocytes and step 7 spermatids were decreased in number in comparison to controls. Serum levels of FSH, LH, PRL, and testosterone were decreased. Activities of testicular delta 5-3 beta-hydroxysteroid dehydrogenase and 17 beta-hydroxysteroid dehydrogenase were suppressed along with a low caudal epididymal sperm count in comparison with controls. When the treatment was prolonged for 20 and 25 days, it showed an additional significant diminution in accessory sex organ weights and number of midpachytene spermatocytes at stage VII in comparison to control animals of corresponding age. It is concluded that lithium has an adverse effect on testicular function in immature rats by reducing serum levels of FSH, LH, PRL, and testosterone. Furthermore, since hormonal changes and altered spermatogenic activities were evident when the serum concentration of lithium was within the therapeutic range, our data may have some potential clinical implications.

29 citations

Journal Article
TL;DR: Effect of ascorbic acid on testicular steroid dehydrogenase activity and testosterone concentration, using in vitro preparation of rat testis, was studied.
Abstract: Effect of ascorbic acid on testicular steroid dehydrogenase activity and testosterone concentration, using in vitro preparation of rat testis, was studied. A significant stimulation of enzyme activity and rise in testosterone content were observed.

29 citations


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TL;DR: Gender differences in susceptibility at lower exposure are uncertain, but recent data indicate that cadmium has estrogenic effects and affect female offspring, and experimental data suggest that females are more susceptible to immunotoxic effects of lead.

599 citations

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TL;DR: Evidence is adduced for the hypothesis that mammalian (including human) sex ratios at birth are partially controlled by the hormone levels of both parents at the time of conception.

456 citations

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TL;DR: An overview of the functional properties of mammalian TRP channels is given, their roles in acquired and hereditary diseases are described, and their potential as drug targets for therapeutic intervention is discussed.
Abstract: The large Trp gene family encodes transient receptor potential (TRP) proteins that form novel cation-selective ion channels. In mammals, 28 Trp channel genes have been identified. TRP proteins exhibit diverse permeation and gating properties and are involved in a plethora of physiologic functions with a strong impact on cellular sensing and signaling pathways. Indeed, mutations in human genes encoding TRP channels, the so-called "TRP channelopathies," are responsible for a number of hereditary diseases that affect the musculoskeletal, cardiovascular, genitourinary, and nervous systems. This review gives an overview of the functional properties of mammalian TRP channels, describes their roles in acquired and hereditary diseases, and discusses their potential as drug targets for therapeutic intervention.

418 citations

Journal ArticleDOI
TL;DR: The present review focuses on mechanism of lead- and cadmium-induced oxidate damages and the ameliorative measures to counteract the oxidative damage and pathotoxicity with the use of supplemented antioxidants for their beneficial effects.
Abstract: Oxidative stress has been implicated to play a role, at least in part, in pathogenesis of many disease conditions and toxicities in animals. Overproduction of reactive oxygen species and free radicals beyond the cells intrinsic capacity to neutralize following xenobiotics exposure leads to a state of oxidative stress and resultant damages of lipids, protein, and DNA. Lead and cadmium are the common environmental heavy metal pollutants and have widespread distribution. Both natural and anthropogenic sources including mining, smelting, and other industrial processes are responsible for human and animal exposure. These pollutants, many a times, are copollutants leading to concurrent exposure to living beings and resultant synergistic deleterious health effects. Several mechanisms have been explained for the damaging effects on the body system. Of late, oxidative stress has been implicated in the pathogenesis of the lead- and cadmium-induced pathotoxicity. Several ameliorative measures to counteract the oxidative damage to the body system aftermath or during exposure to these toxicants have been assessed with the use of antioxidants. The present review focuses on mechanism of lead- and cadmium-induced oxidate damages and the ameliorative measures to counteract the oxidative damage and pathotoxicity with the use of supplemented antioxidants for their beneficial effects.

412 citations

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TL;DR: This review reports current knowledge regarding the roles that cadmium (Cd), mercury (Hg), arsenic (As), lead (PB), manganese (Mn), and zinc (Zn) play as endocrine-disrupting chemicals (EDCs).
Abstract: This review reports current knowledge regarding the roles that cadmium (Cd), mercury (Hg), arsenic (As), lead (PB), manganese (Mn), and zinc (Zn) play as endocrine-disrupting chemicals (EDCs). The influence of these metals on the endocrine system, possible mechanisms of action, and consequent health effects were correlated between experimental animals and humans. Analysis of the studies prompted us to identify some critical issues related to this area and showed the need for more rigorous and innovative studies. Consequently, it was recommended that future studies need to: (1) identify the mechanisms of action, because at the present time only a few have been elucidated-in this context, the possible presence of hormesis need to be determined, as currently this was reported only for exposure Cd and As; (2) study the possible additive, synergistic, or antagonistic effects on the endocrine system following exposure to a mixture of metals since there is a lack of these studies available, and in general or occupational environments, humans are simultaneously exposed to different classes of xenobiotics, including metals, but also to organic compounds that might also be EDCs; (3) assess the potential adverse effects on the endocrine system of low-level exposures to metals, as most of the information currently available on EDCs originates from studies in which exposure levels were particularly high; and (4) assess the effects on the endocrine and reproductive systems of other metals that are present in the general and occupational environment that have not yet been evaluated.

398 citations