Rituparna Ghosh | University of Calcutta (original) (raw)
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Papers by Rituparna Ghosh
Journal of inorganic …, Jan 1, 2007
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Environmental Toxicology …, Jan 1, 2007
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Reproductive …, Jan 1, 2007
The present study investigates the testicular and adrenocortical activities under different doses... more The present study investigates the testicular and adrenocortical activities under different doses and durations of chromium (Cr) exposure and their interactions. Mature male Sprague Dawley rats were injected daily with three different doses (0.2, 0.4, and 0.6 mg/kg bw) of Cr salt (K(2)Cr(2)O(7)) intraperitonealy for 13 and 26 days, respectively. The medium (0.4 mg/kg bw/day) and higher dose (0.6 mg/kg bw/day) of Cr significantly (p<0.05) decrease accessory sex organs weight, testicular Delta(5)3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities, epididymal sperm count, effective spermatid degeneration, serum testosterone, LH level, testicular catalase and superoxide dismutase (SOD) activities while testicular lipid peroxidation, serum FSH, corticosterone level, adrenal weight and adrenal Delta(5)3beta-HSD activity increased significantly than that of control and lower dose (0.2 mg/kg bw/day) Cr exposed animals. Testicular histoarchitechture shows deterioration after critical dose (0.4 mg/kg bw/day) and duration (26 days) of Cr exposure. Cr induced alterations on testicular and adrenocortical activities are dose and duration dependent. Adrecortical hyperactivity accompanied by testicular oxidative stress might have a crucial role for Cr induced male reproductive impairment.
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Molecular and cellular …, Jan 1, 2007
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Toxicology Mechanisms …
Vanadium is a well recognized industrial hazard known to adversely affect male reproductive funct... more Vanadium is a well recognized industrial hazard known to adversely affect male reproductive functions. The intricate mechanistic aspects of this metal and the role of oxidative stress in the deterioration of testicular functions are investigated in the current study. The experiment also focused on the effects of testosterone propionate in testicular and sperm functions in the rat intoxicated with vanadate. Vanadium exposure resulted in a more prominent spermatogenic arrest and consistently abolished the conversion of round to mature spermatids along with decreased epididymal sperm number and increased percentage of abnormal sperm. This is followed by a precipitous decline in the level of serum testosterone and gonadotropins and consequently the testicular steroidogenic and antioxidant enzymes were inhibited. Vanadium induces degeneration in the genital organs of rats and exhibits high indices of lipid oxidative damage. In response to exogenous testosterone propionate (TP) administration, spermatogonial cell populations remained suppressed, while the spermatogenesis was restored quantitatively. In contrast, the hormone treatment had no effect on the dramatically decreased serum FSH level after vanadate treatment. Moreover, TP could ameliorate the toxicity, as indicated by decreased testicular lipid peroxidation with marginal but significant increase in the activities of all the measured enzymes following vanadate-treatment. Taken together all these studies establish that vanadium is a testicular toxicant that perturbs the male reproductive system adversely. However, hormone replacement therapy by testosterone propionate may provide partial protection. The results suggest the feasibility of using endocrine regimens to impede deleterious effects of vanadium on the male reproductive system.
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Food and Chemical …, Jan 1, 2010
Excess chromium (Cr) exposure is associated with various pathological conditions including reprod... more Excess chromium (Cr) exposure is associated with various pathological conditions including reproductive dysfunction. Generation of oxidative stress is one of the plausible mechanisms behind Cr induced cellular deteriorations. The efficacy of vitamin E to combat Cr induced oxidative damage in adult rat testis has investigated in the current study. Adult male rats exposed to hexavalent Cr (intraperitoneal injection with 0.4 mg K(2)Cr(2)O(7)/ kg bw/day) for 26 days resulted in decreased accessory sex organs weight compared to controls. Development of oxidative stress in testis was evidenced by increased lipid peroxidation along with decreased superoxide dismutase (SOD) and catalase activities than control animals. Marked reduction in the activities of testicular steroidogenic enzymes; Delta(5)3beta-hydroxysteroid dehydrogenase (HSD), 17beta-HSD, serum testosterone and Leutinizing Hormone (LH) levels were observed. However significant increase in serum Follicle Stimulating Hormone (FSH) level was observed with Cr treated group. Histological evaluation of testis revealed degeneration of stage VII spermatogenic cycle along with decrease in epithelial cell height in epididymis and seminiferous tubules; number of different germ cells per seminiferous tubule and seminiferous tubular diameter reduced after Cr exposure. Simultaneous oral supplementation of vitamin E (50mg/kg bw/day) in Cr exposed rats showed less oxidative damage and restored the otherwise altered testicular activities. Epididymal sperm number was also restored in vitamin E-supplemented group than Cr induced rats. This study implicates vitamin E as a possible protective agent against Cr induced spermatogenic and steroidogenic alteration.
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Bookmarks Related papers MentionsView impact
Journal of inorganic …, Jan 1, 2007
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Environmental Toxicology …, Jan 1, 2007
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Reproductive …, Jan 1, 2007
The present study investigates the testicular and adrenocortical activities under different doses... more The present study investigates the testicular and adrenocortical activities under different doses and durations of chromium (Cr) exposure and their interactions. Mature male Sprague Dawley rats were injected daily with three different doses (0.2, 0.4, and 0.6 mg/kg bw) of Cr salt (K(2)Cr(2)O(7)) intraperitonealy for 13 and 26 days, respectively. The medium (0.4 mg/kg bw/day) and higher dose (0.6 mg/kg bw/day) of Cr significantly (p<0.05) decrease accessory sex organs weight, testicular Delta(5)3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities, epididymal sperm count, effective spermatid degeneration, serum testosterone, LH level, testicular catalase and superoxide dismutase (SOD) activities while testicular lipid peroxidation, serum FSH, corticosterone level, adrenal weight and adrenal Delta(5)3beta-HSD activity increased significantly than that of control and lower dose (0.2 mg/kg bw/day) Cr exposed animals. Testicular histoarchitechture shows deterioration after critical dose (0.4 mg/kg bw/day) and duration (26 days) of Cr exposure. Cr induced alterations on testicular and adrenocortical activities are dose and duration dependent. Adrecortical hyperactivity accompanied by testicular oxidative stress might have a crucial role for Cr induced male reproductive impairment.
Bookmarks Related papers MentionsView impact
Molecular and cellular …, Jan 1, 2007
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Toxicology Mechanisms …
Vanadium is a well recognized industrial hazard known to adversely affect male reproductive funct... more Vanadium is a well recognized industrial hazard known to adversely affect male reproductive functions. The intricate mechanistic aspects of this metal and the role of oxidative stress in the deterioration of testicular functions are investigated in the current study. The experiment also focused on the effects of testosterone propionate in testicular and sperm functions in the rat intoxicated with vanadate. Vanadium exposure resulted in a more prominent spermatogenic arrest and consistently abolished the conversion of round to mature spermatids along with decreased epididymal sperm number and increased percentage of abnormal sperm. This is followed by a precipitous decline in the level of serum testosterone and gonadotropins and consequently the testicular steroidogenic and antioxidant enzymes were inhibited. Vanadium induces degeneration in the genital organs of rats and exhibits high indices of lipid oxidative damage. In response to exogenous testosterone propionate (TP) administration, spermatogonial cell populations remained suppressed, while the spermatogenesis was restored quantitatively. In contrast, the hormone treatment had no effect on the dramatically decreased serum FSH level after vanadate treatment. Moreover, TP could ameliorate the toxicity, as indicated by decreased testicular lipid peroxidation with marginal but significant increase in the activities of all the measured enzymes following vanadate-treatment. Taken together all these studies establish that vanadium is a testicular toxicant that perturbs the male reproductive system adversely. However, hormone replacement therapy by testosterone propionate may provide partial protection. The results suggest the feasibility of using endocrine regimens to impede deleterious effects of vanadium on the male reproductive system.
Bookmarks Related papers MentionsView impact
Food and Chemical …, Jan 1, 2010
Excess chromium (Cr) exposure is associated with various pathological conditions including reprod... more Excess chromium (Cr) exposure is associated with various pathological conditions including reproductive dysfunction. Generation of oxidative stress is one of the plausible mechanisms behind Cr induced cellular deteriorations. The efficacy of vitamin E to combat Cr induced oxidative damage in adult rat testis has investigated in the current study. Adult male rats exposed to hexavalent Cr (intraperitoneal injection with 0.4 mg K(2)Cr(2)O(7)/ kg bw/day) for 26 days resulted in decreased accessory sex organs weight compared to controls. Development of oxidative stress in testis was evidenced by increased lipid peroxidation along with decreased superoxide dismutase (SOD) and catalase activities than control animals. Marked reduction in the activities of testicular steroidogenic enzymes; Delta(5)3beta-hydroxysteroid dehydrogenase (HSD), 17beta-HSD, serum testosterone and Leutinizing Hormone (LH) levels were observed. However significant increase in serum Follicle Stimulating Hormone (FSH) level was observed with Cr treated group. Histological evaluation of testis revealed degeneration of stage VII spermatogenic cycle along with decrease in epithelial cell height in epididymis and seminiferous tubules; number of different germ cells per seminiferous tubule and seminiferous tubular diameter reduced after Cr exposure. Simultaneous oral supplementation of vitamin E (50mg/kg bw/day) in Cr exposed rats showed less oxidative damage and restored the otherwise altered testicular activities. Epididymal sperm number was also restored in vitamin E-supplemented group than Cr induced rats. This study implicates vitamin E as a possible protective agent against Cr induced spermatogenic and steroidogenic alteration.
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Bookmarks Related papers MentionsView impact