Effect of human chorionic gonadotrophin coadministration on ovarian steroidogenic and folliculogenic activities in cyclophosphamide treated albino rats

Ghosh, Surajit; Misro, M. M.; Das, Ujjal; Maiti, Rajkumar; Debnath, J.; Ghosh, Debidas

doi:10.1016/s0890-6238(01)00114-9

Cited by 17 publications

(15 citation statements)

References 27 publications

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“…A noticeable protection in ovarian histoarchitecture was evident after hCG coadministration in sodium arsenitetreated rats, and probable fact behind this may be the facilitatory effect of hCG on ovarian folliculogenesis and the existence of high plasma level of estradiol [41,42,62]. The reduction in plasma FSH and LH levels after sodium arsenite treatment in this experiment is in agreement with the results of the previous studies.…”

Section: Discussionsupporting

confidence: 92%

“…Significant recovery in ovarian folliculogenesis after hCG coadministration in arsenic-intoxicated rats may be the outcome of direct effect of hCG on ovarian follicles [41,42,62,63,72]. Different parameters of uterine histometry were altered significantly after sodium arsenite treatment, which confirmed the results of our previous experiments.…”

Section: Discussionsupporting

confidence: 89%

“…Inhibition in plasma estradiol after sodium arsenite treatment at this critical dose and duration was again supported by the results of our previous studies [36,[38][39][40]. This normal level of plasma estradiol was protected significantly after hCG coadministration, which may be the outcome of direct stimulatory effect of hCG on ovarian steroidogenic enzymes [41,42,60,61].…”

Section: Discussionsupporting

confidence: 78%

“…The efficacy of hCG is also tested in the amelioration of arsenic-mediated male reproductive disorder in rat [21], in which hCG treatment has been associated with the modulation of arsenic-induced imbalance of pituitary-testicular axis. Moreover, hCG is beneficial in the significant protection against lithium chlorideand cyclophosphamide-induced inhibition of ovarian steroidogenesis [41,42]. In this investigation, our effort was to define the mechanism of action of sodium arsenite in the development of ovarian and uterine toxicity via hCG coadministration.…”

Section: Introductionmentioning

confidence: 99%

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The involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes in arsenic‐mediated ovarian and uterine toxicity: Modulation by hCG

Chattopadhyay

Ghosh

2010

J Biochem & Molecular Tox

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This study evaluated the involvement of hypophyseal-gonadal and hypophyseal-adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle-stimulating hormone, and estradiol along with sluggish ovarian activities of Delta(5),3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic-intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes in arsenic‐mediated ovarian and uterine toxicity: Modulation by hCG

Chattopadhyay

Ghosh

2010

J Biochem & Molecular Tox

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“…Previous studies have proved the protective effect of hCG against lithium chloride and cyclophosphamideinduced changes in the ovary [12].…”

Section: Morphometric and Statistical Studymentioning

confidence: 98%

Arsenic-induced toxicity in the endometrium of adult albino rat and the possible role of human chorionic gonadotropin hormone

Elshawarby

Saleh

Attia

et al. 2014

The Egyptian Journal of Histology

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Lithium induces follicular atresia in rat ovary through a GSK‐3β/β‐catenin dependent mechanism

Mirakhori

Zeynali

Tafreshi

et al. 2013

Molecular Reproduction Devel

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Lithium chloride (LiCl) is a drug used to treat bipolar disorder, but has side effects in the female reproductive system. Although lithium is known to decrease folliculogenesis and induce follicular atresia in rodent ovaries, its cellular and molecular effects in the ovary have not yet been addressed. To investigate these effects, 23-day-old immature female rats were injected with 10 IU pregnant mare serum gonadotropin (PMSG), followed by injections of 250 mg/kg LiCl every 12 hr for four doses. Ovaries were removed 40 and 48 hr after PMSG administration and prepared for histology, immunohistochemistry, Western blotting, and DNA laddering analysis. Our results showed that in the ovaries of LiCl-treated rats, few antral but more atretic follicles were present compared to those of the control rats. The induction of atresia by LiCl was further confirmed by the presence of DNA fragmentation, accompanied by a reduced level of 17β-estradiol in the serum. At the cellular level, lithium significantly decreased the number of proliferating cell nuclear antigen (PCNA)-positive cells and conversely increased the number of TUNEL-positive cells in the granulosa layer of the antral follicles. At the molecular level, lithium increased the level of phosphorylated glycogen synthase kinase-3β, and unexpectedly decreased the expression of active (stabilized) β-catenin. Altogether, our results indicate that lithium disrupts the balance between proliferation and apoptosis in granulosa cells, leading to follicular atresia possibly through the reduction in both the stabilized β-catenin and 17β-estradiol synthesis.

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Effect of human chorionic gonadotrophin coadministration on ovarian steroidogenic and folliculogenic activities in cyclophosphamide treated albino rats

Cited by 17 publications

References 27 publications

The involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes in arsenic‐mediated ovarian and uterine toxicity: Modulation by hCG

The involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes in arsenic‐mediated ovarian and uterine toxicity: Modulation by hCG

Arsenic-induced toxicity in the endometrium of adult albino rat and the possible role of human chorionic gonadotropin hormone

Lithium induces follicular atresia in rat ovary through a GSK‐3β/β‐catenin dependent mechanism

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