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Etiology of ovarian dysfunction in chronic murine toxoplasmosis
1Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201, USA.
Abstract:
Ovarian dysfunction develops in Nya:NYLAR mice chronically infected with Toxoplasma gondii. To differentiate between primary ovarian failure and pituitary gonadotropin insufficiency, we (a) monitored ovarian responsiveness to pregnant mare serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG) and (b) assessed endogenous pituitary gonadotropin capacity by the degree of ovarian compensatory hypertrophy (OCH) developing after unilateral ovariectomy (ULO). PMSG stimulated vigorous folliculogenesis and estrogen synthesis, but not ovulation. HCG given 3 days after PMSG induced "superovulation" within 16 h. These observations indicate the absence of the critical preovulatory surge of endogenous luteinizing hormone (LH) from the pituitary. In addition, ULO did not result in compensatory hypertrophy of the contralateral ovary, an indication of follicle-stimulating hormone (FSH) insufficiency. We hypothesize that cytokines released peripherally in response to the parasite reached the hypothalamus and initiated a sequence of events that inhibited the pulsatile release of gonadotropin-releasing hormone (GnRH), leading to the subsequent impairment of the pituitary-ovarian axis.
Insights
Toxoplasma gondii infection causes ovarian dysfunction in mice by impairing pituitary gonadotropin release. This study reveals a disruption in the hypothalamic-pituitary-ovarian axis, impacting fertility.
Area of Science:
- Reproductive Biology
- Infectious Diseases
- Endocrinology
Background:
- Chronic Toxoplasma gondii infection is linked to reproductive issues.
- Ovarian dysfunction in infected mice requires differentiation between primary ovarian failure and pituitary insufficiency.
Purpose of the Study:
- To investigate the mechanisms of ovarian dysfunction in mice infected with Toxoplasma gondii.
- To determine if the dysfunction stems from ovarian issues or impaired pituitary hormone production.
Main Methods:
- Assessed ovarian response to exogenous gonadotropins (PMSG and hCG).
- Evaluated pituitary gonadotropin capacity via ovarian compensatory hypertrophy (OCH) after unilateral ovariectomy (ULO).
Main Results:
- Pregnant mare serum gonadotropin (PMSG) stimulated folliculogenesis and estrogen, but not ovulation.
- Human chorionic gonadotropin (hCG) induced superovulation, indicating absent endogenous luteinizing hormone (LH) surge.
- Unilateral ovariectomy (ULO) failed to cause compensatory hypertrophy, suggesting follicle-stimulating hormone (FSH) insufficiency.
Conclusions:
- Toxoplasma gondii infection leads to pituitary gonadotropin insufficiency, not primary ovarian failure.
- Cytokine release during infection may inhibit GnRH pulsatility, disrupting the pituitary-ovarian axis.