Impact of Combined Highly Active Antiretroviral Drugs on Ovarian Histoarchitecture, Oxidative Stress Markers and Fertility Outcomes in Female Sprague-Dawley rats. Impact of Combined Highly Active Antiretroviral Drugs on Ovarian Histoarchitecture
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Abstract
Highly Active Antiretroviral Therapy (HAART) has substantially changed positively the clinical direction of human immunodeficiency virus (HIV) infection. Nevertheless, accumulating evidence of its disruptive influence on endocrine homeostasis has raised significant concerns on female reproductive health. The increasing documentation of ovarian pathology among HAART-exposed individuals underscores the urgency of elucidating its mechanistic impact to inform evidence-based therapeutic strategies. The understanding of the potential effects on organ oxidative stress status and impact on ovarian microscopic profile is crucial for developing strategies to preserve reproductive health in HIV-positive women. The present investigation evaluated HAART-associated alterations in ovarian oxidative stress indices and tissue architecture in female Sprague-Dawley rats. Ten animals were allocated into two groups of five: a HAART-treated group (Group A) administered 1.88 mg of the drug combination dissolved in 0.1 ml of normal saline, and a control group (Group B) receiving equivalent volume of normal saline as placebo. Following 28 days of administration, ovarian tissues were subjected to histomorphological examination alongside biochemical quantification of oxidative stress markers. HAART administration resulted in statistically significant suppression of antioxidant enzyme activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and reduced glutathione (GSH), alongside a marked elevation in malondialdehyde (MDA), a principal lipid peroxidation biomarker. Histomorphological evaluation revealed aberrant follicular architecture characterized by cystic formations and vascular congestions. These findings collectively indicate that combined HAART exposure may precipitate oxidative stress-mediated deterioration of ovarian function. Elucidation of the precise molecular pathways underlying these effects remains warranted to facilitate the development of targeted mitigation strategies.
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