L. carnitine modulates oxidative stress, steroidogenic gene disturbance, and testicular histopathology induced by Bisphenol A in male rats

TL;DR

This study shows that L-carnitine can help protect male rats from reproductive damage caused by Bisphenol A by reducing oxidative stress and improving sperm quality.

Contribution

The study demonstrates L-carnitine's protective effects against BPA-induced reproductive toxicity in rats through oxidative stress modulation and gene expression restoration.

Findings

BPA exposure reduced sperm quality, hormone levels, and antioxidant activity while increasing oxidative stress.

L-carnitine co-treatment improved sperm count, motility, and partially restored hormone levels and gene expression.

Histopathological analysis showed less testicular damage in BPA + L-carnitine groups compared to BPA alone.

Abstract

Bisphenol A (BPA) is a widely used endocrine disruptor that has been implicated in reproductive toxicity. L-carnitine (LC), has shown potential protective impacts against various toxicities.

This study aims to assess the protective role of LC against BPA-induced reproductive toxicity in male Sprague Dawley rats.

Sixty adult male Sprague Dawley rats (180–250 g, 3.5 months old) were divided into six groups (n = 10). Group I (control) administered of corn oil, Group II administered LC (500 mg/kg/day), Group III administered BPA (100 mg/kg/day), Group IV administered BPA (300 mg/kg/day), Group V was co-treated with BPA (100 mg/kg/day) and LC , and Group VI administered co-treatment with BPA (300 mg/kg/day) and L-carnitine. After 70 days of treatment, sperm count, motility, and morphology were assessed. Reproductive hormone levels (Follicle Stimulating Hormone (FSH), Luteinizing Hormone (LH), and testosterone) were measured via ELISA. Oxidative stress markers as Malondialdehyde (MDA), Glutathione (GSH), Nitric Oxide (NO), Catalase (CAT), and Superoxide Dismutase (SOD), the expression levels of StAR (Steroidogenic Acute Regulatory Protein), 3β-HSD (3β-Hydroxysteroid Dehydrogenase), Cyp17a (Cytochrome P450 17A1), and aromatase were evaluated. Testicular histopathological examination was performed.

BPA exposure significantly reduced sperm quality, hormone levels, and antioxidant enzyme activities, while increasing oxidative stress markers. LC co-treatment ameliorated these impacts, improving sperm count, motility, and morphology, and partially restoring hormone levels. Gene expression of steroidogenic proteins was partially restored with LC treatment, and histopathological analysis revealed less severe testicular damage compared to the BPA-alone groups.

L-carnitine demonstrates a protective role against BPA-induced reproductive toxicity in male rats.

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