Melatonin alleviates oxidative stress damage in mouse testes induced by bisphenol A

Qi Qi ^1,2, Jiaxin Yang ¹, Shuang Li ^1,2

⁰Center for Reproductive Medicine, Jilin Medical University, Jilin, China.

Frontiers in Cell and Developmental Biology +

|

March 5, 2024

View abstract on PubMed

Summary

Melatonin effectively combats bisphenol A (BPA) induced testicular damage by reducing oxidative stress and apoptosis. This study shows melatonin enhances antioxidant capacity, boosts testosterone production, and improves sperm health in mice exposed to BPA.

Area Of Science

Reproductive Toxicology
Endocrinology
Oxidative Stress Research

Background

Bisphenol A (BPA) is an endocrine-disrupting chemical linked to male reproductive toxicity.
Oxidative stress plays a critical role in BPA-induced testicular damage.
Melatonin, a hormone with antioxidant properties, may offer protective effects against reproductive toxicants.

Purpose Of The Study

To investigate the protective effects of melatonin against BPA-induced oxidative stress and damage in mouse testicular tissue and Leydig cells.
To evaluate melatonin's impact on sperm parameters, testicular morphology, oxidative stress markers, and steroidogenesis in BPA-exposed mice.

Main Methods

Mice were exposed to BPA (50 mg/kg) for 30 days, with concurrent administration of melatonin (10 and 20 mg/kg).
In vitro studies involved treating Leydig cells with BPA and melatonin (10 μmol/L).
Evaluated parameters included testicular and epididymis indices, sperm viability and density, oxidative stress markers (malondialdehyde, glutathione, antioxidant enzymes), steroidogenic enzyme expression, hormone levels (testosterone, estradiol), and apoptosis (TUNEL assay).

Main Results

Melatonin (20 mg/kg) significantly improved testicular and epididymis indices, seminiferous tubule development, sperm viability, and density in BPA-treated mice.
Melatonin treatment reduced malondialdehyde levels, increased antioxidant enzyme expression and glutathione content, and decreased Leydig cell and spermatogonia apoptosis.
Melatonin enhanced the expression of melatonin receptor 1A and luteinizing hormone receptor, promoted steroidogenic enzyme expression, and increased testosterone levels, while reducing aromatase expression and estradiol levels.

Conclusions

Melatonin demonstrates significant potential in alleviating BPA-induced testicular oxidative stress and damage.
The protective mechanisms involve enhancing testicular antioxidant capacity, promoting testosterone synthesis, and reducing cellular apoptosis.
Melatonin may serve as a therapeutic agent to mitigate the adverse reproductive effects of BPA exposure.

Keywords:

bisphenol A melatonin oxidative stress testis testosterone