Reproductive toxicology (Elmsford, N.Y.) · 2026
Melatonin attenuates BPA-induced testicular tissue oxidative stress damage by protecting testicular mitochondrial function and reducing cell apoptosis in mice.
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Liu Jingjing, Zhang Wansheng, Qi Qi, Li Shuang, Wang Xuenan, Pan Xiaoyan
Аннотация
OBJECTIVE: This study explores the protective role of melatonin against Bisphenol A (BPA)-induced oxidative stress in the testes of adult mice.
METHODS: Adult male mice were orally administered 50 mg/kg BPA for 30 days, with or without melatonin (20 mg/kg). Testicular function, network pharmacology targets, melatonin receptor 1 A (MT1R) expression, oxidative stress markers, and mitochondrial function were assessed. Testosterone, luteinizing hormone, and proteins associated with steroid hormone synthesis were measured by an enzyme-linked immunosorbent assay (ELISA) and apoptosis by TUNEL.
RESULTS: Melatonin treatment increased testicular/epididymal indices, restored seminiferous tubule morphology, and improved sperm density and viability in BPA-treated mice. A total of 262 common targets associated with melatonin and BPA-related testicular diseases were identified, primarily involved in regulating oxidative stress, mitochondrial function, steroid hormone synthesis, and apoptosis. Melatonin treatment boosted MT1R expression and elevated levels of catalase, superoxide dismutase 2, and glutathione while reducing malondialdehyde. Furthermore, melatonin treatment increased the expression of OPA1, MFN1, MFN2, NRF1, and TFAM while decreasing DRP1 and FIS1, restoring mitochondrial dynamics and biogenesis. It also enhanced adenosine triphosphate (ATP) production and the activities of the mitochondrial respiratory chain complexes I-V. Additionally, melatonin treatment increased testosterone levels and the expression of steroidogenic acute regulatory protein and cytochrome P450 11A1 while decreasing luteinizing hormone levels and inhibiting testicular cell apoptosis.
CONCLUSION: In BPA-treated mice, exogenous melatonin alleviated testicular cell oxidative stress damage and mitochondrial dysfunction, increased testosterone synthesis and secretion, and inhibited testicular cell apoptosis; this could offer significant testicular protection in man.
METHODS: Adult male mice were orally administered 50 mg/kg BPA for 30 days, with or without melatonin (20 mg/kg). Testicular function, network pharmacology targets, melatonin receptor 1 A (MT1R) expression, oxidative stress markers, and mitochondrial function were assessed. Testosterone, luteinizing hormone, and proteins associated with steroid hormone synthesis were measured by an enzyme-linked immunosorbent assay (ELISA) and apoptosis by TUNEL.
RESULTS: Melatonin treatment increased testicular/epididymal indices, restored seminiferous tubule morphology, and improved sperm density and viability in BPA-treated mice. A total of 262 common targets associated with melatonin and BPA-related testicular diseases were identified, primarily involved in regulating oxidative stress, mitochondrial function, steroid hormone synthesis, and apoptosis. Melatonin treatment boosted MT1R expression and elevated levels of catalase, superoxide dismutase 2, and glutathione while reducing malondialdehyde. Furthermore, melatonin treatment increased the expression of OPA1, MFN1, MFN2, NRF1, and TFAM while decreasing DRP1 and FIS1, restoring mitochondrial dynamics and biogenesis. It also enhanced adenosine triphosphate (ATP) production and the activities of the mitochondrial respiratory chain complexes I-V. Additionally, melatonin treatment increased testosterone levels and the expression of steroidogenic acute regulatory protein and cytochrome P450 11A1 while decreasing luteinizing hormone levels and inhibiting testicular cell apoptosis.
CONCLUSION: In BPA-treated mice, exogenous melatonin alleviated testicular cell oxidative stress damage and mitochondrial dysfunction, increased testosterone synthesis and secretion, and inhibited testicular cell apoptosis; this could offer significant testicular protection in man.