Melatonin protects rats against bisphenol A-induced testicular dysfunction through the upregulation of α-smooth muscle actin, vimentin, and S-100 proteins
Abstrak
Bisphenol A (BPA) is a widely used chemical in the plastic industry and a known endocrine disruptor which causes reproductive toxicity in animals. Also, melatonin is an antioxidant that can alleviate the toxicity caused by endocrine disruptors. Previous studies have demonstrated that melatonin protects the male reproductive functions. However, the protective mechanisms of melatonin are not well elucidated. This study investigated how melatonin protects against BPA-induced testicular dysfunction in rats. Forty male Wistar rats were grouped randomly into four. Animals in group A (control) received 0.2 mL of olive oil orally, B: melatonin (10 mg/kg) intraperitoneally, C: BPA (10 mg/kg) orally, and D: co-exposed with BPA and melatonin. All rats were treated daily for 45 days. Testicular samples were harvested and analysed on the 46th day. Results from this study showed that melatonin prevented the BPA-induced testicular necrosis and distortion of spermatozoa flagellar axoneme arrangement in the co-exposed rats. In addition, the induction of alpha-smooth muscle actin, vimentin, and S-100 proteins in the testes was significantly reduced in the BPA alone-treated rats. The melatonin upregulated the proteins in the co-treated group. Increased expression of alpha-smooth muscle actin, vimentin, and S-100 proteins in normal tissue have been associated with effective regulation of fibroblast contractile activity, cell migration and metastasis, and apoptosis, proliferation, differentiation, and inflammation in different cell types, respectively. Therefore, our findings provide insights into the protective mechanisms of melatonin against the bisphenol A-induced reproductive toxicity.
Topik & Kata Kunci
Penulis (4)
Olumide Samuel Ajani
Samuel Gbadebo Olukole
Matthew Olugbenga Oyeyemi
Ekundayo Stephen Samuel
Akses Cepat
- Tahun Terbit
- 2025
- Sumber Database
- DOAJ
- DOI
- 10.52331/v30i2512
- Akses
- Open Access ✓