{"title":"Combined vitamin D and coconut oil are promising protective approaches against aluminum-induced testicular damage in rats.","authors":"Fatma A Al-Nefeiy","doi":"10.1016/j.toxrep.2025.102051","DOIUrl":null,"url":null,"abstract":"<p><p>Exposure to high levels of aluminum (Al) is a widespread environmental problem where its use is continuously increasing. Al may play a substantial role in male fertility decline. This study was designed experimentally in rats to explore the protective effect of both vitamin D (VD) and virgin coconut oil (VCO) against aluminum chloride (AlCl<sub>3</sub>) on the biochemical and histopathological changes of the testis. Male rats were divided into 7 groups: Control group, VD group, VCO group, AlCl3-treated group, AlCl3 co-treated with VD group, AlCl3 co-treated with VCO group, AlCl<sub>3</sub> co-treated with both VD and VCO group. After six weeks of treatment, the rats of each group were sacrificed where blood and testicular samples were assembled and processed for different biochemical and histopathological studies. The results showed that AlCl<sub>3</sub> reduced body weight gain, testis weights, reproductive hormones (FSH, LH, testosterone), and antioxidant enzymes (SOD, GPx, CAT), while elevating oxidative stress (MDA). These effects were notably reversed by VD, VCO, or their combination, with combined therapy showing the greatest improvement. Histologically, AlCl<sub>3</sub> caused severe testicular damage, including disrupted seminiferous tubules, degenerated spermatogenic cells, interstitial fibrosis, and Leydig cell loss, findings partially restored by VD or VCO and nearly normalized with their combination. Immunohistochemistry further confirmed these improvements, with combined treatment reducing caspase-3 (apoptosis) and restoring Ki-67 (proliferation) expression. In conclusion, AlCl<sub>3</sub> exposure impaired testicular function by disrupting hormone levels, antioxidant defenses, and tissue integrity. VD and VCO, especially in combination, effectively counteracted these effects, restoring hormonal balance, antioxidant status, and normal tissue structure with reducing apoptosis and enhancing proliferation. Collectively, these findings suggest that VD and VCO synergistically counteract AlCl<sub>3</sub>-induced testicular toxicity, offering anti-inflammatory, antioxidant, anti-apoptotic, and proliferative mechanisms.</p>","PeriodicalId":23129,"journal":{"name":"Toxicology Reports","volume":"14 ","pages":"102051"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12152672/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1016/j.toxrep.2025.102051","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"Environmental Science","Score":null,"Total":0}
引用次数: 0
Abstract
Exposure to high levels of aluminum (Al) is a widespread environmental problem where its use is continuously increasing. Al may play a substantial role in male fertility decline. This study was designed experimentally in rats to explore the protective effect of both vitamin D (VD) and virgin coconut oil (VCO) against aluminum chloride (AlCl3) on the biochemical and histopathological changes of the testis. Male rats were divided into 7 groups: Control group, VD group, VCO group, AlCl3-treated group, AlCl3 co-treated with VD group, AlCl3 co-treated with VCO group, AlCl3 co-treated with both VD and VCO group. After six weeks of treatment, the rats of each group were sacrificed where blood and testicular samples were assembled and processed for different biochemical and histopathological studies. The results showed that AlCl3 reduced body weight gain, testis weights, reproductive hormones (FSH, LH, testosterone), and antioxidant enzymes (SOD, GPx, CAT), while elevating oxidative stress (MDA). These effects were notably reversed by VD, VCO, or their combination, with combined therapy showing the greatest improvement. Histologically, AlCl3 caused severe testicular damage, including disrupted seminiferous tubules, degenerated spermatogenic cells, interstitial fibrosis, and Leydig cell loss, findings partially restored by VD or VCO and nearly normalized with their combination. Immunohistochemistry further confirmed these improvements, with combined treatment reducing caspase-3 (apoptosis) and restoring Ki-67 (proliferation) expression. In conclusion, AlCl3 exposure impaired testicular function by disrupting hormone levels, antioxidant defenses, and tissue integrity. VD and VCO, especially in combination, effectively counteracted these effects, restoring hormonal balance, antioxidant status, and normal tissue structure with reducing apoptosis and enhancing proliferation. Collectively, these findings suggest that VD and VCO synergistically counteract AlCl3-induced testicular toxicity, offering anti-inflammatory, antioxidant, anti-apoptotic, and proliferative mechanisms.