Sahin Serkan, Mortas Tulay, Muderrisoglu Ahmet, Turksoy Vugar Ali
Department of Medical Pharmacology, Yozgat Bozok University Faculty of Medicine, Yozgat, Turkey.
Department of Histology, Kırıkkale University Faculty of Medicine, Kırıkkale, Turkey.
Basic Clin Pharmacol Toxicol. 2025 Feb;136(2):e14131. doi: 10.1111/bcpt.14131.
Current chelation treatments used for cadmium poisoning may cause some serious side effects. Thus, safer novel treatments could be promising for clinical use. This study evaluated the effects of cannabidiol on Cd toxicity. Four groups of 10 mice were formed: Groups I and III were cadmium-free, while groups II and IV received 50 mg/L cadmium in drinking water. Groups III and IV received daily cannabidiol (25 mg/kg) via intragastric gavage. After 30 days, the animals were killed, and blood and tissue samples were collected. Oxidative stress and inflammation markers, including glutathione, catalase, myeloperoxidase, TNF-α, IL-1β and IL-6, were analysed using ELISA. Additionally, histological evaluations of the liver, kidney and testis were performed. Cadmium exposure reduced glutathione and catalase levels in the blood, liver, kidney and testis, while increasing myeloperoxidase. Cannabidiol mitigated these effects on oxidative stress markers. Cannabidiol also reduced the increase in proinflammatory cytokines. Histopathological analysis revealed reduced liver and kidney damage in cannabidiol-treated groups compared to cadmium-only groups. In addition, histopathological evaluation showed CBD had no protective effect on the testicular tissue against Cd toxicity. Our results indicate that cannabidiol protects against some toxic effects of cadmium. If confirmed by future studies, cannabidiol may be proposed as a novel treatment for cadmium toxicity.
目前用于镉中毒的螯合疗法可能会引起一些严重的副作用。因此,更安全的新型疗法有望用于临床。本研究评估了大麻二酚对镉毒性的影响。将40只小鼠分成四组:第一组和第三组不接触镉,而第二组和第四组的饮用水中含有50毫克/升的镉。第三组和第四组每天通过灌胃给予大麻二酚(25毫克/千克)。30天后,处死动物并采集血液和组织样本。使用酶联免疫吸附测定法分析氧化应激和炎症标志物,包括谷胱甘肽、过氧化氢酶、髓过氧化物酶、肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6。此外,对肝脏、肾脏和睾丸进行了组织学评估。镉暴露降低了血液、肝脏、肾脏和睾丸中的谷胱甘肽和过氧化氢酶水平,同时增加了髓过氧化物酶。大麻二酚减轻了这些对氧化应激标志物的影响。大麻二酚还降低了促炎细胞因子的增加。组织病理学分析显示,与仅接触镉的组相比,大麻二酚治疗组的肝脏和肾脏损伤减轻。此外,组织病理学评估显示,大麻二酚对睾丸组织免受镉毒性没有保护作用。我们的结果表明,大麻二酚可预防镉的一些毒性作用。如果未来的研究证实,大麻二酚可能会被提议作为一种治疗镉中毒的新型疗法。