Sun Jianxia, Xu Wei, Zhu Cuijuan, Hu Yunfeng, Jiang Xinwei, Ou Shiyi, Su Zhijian, Huang Yadong, Jiao Rui, Bai Weibin
Faculty of Chemical Engineering and Light Industry, Guangdong University of TechnologyGuangzhou, China; Department of Food Science and Engineering, Institute of Food Safety and Nutrition, Jinan UniversityGuangzhou, China.
Department of Food Science and Engineering, Institute of Food Safety and Nutrition, Jinan University Guangzhou, China.
Front Pharmacol. 2016 Nov 4;7:399. doi: 10.3389/fphar.2016.00399. eCollection 2016.
1,3-Dichloro-2-propanol (1,3-DCP) is a food processing contaminant and has been shown to perturb male reproductive function. Cyanidin-3--glucoside (C3G), an anthocyanin antioxidant, is reported to have protective effects on many organs. However, it remains unclear whether C3G protects against chemical-induced reproductive toxicity. The present study was therefore to investigate the intervention of C3G on 1,3-DCP-induced reproductive toxicity in R2C Leydig cells. Results demonstrated that C3G inhibited the 1,3-DCP-induced cytotoxicity and cell shape damage with the effective doses being ranging from 10 to 40 μmol/L. In addition, 1,3-DCP (2 mmol/L) exposure significantly increased the ROS level and mitochondrial membrane potential damage ratio, leading to a decrease in progesterone production, while C3G intervention reduced the ROS level, and increased the progesterone production after 24 h treatment. Most importantly, C3G intervention could up-regulate the cyclic adenosine monophosphate (cAMP) level and protein expression of steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase. It was concluded that C3G is effective in reducing 1,3-DCP-induced reproductive toxicity via activating steroidogenic enzymes and cAMP level.
1,3-二氯-2-丙醇(1,3-DCP)是一种食品加工污染物,已被证明会干扰雄性生殖功能。矢车菊素-3-O-葡萄糖苷(C3G)是一种花青素抗氧化剂,据报道对许多器官具有保护作用。然而,C3G是否能预防化学诱导的生殖毒性仍不清楚。因此,本研究旨在探讨C3G对1,3-DCP诱导的R2C Leydig细胞生殖毒性的干预作用。结果表明,C3G抑制了1,3-DCP诱导的细胞毒性和细胞形态损伤,有效剂量范围为10至40μmol/L。此外,暴露于1,3-DCP(2 mmol/L)显著增加了活性氧水平和线粒体膜电位损伤率,导致孕酮分泌减少,而C3G干预降低了活性氧水平,并在处理24小时后增加了孕酮分泌。最重要的是,C3G干预可上调环磷酸腺苷(cAMP)水平以及类固醇生成急性调节蛋白和3β-羟基类固醇脱氢酶的蛋白表达。得出的结论是,C3G通过激活类固醇生成酶和cAMP水平,有效降低了1,3-DCP诱导的生殖毒性。