Proanthocyanidins Antagonize Arsenic-Induced Oxidative Damage and Promote Arsenic Methylation through Activation of the Nrf2 Signaling Pathway

• Published in: Oxidative medicine and cellular longevity 2019, Vol.2019 (2019), p.1-19
• Main Authors: Wang, Hai-Xia, Feng, Gangling, Hu, Yun-Hua, Niu, Qiang, Xu, Meng-Chuan, Li, Shugang
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Apoptosis; Arsenic; Arsenic - toxicity; Cell Line; Cell Survival - drug effects; Cytotoxicity; Enzymes; Free radicals; Grape Seed Extract - pharmacology; Lipid peroxidation; Liver; Liver - drug effects; Liver - pathology; Liver - physiopathology; Metabolism; Methylation; NF-E2-Related Factor 2 - genetics; NF-E2-Related Factor 2 - metabolism; Oxidative stress; Oxidative Stress - drug effects; Penicillin; Poisoning; Proanthocyanidins - pharmacology; Proteomics; R&D; Reactive Oxygen Species - metabolism; Research & development; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Signal Transduction - drug effects
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2019/8549035

Purpose. To investigate the effects of grape seed proanthocyanidin extract (GSPE) on oxidative damage and arsenic (As) methylation and to clarify the role of Nrf2 in the process. Methods. L-02 cells were treated with arsenic (25 μM) and GSPE (10, 25, and 50 mg/L) for 24 h. Cell viability was analyzed by MTT assay. Cell apoptosis and ROS fluorescence were detected by flow cytometry. Oxidative stress marker levels were measured using commercial kits. mRNA and protein expression were detected by qRT-PCR and western blotting. The cellular concentrations of methylation products were measured by HPLC-HGAFS. Arsenic methylation ability of cells was determined. Results. Cell survival rate was significantly lower in the As group than in the control group (P