Department of Chemistry, Wakayama Medical University, 580 Mikazura, Wakayama 641-0011, Japan.
J Clin Biochem Nutr. 2011 Nov;49(3):207-15. doi: 10.3164/jcbn.11-16. Epub 2011 Aug 24.
In order to clarify the mechanism by polyphenols of protective effects against oxidative damage or by quinolinic acid of its neurotoxic and inflammatory actions, effects of polyphenols or quinolinic acid on the radical formation were examined. The ESR measurements showed that some polyphenols such as caffeic acid, catechol, gallic acid, D-(+)-catechin, L-dopa, chlorogenic acid and L-noradrenaline inhibited the formation of radicals in the reaction mixture of rat liver microsomes with ADP, Fe(3+) and NADPH. The ESR measurements showed that α-picolinic acid, 2,6-pyridinedicarboxylic acid and quinolinic acid (2,3-pyridinedicarboxylic acid) enhanced the formation of radicals in the reaction mixture of rat liver microsomes with Fe(3+) and NADPH. Caffeic acid and α-picolinic acid had no effects on the formation of radicals in the presence of EDTA, suggesting that the chelation of iron ion seems to be related to the inhibitory and enhanced effects. The polyphenols may exert protective effects against oxidative damage of erythrocyte membrane, ethanol-induced fatty livers, cardiovascular diseases, inflammatory and cancer through the mechanism. On the other hand, quinolinic acid may exert its neurotoxic and inflammatory effects because of the enhanced effect on the radical formation.
为了阐明多酚对氧化损伤的保护作用机制或喹啉酸的神经毒性和炎症作用机制，研究了多酚或喹啉酸对自由基形成的影响。ESR 测量结果表明，一些多酚，如咖啡酸、儿茶酚、没食子酸、D-（+）-儿茶素、左旋多巴、绿原酸和去甲肾上腺素，抑制了大鼠肝微粒体与 ADP、Fe(3+)和 NADPH 反应混合物中自由基的形成。ESR 测量结果表明，α-吡啶甲酸、2,6-吡啶二甲酸和喹啉酸（2,3-吡啶二甲酸）增强了大鼠肝微粒体与 Fe(3+)和 NADPH 反应混合物中自由基的形成。在 EDTA 存在下，咖啡酸和 α-吡啶甲酸对自由基的形成没有影响，这表明铁离子的螯合作用可能与抑制和增强作用有关。多酚可能通过这种机制发挥对红细胞膜氧化损伤、乙醇诱导的脂肪肝、心血管疾病、炎症和癌症的保护作用。另一方面，由于对自由基形成的增强作用，喹啉酸可能发挥其神经毒性和炎症作用。
