Andrade Roberto G, Ginani Janini S, Lopes George K B, Dutra Fernando, Alonso Antonio, Hermes-Lima Marcelo
Oxyradical Research Group, Departamento de Biologia Celular, Universidade de Brasília, Brasília, DF, 70910-900, Brazil.
Biochimie. 2006 Sep;88(9):1287-96. doi: 10.1016/j.biochi.2006.02.006. Epub 2006 Mar 15.
The antioxidant activity of tannic acid (TA), a plant polyphenol claimed to possess antimutagenic and anticarcinogenic activities, was studied by monitoring (i) 2-deoxyribose degradation (a technique for OH detection), (ii) ascorbate oxidation, (iii) ascorbate radical formation (determined by EPR analysis) and (iv) oxygen uptake induced by the system, which comprised Fe(III) complexes (EDTA, nitrilotriacetic acid (NTA) or citrate as co-chelators), ascorbate and oxygen. TA removes Fe(III) from the co-chelators (in the case of EDTA, this removal is slower than with NTA or citrate), forming an iron-TA complex less capable of oxidizing ascorbate into ascorbate radical or mediating 2-deoxyribose degradation. The effectiveness of TA against 2-deoxyribose degradation, ascorbate oxidation and ascorbate radical formation was substantially higher in the presence of iron-NTA (or iron-citrate) than with iron-EDTA, which is consistent with the known formation constants of the iron complexes with the co-chelators. Oxygen uptake and 2-deoxyribose degradation induced by Fe(II) autoxidation were also inhibited by TA. These results indicate that TA inhibits OH formation induced by Fe(III)/ascorbate/O(2) mainly by arresting Fe(III)-induced ascorbate oxidation and Fe(II) autoxidation (which generates Fe(II) and H(2)O(2), respectively), thus limiting the production of Fenton reagents and OH formation. We also hypothesize that the Fe(II) complex with TA exhibits an OH trapping activity, which explains the effect of TA on the Fenton reaction.
单宁酸（TA）是一种据称具有抗诱变和抗癌活性的植物多酚，通过监测以下各项研究了其抗氧化活性：（i）2-脱氧核糖降解（一种检测羟基的技术）；（ii）抗坏血酸氧化；（iii）抗坏血酸自由基形成（通过电子顺磁共振分析测定）；以及（iv）由包含Fe（III）配合物（乙二胺四乙酸（EDTA）、次氮基三乙酸（NTA）或柠檬酸盐作为共螯合剂）、抗坏血酸和氧气的体系诱导的氧气摄取。TA从共螯合剂中去除Fe（III）（就EDTA而言，这种去除比NTA或柠檬酸盐慢），形成一种铁-TA配合物，其氧化抗坏血酸生成抗坏血酸自由基或介导2-脱氧核糖降解的能力较弱。在存在铁-NTA（或铁-柠檬酸盐）的情况下，TA对2-脱氧核糖降解、抗坏血酸氧化和抗坏血酸自由基形成的有效性明显高于铁-EDTA，这与铁配合物与共螯合剂的已知形成常数一致。TA也抑制了Fe（II）自氧化诱导的氧气摄取和2-脱氧核糖降解。这些结果表明，TA主要通过阻止Fe（III）诱导的抗坏血酸氧化和Fe（II）自氧化（分别产生Fe（II）和H₂O₂）来抑制Fe（III）/抗坏血酸/O₂诱导的羟基形成，从而限制芬顿试剂的产生和羟基形成。我们还假设与TA形成的Fe（II）配合物具有羟基捕获活性，这解释了TA对芬顿反应的影响。
