Mechanism for the protection of oxidative stress in digestive tract by phytic acid

植酸（IP_6）能够螯合铁离子，从而阻断Fenton反应产生活性氧自由基。一些证据表明，富含植酸的饮食可以保护肠上皮细胞免受铁离子诱导的氧化损伤。在消化过程中，植酸被去磷酸化，生成低磷酸化形式的磷酸肌醇（IP_5 ~ IP_1）。在这项研究中，我们评估了其水解产物的抗氧化性能。它们螯合铁离子的能力随着肌醇结构上磷酸基团数量的减少而降低。ip2对铁离子诱导的脱氧核糖降解具有独特的抑制作用，IP3对铁离子诱导的大肠黏膜均浆氧化具有较强的抑制作用，与IP6相似。有趣的是，在脂质体混悬液中添加维生素E可显著提高IP3的抗氧化活性，提示其具有协同抗氧化作用。此外，口服IP6可保护大肠黏膜免受铁离子诱导的脂质过氧化。这些观察结果表明植酸水解产物具有重要的抗氧化功能，并表明它们与维生素E的协同作用是预防大肠黏膜氧化损伤的重要因素。

Phytic acid (IP_6) is capable of chelating iron ion and thereby blocking the generation of reactive oxygen radical via Fenton reaction. Some evidences suggest that the consumption of diets rich in phytic acid protect intestinal epithelial cells against iron ion-induced oxidative damage. During digestion, phytic acid is dephosphorylated yielding lower phosphorylated forms of inositol phosphate (IP_5〜IP_1). In this study, we evaluated the antioxidant properties of its hydrolysis products. Their ability to chelate iron ion decreased with the decrease in the number of phosphate groups on inositol structure. However, IP_2 showed a unique ability to prevent iron ion- induced deoxyribose degradation and IP3, as similarly to IP6, showed strong inhibitory effect against iron ion-induced oxidation of large intestinal mucosa homogenate. Interestingly, addition of vitamin E into liposomal suspension greatly incressed IP3 antioxidant activity, suggesting a synergistic antioxidant effect. Moreover, oral administration of IP6 protected large intestinal mucosa against iron ion-induced lipid peroxidation. These observations indicate an important antioxidant function for phytic acid hydrolysis products and suggest that their synergistic effect with vitamin E is an essential factor in the prevention of oxidative damage occurring in large intestinal mucosa.