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

植酸(IP_6)能螯合铁离子，从而阻止Fenton反应产生活性氧自由基。一些证据表明，食用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，产生较低形式的肌醇磷酸(IP_5~IP_1)。在本研究中，我们对其水解物的抗氧化性能进行了评价。它们对铁离子的螯合能力随着肌醇结构上磷酸基团的减少而降低。但IP2对铁离子诱导的脱氧核糖降解有独特的抑制作用，与IP6类似，IP3对铁离子诱导的大肠黏膜匀浆氧化也有很强的抑制作用。有趣的是，在脂质体悬浮液中添加维生素E显著提高了IP3的抗氧化活性，这表明了协同抗氧化作用。此外，口服IP6对铁离子诱导的大肠粘膜脂质过氧化有保护作用。这些观察结果表明，植酸水解物具有重要的抗氧化功能，并表明它们与维生素E的协同作用是防止大肠粘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.