Phytate peroxidation

The occupation of all available coordination sites by phytate suppresses other iron-mediated processes, such as lipid peroxidation ( 0). Figure 6 demonstrates that 0.24 mM phytate prevents the peroxidation of arachidonic acid driven by ascorbic acid and iron, whereas substantial amounts of malondialdehyde arise in the presence of free iron or of an iron-ADP chelate. 

By virtue of rendering iron catalytically inactive, dietary phytate may also suppress the incidence of colonic cancer (J2j>). Intestinal aerobic bacteria and/or minor inflammatory events generate substantial amounts of O27 leading to OH formation and lipid peroxidation. These two processes are thought to be important elements in tissue injury which occurs during inflammation. This argument is compatible with the observation that colonic cancer is frequently preceded, or accompanied, by pigmentation of the colonic epithelium lipofuscin, a byproduct of lipid... 

Figure 6. Effect of ADP and phytate on iron-mediated OH formation (A) and lipid peroxidation (B). The mean and standard deviation of 3 determinations are shown.

Iron absorption occurs predominantly in the duodenum and upper jejunum. The physical state of iron entering the duodenum greatly influences its absorption. At physiological pH, ferrous iron is rapidly oxidized to the insoluble ferric form. Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of ferric iron. When gastric acid production is impaired, iron absorption is reduced substantially. Ascorbic acid enhances iron absorption. Ascorbic acid mobilizes iron from iron-binding proteins in vivo, which in turn could catalyze lipid peroxidation. Iron absorption is inhibited by antacids, phytates, phosphates and tetracyclines. 

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