Evidence for superoxide-dependent reduction of Fe3+ and its role in enzyme-generated hydroxyl radical formation

Because the conditions for such reactions appear to exist in animal tissues, the results indicate a mechanism for the initiation and promotion of peroxidative attacks on membrane lipids and suggest that the role of antioxidants in intracellular metabolism may be to inhibit initiation of degradative reactions by the highly reactive radicals formed extraneously during metabolic activity

Kuo-Lan Fong; Paul B. McCay; J.Lee Poyer; Hara P. Misra; Bernard B. Keele

2002

Scholarcy highlights

  • The data reported below provide additional support for the occurrence of these reactions, especially the reduction of Fe3+ by superoxide
  • The phenomenon appears to be an intrinsic property of certain enzyme systems which produce superoxide and H2O2, and can result in extensive oxidative degradation of membrane lipids
  • Earlier studies had suggested that iron augmented production of the hydroxyl radical in such systems according to the following reaction sequence:
  • Because the conditions for such reactions appear to exist in animal tissues, the results indicate a mechanism for the initiation and promotion of peroxidative attacks on membrane lipids and suggest that the role of antioxidants in intracellular metabolism may be to inhibit initiation of degradative reactions by the highly reactive radicals formed extraneously during metabolic activity
  • (3)The O2-dependent reduction of Fe3+ to Fe2+ by xanthine oxidase activity is inhibited by Mn2+, which, in view of statement 2 above, is a further indication that the reduction of the iron involves superoxide anion
  • (6)The reoxidation of reduced cyt c in the xanthine oxidase system is markedly enhanced by Fe3+ and is apparently due to enhanced HO¬∑ radical formation since the Fe3+-stimulated reoxidation is inhibited by free radical scavengers, including those with specificity for the hydroxyl radical
  • From the Biomembrane Research Laboratory, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, and supported by Grants No AM-06978 and AM-08397 from the National Institutes of Health, U.S Public Health Service

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