Effects of iron on Vitamin C/copper-induced hydroxyl radical generation in bicarbonate-rich water

• Published in: Free radical research 2005-05, Vol.39 (5), p.565-570
• Main Authors: Jansson, Patric J., Del Castillo, Urko, Lindqvist, Christer, Nordström, Tommy
• Format: Article
• Language: English
• Subjects: Ascorbic Acid - chemistry; bicarbonate; Bicarbonates - chemistry; Chromatography, High Pressure Liquid; copper; Copper - chemistry; Food Contamination; Hydroxyl Radical - analysis; Hydroxyl Radical - chemical synthesis; iron; Iron - chemistry; Vitamin C; water; Water - chemistry
• ISSN: 1071-5762; 1029-2470
• DOI: 10.1080/10715760400009233

The aim of this study was to evaluate whether iron, like copper, could support Vitamin C mediated hydroxyl radical formation in bicarbonate-rich water. By using the hydroxyl radical indicator coumarin-3-carboxylic acid, we found that iron, in contrast to copper, was not capable to support Vitamin C induced hydroxyl radical formation. However, when 0.2 mg/l iron and 0.1 mg/l copper were both added to bicarbonate supplemented Milli-Q water, the Vitamin C induced formation of 7-hydroxycoumarin, as measured by HPLC analysis, was inhibited by 47.5%. The inhibition of hydroxyl radical formation by iron was also evident in the experiments performed on copper contaminated bicarbonate-rich household drinking water samples. In the presence of 0.2 mg/l of ferric iron the ascorbic acid induced hydroxyl radical formation was inhibited by 36.0-44.6%. This inhibition was even more significant, 47.0-59.2%, when 0.8 mg/l of ferric iron was present. None of the other redox-active metals, e.g. manganese, nickel or cobalt, could support ascorbic acid induced hydroxyl radical formation and did not have any impact on the ascorbic acid/copper-induced hydroxyl radical generation. Our results show, that iron cannot by itself produce hydroxyl radicals in bicarbonate rich water but can significantly reduce Vitamin C/copper-induced hydroxyl radical formation. These findings might partly explain the mechanism for the iron-induced protective effect on various copper related degenerative disorders that earlier has been observed in animal model systems.