Abstract
Ni 2+, a toxic, carcinogenic and allergenic agent, affected both the kinetic and chemical courses of the Fe 2+-induced oxidation of arachidonic acid (AA) in 0.05 M phosphate buffer (pH 7.4) and at 37 °C. At 10 μM concentration, Ni 2+ decreased the rate of oxidation of peroxide-free AA (200 μM) promoted by 50 μM Fe 2+, as determined by measurement of thiobarbituric acid reactive species (TBARS) and 1H NMR analysis. However, in the presence of low levels of peroxides (e.g. 2%), Ni 2+ exerted a significant stimulatory effect on Fe 2+-induced AA oxidation and TBARS formation. 1H NMR analysis showed that Ni 2+ (10 μM) enhanced formation of genotoxic alkenals including 4-hydroxy-2-nonenal (4-HNE, GC/MS evidence) by Fe 2+-promoted degradation of both AA and 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid (15-HPETE) methyl esters. The observed stimulatory effects of Ni 2+ on peroxide breakdown and cytotoxic aldehyde formation provide an attractive explanation to the enhanced sensitization capacity of nickel in inflammatory states compared to normal states.
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