Interactions of human blood plasma with hydrogen peroxide and hypochlorous acid
van der Vliet, A.; Hu, M.L.; O'Neill, C.A.; Cross, C.E.; Halliwell, B.
Journal of Laboratory and Clinical Medicine 124(5): 701-707
1994
ISSN/ISBN: 0022-2143 PMID: 7964128 Document Number: 434433
Activated neutrophils produce both hydrogen peroxide (H-2O-2) and hypochlorous acid (HOCI). Previous work has shown that HOCI depletes antioxidants, modifies proteins, and forms fatty acid chlorohydrins but does not cause significant lipid peroxidation in human plasma. Because activated phagocytes have been claimed to stimulate lipid peroxidation in plasma, we examined the effects of H-2O-2 and HOCI alone and in combination on plasma constituents. Hydrogen peroxide at concentrations below 0.5 mmol/L had little effect, but 1 to 2 mmol/L H-2O-2 caused loss of ascorbic acid and protein thiol groups, an effect potentiated by preincubation of the plasma with sodium azide to inhibit catalase. H-2O-2 caused no detectable lipid peroxidation or loss of alpha-tocopherol in plasma, but some depletion of ubiquinol occurred. The combination of HOCI and H-2O-2 caused more lipid peroxidation than either agent alone. Peroxidation was not inhibited by the metal chelators ethylenediaminetetraacetic acid and deferoxamine or by the singlet O-2/hydroXyl radical scavenger histidine. We hypothesize that the phagocyte-derived H-2O-2 and HOCI could interact in the microenvironment of the activated leukocyte to induce lipid peroxidation of plasma lipoproteins or cell membranes (or both).