HYPOCHLOROUS ACID-INDUCED ZINC RELEASE FROM THIOLATE BONDS - A POTENTIAL PROTECTIVE MECHANISM TOWARDS BIOMOLECULES OXIDANT DAMAGE DURING INFLAMMATION

It has been proposed that metalloprotein zinc mobilization mediated by hypochlorous acid (HOCl) may induce cell injury (see H. Fliss and M. Menard (1991), Archives of Biochemistry and Biophysics, 287, 175-179). In the present paper, we have demonstrated using a dimercaptopropanol -zinc complex that, once released from thiolate bonds by HOCl, zinc ca n exert a significant antioxidant effect on both linolenic acid and de oxyribose oxidation induced by iron. In these experimental conditions, however, the antagonism towards deoxyribose oxidation is notably less than that towards linolenic acid peroxidation, thus suggesting a more specific inhibitory effect of zinc on iron-mediated oxidant damage wh en polyunsaturated fatty acids represent the oxidizable substrate. The antioxidant effects of zinc are strictly related to the ''free'' form ; indeed, the dimercaptopropanol-zinc complex per se is stimulatory ev en on biomolecules oxidant damage, apparently as a result of the proox idant interaction of the thiol compound with iron. In light of these r esults, it may be proposed that the zinc released from thiolate bonds by HOCl could specifically limit tissue oxidative burden in pathologic al conditions involving neutrophil accumulation and activation, such a s inflammation and ischemia-reperfusion.