Antioxidant properties hydrogen peroxide

At the same time the interaction of superoxide with MPO may affect a total superoxide production by phagocytes. Thus, the superoxide adduct of MPO (Compound III) is probably quantitatively formed in PMA-stimulated human neutrophils [223]. Edwards and Swan [224] proposed that superoxide production regulate the respiratory burst of stimulated human neutrophils. It has also been suggested that the interaction of superoxide with HRP, MPO, and LPO resulted in the formation of Compound III by a two-step reaction [225]. Superoxide is able to react relatively rapidly with peroxidases and their catalytic intermediates. For example, the rate constant for reaction of superoxide with Fe(III)MPO is equal to 1.1-2.1 x 1061 mol 1 s 1 [226], and the rate constants for the reactions of Oi and HOO with HRP Compound I are equal to 1.6 x 106 and 2.2 x 1081 mol-1 s-1, respectively [227]. Thus, peroxidases may change their functions, from acting as prooxidant enzymes and the catalysts of free radical processes, and acquire antioxidant catalase properties as shown for HRP [228] and MPO [229]. In this case catalase activity depends on the two-electron oxidation of hydrogen peroxide by Compound I. 

Bedard et al. [7] studied quantitatively the initiation of the peroxidation of human low-density lipoproteins (LDL) with H00702 . In accord with the above findings the initiation rate increased when pH decreased from 7.6 to 6.5. It was suggested that initiation occurred via hydrogen atom abstraction by perhydroxyl radical from endogenous a-tocopherol, which in this process exhibited prooxidant and not antioxidant properties. Neutral, positively, and negatively charged alkyl peroxyl free radicals were the more efficient initiators of LDL peroxidation compared to superoxide. 

The absence of substituents with free radical scavenging properties in most of the (3-blockers makes doubtful their efficacy as powerful antioxidants. Arouma et al. [293] tested the antioxidative properties of several 3-blockers in reactions with superoxide, hydroxyl radicals, hydrogen peroxide, and hypochlorous acid. It was demonstrated that most of the compounds tested were inactive in these experiments. Nonetheless, propranolol, verapamil, and flunarizine effectively inhibited iron ascorbate-stimulated microsomal lipid peroxidation and all drugs (excluding flunarizine) were effective scavengers of hydroxyl radicals. Contrary to Janero et al. [292], these authors did not find the inhibition of xanthine oxidase by propranolol. It was concluded that 3-blockers are not the effective in vivo antioxidants. 

Furthermore, lacidipine was found to possess antioxidant activity at the same level of that of vitamin E in many tests, including hydrogen peroxide oxidation of rat neuronal cells [14]. The antioxidant property of lacidipine was further confirmed by experiments in vivo, in which low-density lipoprotein (LDL) oxidation was completely abolished [15]. Lacidipine also shows a direct protective effect on the vasculature at non-antihypertensive doses, indicating that its high lipophilicity combined with antioxidant potential can exert an additional therapeutic benefit [16-18]. 

Kim AT, Sarafian TA, Shau H (1997) Characterization of antioxidant properties of natural killer-enhancing factor-B and induction of its expressionby hydrogen peroxide. Toxicol Appl Pharmacol 147 135-142... 

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