Untitled

Abstract

It was established that nitrite in the presence of chloride, bromide, and thiocyanate decreases the rate of hydrogen peroxide decomposition by catalase. The decrease was recorded by the permanganatometric method and by a method of dynamic calorimetry. Nitrite was not destroyed in the course of the reaction and the total value of heat produced in the process was not changed by its presence. These facts suggest that nitrite induces inhibition of catalase with no change in the essence of the enzymatic process. Even micromolar nitrite concentrations induced a considerable decrease in catalase activity. However, in the absence of chloride, bromide, and thiocyanate inhibition was not observed. In contrast, fluoride protected catalase from nitrite inhibition in the presence of the above-mentioned halides and pseudohalide. As hydrogen peroxide is a necessary factor for triggering a number of important toxic effects of nitrite, the latter increases its toxicity by inhibiting catalase. This was shown by the example of nitrite-induced hemoglobin oxidation. The naturally existing gradient of chloride and other anion concentrations between intra- and extracellular media appears to be the most important mechanism of cell protection from inhibition of intracellular catalase by nitrite. Possible mechanisms of this inhibition are discussed.

Proposed Mechanism of Nitrite-Induced Methemoglobinemia

“…70 No. As we reported in the previous study [11], we showed that nitrite reversibly inhibits catalase in the presence of halide ions and thio cyanate, while in their absence the above effect is not recorded. All these proce dures can result in artifacts [12].…”

“…Rabbit erythrocyte hemolysate was obtained by 20 fold dilution of erythro cyte mass (thrice washed with physiological solution) with 2.5 mM phosphate buffer, pH 7.2 [11]. NaH 2 PO 4 , NaCl, KBr, hydrogen perox ide, and ethanol were from Reakhim (Russia); KSCN, NaN 3 , potassium nitrite, ascorbic acid, bovine liver cata lase, methemoglobin, lactoperoxidase, and horseradish peroxidase (RZ 3.0) were from Sigma (USA); β estradiol and testosterone were from Merck (Germany); sero tonin creatinine sulfate and benzidine were from Reanal (Hungary); mannitol, β naphthol, and EDTA were from Chemapol (Czech Republic).…”

“…Rabbit erythrocyte hemolysate was obtained by 20 fold dilution of erythro cyte mass (thrice washed with physiological solution) with 2.5 mM phosphate buffer, pH 7.2 [11].Estimation of nitrite content in erythrocyte hemolysate. There are several aspects within this line to be studied: nitrite induced hemoglobin oxidation as one of the principal factors of nitrite toxicity and as one of the ways of its metabolism in an organism, which is closely interconnected with the metabolism of nitrogen oxide, nitrogen dioxide, and nitrate [1 4].…”

Acute oral dose of sodium nitrite induces redox imbalance, DNA damage, metabolic and histological changes in rat intestine

“…NO forms complexes with transition metal ions and can thus directly interact with these enzymes and interfere in their activity. Direct inhibition of CAT by nitrite in presence of specific anions has also been reported [59]. A decrease in the activities of TR, GR and GPx could also be due to oxidative modification of these enzymes.…”

The Reaction between Nitrite and Oxyhemoglobin

“…In these experiments we employed relatively high catalase concentrations to overcome any potential nitrite-catalase interaction (28), and also the possible competition between catalase and metHb (29). Interestingly, catalase was only effective when added at the start of the reaction but not when added toward the end of the lag period.…”