Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.8.1.4 (diaphorase)
 2,754 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial dihydrolipoamide dehydrogenase (LADH) is inactivated after incubation at 30 degree C, with myeloperoxidase (MPO)-dependent systems. The enzyme inactivation was a function of the pro-oxidant system composition and the time of incubation. The standard inactivating system contained 50 mM KH2PO4-K2HPO44, pH 7.4, 0.5-1.0 muM LADH, and pro-oxidant system. After 30 or 60 min of incubation with the MPO/H2O2/NaCl system, LADH inactivation was 64 and 87%, respectively (Figure 1). In the absence of NaCl, inactivation values were 9 and 27%, respectively, whereas in the absence of MPO the inactivation values were 4.0 and 11%, respectively (Figure 1). Under similar experimental conditions, sodium hypochlorite significantly inactivated LADH, thus supporting the role of hipochlorous acid as agent of the MPO/H2O2/CINa system. With the MPO/H2O2/Kl, MPO/H2O2/SCN or the MPO/H2O2/NaNO2 systems LADH inactivation depended on the anion nature, 1-being the most effective (Figure 2). NaNo2 effectively replaced halides as pro-oxidant (Figure 3). The MPO/NADH/halide systems, where NADH replaced H2O2, also inactivated LADH. Native (not denatured) catalase completely prevented the MPO/NADH/Kl system effect (Table 1), in close agreement with H2O2 production by the LADH-catalysed NADH oxidation and the role of H2O2 in LADH inactivation. LADH was also inactivated after incubation with MPO-generated free radicals such as the Chloropromazine and Paracetamol radicals (Table 2). Thiol compounds (Captopril, penicillamine, cysteine, N-acetylcysteine and mercaptopropionylglycine) (Table 3 and Figure 4), as well as taurine, ascorbate (Table 4), GSSG and trypanothione (Figure 5), protected LADH against the MPO-dependent oxidizing systems, and also against NaCIO (Table 4). The summarized observations are discussed in relation to MPO function in free radical production and pathologies such as ischemia-reperfusion injury and inflammation.
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PMID:[Myeloperoxidase as a factor of oxidative damage of the myocardium: inactivation of dihydrolipoamide dehydrogenase]. 970 51