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[The mechanism of action of d-amino acid oxidase. I. Evidence for a free radical mechanism of the reaction catalyzed b a dimeric form of the enzyme].

d-Amino acid oxidase can oxidize the substrate to a ketoacid in the absence of oxygen. The stoichiometry of this reaction is precisely 1 molecule of keto acid for 1 molecule of enzyme, containing two flavin groups. Hence, the flavin must be in the semi-reduced free radical state. But these free radicals cannot be visualized by ESR spectroscopy because of closeness and strong interaction. After the acid denaturation of the protein the coenzyme is released as a semi-reduced free radical. An alternative method of registration is the transfer of the free radical state to an added excess of free flavin molecules. By both methods it is quantitatively determined that each flavin of the enzyme is reduced to a free radical. Therefore, we believe to have evidenced unambiguously that this enzymatic reaction proceeds via a free radical transition state.

Animals↗

Crystalline free radical of chloropromazine.

The method of preparation and the spectral characteristic of the crystalline free radical of chlorpromazine are described. Two absorption maxima at 770 and 860 nm concomitant with those at 530 and 277 nm were found. The highest rate of dismutation of the radical was 4-4.10(-1) M. sec-1 at pH 7-2. The mechanism of luminescence during the decay of the peroxide form of th radical is discussed.

Chemical Phenomena↗

Kinetics of drug decomposition. Part 38. Hydrolysis and autoxidation of sodium phenylbutazone and aminophenazone in binary kinetic system.

The kinetics of hydrolysis and autoxidation of sodium phenylbutazone (PhB-Na) and aminophenazone (APh) was studied in ammonia-acetate, Carmody and Welford buffers at different buffer concentration, pH, ionic strengths and temperatures. The reaction in N2 atmosphere and under a constant O2 pressure, carried out in calibrated ampoules, followed the first order reaction kinetics. The assay of PhB-Na and APh in the presence of their degradation produces was carried out spectrophotometrically in the degraded solutions.

Aminopyrine↗

[Dinitroorthocresol dissociation of oxidative phosphorylation in the rat liver perfused in situ].

Perfusion of the rat liver in situ for 150 min provides for maintaining optimal values of acid-base balance for the following indexes: surplus of bases, content of standard bicarbonate, buffer bases pH, pO2, pCO2, HbO2, the level of bile secretion, content of lactate, pyruvate, ATP, ADP, that evidences for a high functional activity in the tissue. Introduction of dinitro-ortho-cresol (DNC) into the perfusion liquid causes development of acidosis. DNC results in dissociation of oxidative phosphorylation: the content of ATP and intensity of inorganic phosphorus utilization decrease, oxygen uptake intensifies. A compensatory increase in the glycolysis intensity directed to maintaining the level of macroergs under these conditions is is pronounced in the intensified uptake of glucose, in a rise in the content of lactate in perfusate and an increase in the pyruvate kinase activity in the liver. The redox state of NAD-pairs (ratio of [NAD+] : [NADN] calculated from the content of redox metabolites and the equilibrium constant for the lactate dehydrogenase system shifts toward an increase in the reducing properties of hepatocytes cytoplasm. The phosphate potential value calculated from the ratio [ATP] : [ADP] - [Pinor] lowers under conditions of the experiment.

Acid-Base Equilibrium↗

[Cellular energy metabolism in rats receiving diets contaminated with lindane].

Young male rats, Wistar CF strain, about 70 g body weight, were fed a well-balanced diet containing 0 (control), 60 or 240 ppm lindane. The day before the experiment, all the animals were fasted, and some of them placed in a restraint wheel forcing them to walk on during 18 hrs; another group was given an i.p. injection of 2.6 g/kg glucose 30 minutes before their sacrifice. The redox and energy potentials of liver and muscle tissues were estimated after the determination of the following compounds: lactate, pyruvate, beta-hydroxybutyrate, acetoacetate, ATP, ADP, AMP, inorganic phosphate, NADP and NADPH. No effect of lindane was observed on muscle metabolism and the 60 ppm dose was without significant effect on liver metabolism. At the 240 ppm dosage: a. Lindane ingestion increased the liver betaHOB/AcAc ratio and decreased the Lac/pyr ratio. The ATP/ADP ratio was not significantly lowered, although the ATP concentration was diminished and, conversely, the AMP and inorganic P ones were elevated; b. Whereas lindane lowered the glucose effect on the mitochondrial redox potential, it had no influence on the increasing of the ATP/ADP ratio by glucose, or on the antiketogenic effect of this sugar; c. In the animals fed the lindane-contaminated diet, muscular exercise increased the liver betaHOB/AcAc and NADPH/NADP ratios, while the lac/pyr and ATP/ADP ratios were unaltered. But blood pyruvate was increased. The following interpretation has been given. Lindane ingestion inhibits liver mitochondrial activity and increases ketogenesis. The glucose treatment results in a poor glucose utilization for energy needs in the contaminated animals and the forced muscular exercise shows that gluconeogenesis proceeds at a slower rate than in the controls. It is suggested that an increased demand in NADPH, as resulting from the induction of the microsomal enzymes by lindane, is one of the mechanisms by which the pesticide inhibits the activity of the tricarboxylic acid cycle.

Animals↗

Nucleophilic addition reactions of free and enzyme-bound deazaflavin.

DeazaFMN-containing glycolate oxidase has been prepared and shown to catalyze the stereospecific transfer of the alpha-hydrogen from substrate to enzyme-bound deazaFMN. The reaction of sulfite, cyanide, and hydroxylamine with several deazaflavin-containing enzymes (glycolate oxidase, D-amino acid oxidase, glucose oxidase, N-methylglutamate synthetase) and free deazaFMN has been examined. All the deazaflavin systems tested form reversible 1:1 complexes with sulfite and cyanide. The pH dependence of the reaction of free deazaFMN with cyanide indicates that cyanide anion is the reacting nucleophile. Hydroxylamine complexes are formed with deazaFMN glycolate oxidase and deazaFAD glucose oxidase. The effectiveness of the various nucleophilic reagents in complex formation decreases in the following order: sulfite greater than cyanide greater than hydroxylamine. The relative stability observed for the sulfite and cyanide complexes formed with various deazaflavin systems (glycolate oxidase greater than D-amino acid oxidase greater than free deazaFMN) follows the same trend observed for the stability of the sulfite complexes formed with the corresponding flavin system. A correlation is also observed between the reduction potential (E'o) of the deazaflavin system (glycolate oxidase (- 170 mV) greater than D-amino acid oxidase (-240 mV) greater than free deazaFMN (-178 mV) and the stability of the deazaflavin-nucleophile complexes. The following evidence indicates that deazaflavin systems are generally more susceptible toward nucleophilic attack than corresponding flavin system: (a) with the exception of glucose oxidase, the dissociation constants for the deazaflavin-sulfite complexes are at least 1 order of magnitude less than the corresponding flavin sulfite complexes; (b) the least reactive nucleophile, hydroxylamine, does not form a complex with any of the flavin systems. In the case of cyanide, a complex is formed only with native glycolate oxidase, which is the flavin-containing system most susceptible to attack by the more reactive sulfite. Formation of the various (deaza)flavin-nucleophile complexes is characterized by a bleaching of the longer wavelength absorption band of the chromophore and increases in absorption below the isosbestic point of the reaction in the near-ultraviolet region of the spectrum. These results are consistent with the formation of covalent adducts via attack of the various nucleophiles at position 5 of (deaza)flavin. The reaction with cyanide provides the first example of a reversible addition of carbanion to enzyme-bound (deaza)flavin.

Alcohol Oxidoreductases↗

Reduced nicotinamide adenine dinucleotide phosphate, a structural and conformational probe of chicken liver fatty acid synthetase.

Structural and conformational organization of chicken liver fatty acid synthetase has been probed using its fluorescent coenzyme, NADPH. Three NADPH binding sites per mole of the enzyme complex, of apparently identical dissociation constant (KD = 0.6 muM) can be titrated at temperatures above 12 degrees. These results are in disagreement with the earlier studies of Hsu and Wagner (Hsu, R. Y., and Wagner, B. J. (1970) Biochemistry, 9, 245-251) in which four such sites could be titrated. At 12 degrees, the composite sites split into two subsets: a pair of sites with a KD of 0.3 muM and a third site with a Kd of 1.1 muM. At lower temperatures (5 degrees or 2 degrees), the site with weak affinity disappears, leaving a pair of sites with a Kd of 0.5 muM. Similar observations were made when the enzyme was modified with phenylmethylsulfonyl fluoride, a specific and selective inhibitor of fatty acyl-CoA deacylase (s) of the pigeon liver enzyme complex (Kumar, S. (1975) J. Biol. Chem. 250, 5150-5158). Partial modification with phenylmethylsulfonyl fluoride elicits a NADPH binding response similar to the binding observed at 12 degrees, i.e. two sets of binding sites with nonidentical dissociation constants. Further modification corresponding to the complete loss of deacylase function results in a set of two apparently identical binding sites, and the third site is not available for titration. The modified enzyme retains the two reductase functions as measured by the model substrates, acetoacetyl-N-acetylcysteamine and crotonyl-CoA. Furthermore, the addition of acetyl- and malonyl-CoA (100 muM each) to the modified enzyme lowers the NADPH binding affinity by a factor of 3. Other observations show that the quantum yield, as measured by the ratio of fluorescence intensity of bound and free NADPH, changes with temperature and ionic strength. Lowering the temperature from 30 degrees to 2 degrees increases the enhancement ratio by 50%, whereas increase in ionic strength from 0.05 to 0.2 M potassium phosphate lowers it to 50% of the original level. Measurement of NADPH binding in the presence of NADP+, NADH, NAD+ and adenosine-2'-monophospho-5'-diphosphoribose demonstrates that NADP+ shows competitive behavior for NADPH sites (KD = 10.6 muM), whereas NADH and NAD+ show noncompetitive (KD (apparent) = nearly 600 muM) and rather complicated interactions implicating nonspecific conformational alteration of the enzyme complex. The behavior of adenosine 2'-monophospho-5'-diphosphoribose is intermediate between NADP+ and NADH. These data are discussed in terms of substrate-mediated conformational changes and the moles of each of the reductase enzymes per mole of the enzyme complex, the polarity of the NADPH binding region, and the probable structure of the nicotinamide moiety when bound to the enzyme.

Animals↗