A colorimetric method for the estimation of monoamine oxidase.
TL;DR: Michael, S. E. & Charlwood, P. A. (1958).
Abstract: Michael, S. E. (1958). Ab8tr. Comm. 4thint,. Congr. Biochem., Vienna, no. 2-106, p. 28. Pedersen, K. 0. (1958). J. phys. Chem. 62, 1282. Popjaik, G. & McCarthy, E. F. (1946). Biochem. J. 40, 789. Ram, J. S. & Maurer, P. H. (1958). Arch. Biochem. Biophys. 76, 28. Reichmann, M. E. & Charlwood, P. A. (1954). Canad. J. Chem. 32, 1092. Schwert, G. W. (1957). J. Amer. chem. Soc. 79, 139. Smith, D. B., Wood, G. C. & Charlwood, P. A. (1956). Canad. J. Chem. 34, 364. Svedberg, T. & Pedersen, K. 0. (1940). The Ultracentrifuge. Oxford University Press. Warren, R. L. & Charlwood, P. A. (1953). Nature, Lond., 171, 353. Wieme, R. J. (1959). Clin. chim. Acta, 4, 317. Williams, J. W., van Holde, K. E., Baldwin, R. L. & Fujita, H. (1958). Chem. Rev. 58, 715.
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TL;DR: The present investigation was undertaken to develop methods for preparation of banana polyphenoloxidase (PPO)3 and to determine some of its properties in comparison with phenol oxidases from other sources.
Abstract: Griffiths (13) has presented evidence indicating that the browning reactions of banana fruit result from the enzymic oxidation of dopamine (3,4 dihydroxyphenylethyliamine) by polyphenoloxidase. Although dopamine does occur in various fruits and vegetables (23), it has not previously been implicated as an important substrate in browning reactions. The present investigation was undertaken to develop methods for preparation of banana polyphenoloxidase (PPO)3 and to determine some of its properties in comparison with phenol oxidases from other sources.
171 citations
Cites background from "A colorimetric method for the estim..."
...However, the detergent extracts were free of significant amounts of these enzymes as determined by appropriate assay (12, 20) and by failure of the extracts to oxidize monophenols, /3-phenylethylamine, p-phenylenediamine or ascorbic acid (3, 6, 22)....
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TL;DR: Kinetic parameters of liver and brain monoamine oxidase with various substrates and inhibitors appeared to be the same when determined by either colorimetric or radiometric methods.
110 citations
TL;DR: The inhibitor of γ‐aminobutyrate transaminase (GABA‐T), amino‐oxyacetic acid (AOAA), drastically reduced the activity of GABA‐T to 30 per cent of the control value, with a corresponding increase of brain GABA, but had no effect on theActivity of glutamate decarboxylase (GAD).
Abstract: —
(1) The inhibitor of γ-aminobutyrate transaminase (GABA-T), amino-oxyacetic acid (AOAA), drastically reduced the activity of GABA-T to 30 per cent of the control value, with a corresponding increase of brain GABA, but had no effect on the activity of glutamate decarboxylase (GAD)
(2) The monoamine oxidase (MAO) inhibitors phenelzine, phenylpropylhydrazine and phenylvalerylhydrazine, lowered GABA-T activity to 58, 49 and 48 per cent, respectively; this was associated with a marked elevation of brain GABA
(3) The action of phenelzine and phenylpropylhydrazine in vivo and in vitro could be abolished by pre-treatment of the tissue with the structurally related MAO inhibitors phenylisopropylhydrazine and trans-2-phenylcyclopropylamine These had no action on the GABA system in vivo, either on the GABA content or on the GABA-T activity These latter drugs, however, were unable to influence the effects of AOAA either on GABA or on GABA-T
(4) The possible mechanism of action on GABA and the enzyme activities of the GABA system is discussed
87 citations
TL;DR: The data suggest that Pb‐exposure perturbs the aminergic system in the cerebral cortex, cerebellum and hippocampus and may contribute to the cognitive and behavioural impairments observed in P b‐exposed rats.
85 citations
Cites methods from "A colorimetric method for the estim..."
...The activity of MAO was estimated by the method of Green and Haughton (1961)....
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TL;DR: The results suggest that yohimbine releases noradrenaline from stores or nerves as a consequence of increased central sympathetic activity, and the lethal effects of a high dose of yOHimbine alone are not reduced by any of the treatments tested, and appear not to result from activation of sympathetic mechanisms.
Abstract: In mice, yohimbine appears to accentuate the normal "alarm" reactions (alerting, flight) to external stimuli. Imipramine increases this effect and at the same time converts a non-lethal dose of yohimbine into a lethal one. The effect of imipramine is greatly reduced by adrenalectomy or by treatment with reserpine, syrosingopine, ganglion-blocking drugs or adrenaline antagonists acting on sympathetic beta-receptors. Hypnotic, anti-convulsant or anaesthetic agents, tetrabenazine or antagonists of 5-hydroxytryptamine do not reduce the imipramine effect. A variety of drugs which, like imipramine, are known to interfere with the tissue binding of noradrenaline also increase the toxicity of yohimbine. Yohimbine significantly reduces brain noradrenaline content; adrenal catechol amines are slightly reduced. The results suggest that yohimbine releases noradrenaline from stores or nerves as a consequence of increased central sympathetic activity. Imipramine increases the actions and toxicity of yohimbine by increasing the effects of the released noradrenaline on beta-receptors. The lethal effects of a high dose of yohimbine alone are not reduced by any of the treatments tested, and appear not to result from activation of sympathetic mechanisms.
69 citations
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