Effects of Some Hypnotic Drugs on Respiration and Oxidative Phosphorylation in Rat Brain

Erwin, V. Gene; Heim, Harold C.

doi:10.1002/jps.2600520808

Cited by 9 publications

(1 citation statement)

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“…These compounds, on the other hand, were found to have no effect on the oxidation of succinate (Table 1) where such an oxidation is independent of NAD. Similar results have been reported by other investigators (8)(9)(10)(11) where inhibition of the oxidation of glucose, pyruvate, malate and glutamate by rat brain homogenate was observed by certain hypnotics such as phenobarbitone, glutethimide and 2-methyl-3…”

Section: Resultssupporting

confidence: 91%

Correlation Between Selective Inhibition of Nad-Dependent Oxidations and Anticonvulsant Property of Quinazolone Allylethers and Quinazolone Allylphenols

Parmar

Rastogi

Gupta

et al. 1970

Japanese Journal of Pharmacology

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Inhibition of certain metabolic processes has been shown to be the property of various central nervous system depressants (1, 2) and a parallelism exists between in vitro and in vivo effects. Furthermore, the structure activity relationship of various psychopharma cological agents has been shown to be due to their interaction with receptor surfaces (3). Amongst 2,3-disubstituted quinazolones possessing central nervous system depressant activity (4-6), 2-methyl-3-(o-tolyl)-4-quinazolone (QZ-2) was found to be a potent anticonvulsant as compared to sodium phenobarbitone against pentylenetetrazole induced seizures (7). Such quinazolones exhibiting profound influence on the normal functional activity of the brain, were found to inhibit selectively nicotinamide adenine dinucleotide (NAD) dependent oxidation of the substrates of tricarboxylic acid cycle, L-glutamate and 19-hydroxybutyrate (8, 9). The ability of quinazolone allyl ethers and quinazolone allyl phenols to inhibit the oxidation of pyruvic acid by rat brain homogenate (10) led us to in vestigate the effects of these quinazolones on the oxidation of NAD-dependent and NAD independent substrates. In the present study attempts have also been made to correlate the enzyme (s) inhibitory activity of quinazolone allyl ethers and quinazolone allyl phe nols with their anticonvulsant property. BIOCHEMICAL STUDIES Materials and methods Commercial chemicals were used in the present study. Adenosine monophosphate (AMP), DL-isocitrate, and cytochrome-C were obtained from Sigma Chemical Co., St. Louis; a-ketoglutaric acid, Q-hydroxybutyric acid, and L-malate was obtained from Mann Research Laboratories Inc., New York; L-glutamic acid was obtained from E. Merck, Darmstadt, and sodium citrate and other common chemicals were obtained from British Drug House, Bombay.

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Section: Resultssupporting

confidence: 91%