Abstract
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 psychopharmacological 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 β-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 investigate 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 phenols with their anticonvulsant property.
