The effects of intragastric administration of μ-, δ, and Κ-opioid receptor agonists DAMGO, DADLE, and ICI 204,448, respectively, on the anxiety and motor activity of rats in an elevated plus-maze were studied. Peripheral administration of ICI 204,448 produced an anxiolytic effect, but had no effect on motor activity of rats. DAMGO and DADLE reduced motor activity; DADLE also increased anxiety. The data on the opposite effects of ICI 204,448 and DADLE on anxiety confirmed our previous hypothesis on the interactions between the central and peripheral components of the endogenous opioid system.
Unlike other intradiol-cleaving dioxygenases, hydroxyquinol 1,2-dioxygenase (HQ-DO) from Azotobacter sp. GP1 (for this enzyme an improved purification is described) and 6-chlorohydroxyquinol 1,2-dioxygenase (CHQ-DO) from Streptomyces rochei 303 only convert 1,2,4-trihydroxybenzene compounds and do not accept catechols as substrate. Inhibition studies revealed the ability of the two enzymes to interact with hydroxylated aromatic and chloroaromatic compounds. Thus polychlorinated catechols strongly inhibited both enzymes by fully mixed mechanism. Also for both enzymes, chlorophenols were weak or no inhibitors and methylcatechols were found to be less effective inhibitors than the corresponding chlorocatechols. Nonchlorinated hydroxylated aromatic compounds inhibited HQ-DO but not CHQ-DO. Mono-and dichlorinated hydroquinones and catechols were competitive inhibitors for HQ-DO but they acted upon CHQ-DO by two different mechanisms: fully competitive and fully mixed inhibition. Differences and similarities in inhibition effect and mechanism are discussed with regard to the interaction of hydroxyaromatic compounds with either enzyme. A hypothesis is presented to explain why hydroxyquinol cleaving enzymes are unable to catalyze the ring fission of catechol.
Unlike other intradiol‐cleaving dioxygenases, hydroxyquinol 1,2‐dioxygenase (HQ‐DO) from Azotobacter sp. GP1 (for this enzyme an improved purification is described) and 6‐chlorohydroxyquinol 1,2‐dioxygenase (CHQ‐DO) from Streptomyces rochei 303 only convert 1,2,4‐trihydroxybenzene compounds and do not accept catechols as substrate. Inhibition studies revealed the ability of the two enzymes to interact with hydroxylated aromatic and chloroaromatic compounds. Thus polychlorinated catechols strongly inhibited both enzymes by fully mixed mechanism. Also for both enzymes, chlorophenols were weak or no inhibitors and methylcatechols were found to be less effective inhibitors than the corresponding chlorocatechols. Nonchlorinated hydroxylated aromatic compounds inhibited HQ‐DO but not CHQ‐DO. Mono‐ and dichlorinated hydroquinones and catechols were competitive inhibitors for HQ‐DO but they acted upon CHQ‐DO by two different mechanisms: fully competitive and fully mixed inhibition. Differences and similarities in inhibition effect and mechanism are discussed with regard to the interaction of hydroxyaromatic compounds with either enzyme. A hypothesis is presented to explain why hydroxyquinol cleaving enzymes are unable to catalyze the ring fission of catechol.
Aim. A comparative study of the influence of nitric oxide synthase (NO-synthase) inhibitors on the parameters of anxiety, motor activity and pain sensitivity of rats. Materials and Methods. The work was conducted on male rats of Wistar line. The anxiety level and locomotor activity of rats were studied in the elevated plus maze (EPM) test. Pain sensitivity of the animals was tested on the hotplate apparatus. In the work, selective inhibitor of inducible isoform of NO-synthase aminoguanidine at a dose of 50 mg/kg, and non-selective inhibitor of this enzyme N-nitro-L-arginine at a dose of 50 mg/kg, were used. Rats of the control group were introduced the equivalent quantity of normal saline. NO-synthase inducible inhibitor aminoguadinine did not produce any influence on the anxiety level, but led to reduction of the horizontal motor activity of rats. Introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by reduction of the anxiety and of the locomotor activity of animals in the EPM test. Both investigated NO-synthase inhibitors induced alteration of pain sensitivity of rats in the form of hypoalgesia. Here, the most pronounced nociceptive effect was observed with introduction of non-selective NO-synthase inhibitor. Conclusion. In the work the evidence of participation of inducible isoform of NO-synthase in realization of the motor activity and pain sensitivity processes in rats is shown. In result of the conducted experiments it was found that introduction of non-selective NO-synthase inhibitor N-nitro-L-arginine was accompanied by evident alterations of anxious behavior, locomotor activity and nociceptive sensitivity of rats. The results obtained confirm the important role of the system of regulation of nitric oxide synthesis in neurochemical mechanisms of behavioral reactions in rats.
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