Adenosine deaminase isoenzyme 2 (ADA2) was isolated from human pleural fluid for the first time. Molecular and kinetic properties were characterized. It was shown that the inhibitors of adenosine deaminase isoenzyme 1 (ADA1), adenosine, and erithro-9-(2-hydroxy-3-nonyl)adenine (EHNA) derivatives are poor inhibitors of ADA2. Comparison of the interaction of ADA2 and ADA1 with adenosine and its derivative, 1-deazaadenosine, indicates that the isoenzymes have similar active centers. The absence of ADA2 inhibition by EHNA is evidence of a difference of these active centers in a close environment. The possible role of Zn 2+ ions and the participation of acidic amino acids Glu and Asp in adenosine deamination catalyzed by ADA2 were shown.

Institute of fine organic chemistry (FOC) of scientific technological center of organic and pharmaceutical chemistry NAS, Republic of Armenia EXPERIMENTAL Materials Depakine, containing sodium valproate (VPA) (Sanofi-Aventis U.S. LLC) as an active substance, d-amphetamine

Aim. To study subcellular nitrergic response in the rat brain regions following chronic stress-induced depression-like behavior. Methods. An animal model of depression induced by chronic circadian stress (CCS) established in our laboratory was used. The L-arginine, L-citrulline and reactive nitrogen species (RNS) levels were determined spectrophotometrically. Results. Immediately after CCS and four days later, a depression-like behavior of rats was observed and accompanied by a substantial persistent elevation of the L-arginine, L-citrulline and RNS levels with a simultaneous up-regulation of the inducible nitric oxide synthase (iNOS) in both cytosolic and mitochondrial compartments of the rat prefrontal cortex, striatum, hippocampus, and hypothalamus, and a down-regulation of their cytosolic constitutive NOS isoforms (cNOS), mitochondrial cNOS was not significantly changed, with the exception for hypothalamus, in which the latter dropped. Conclusions. Compromised balance of the L-arginine levels and NO synthesis in both mitochondria and cytosol in the limbic brain appears to be implicated in the pathogenesis of depression and pathological anxiety

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