Disease relevance of Aminooxyacetic acid

• Atropine 1 mg/kg, thiosemicarbazide 4 mg/kg, aminooxyacetic acid 100 mg/kg, theophylline 100 mg/kg, and phenytoin 50 mg/kg were associated with a reduced survival after cerebral ischemia [1].
• Aminooxyacetic acid: correlation between biochemical effects, anticonvulsant action and toxicity in mice [2].
• As regards pharmacological effects, AOAA caused marked hypothermia, which was maximal by 1 hr and could be reversed by increasing ambient temperature, whereas effects of VPA on body temperature were only moderate [3].
• Aminooxyacetic acid produces excitotoxic brain injury in neonatal rats [4].
• In contrast, pretreatment of immature puppies with aminooxyacetic acid severely impaired recovery after 45 minutes of normothermic global ischemia (30% versus 85% recovery in untreated hearts, p less than 0.05) [5].

Psychiatry related information on Aminooxyacetic acid

• A further suppression of ethanol-induced hyperactivity was reached by pretreatment with aminooxyacetic acid (AOAA, 15 mg/kg i.p.). The stimulation of motor activity induced by morphine (10 mg/kg i.p.) remained unaffected by even high doses of i.p. GABA [6].
• GABA agonists showed an antiamnesic action as follows: in the passive avoidance task, 1) picrotoxin-induced amnesia was antagonized by muscimol, baclofen and AOAA [7].
• However, at sexual arousal, the bicuculline blockade of GABA receptors significantly reduced the inhibitory effects of both AOAA administration and emotional stress on plasma testosterone levels [8].

High impact information on Aminooxyacetic acid

• Inhibiting the covalent binding with a beta-lyase inhibitor, aminooxyacetic acid, blocked the increase in hsp70 mRNA [9].
• We have partially purified ACC synthase 6,000-fold from Cucurbita fruit tissue treated with indoleacetic acid + benzyladenine + aminooxyacetic acid + LiCl [10].
• S-(1,2-Dichlorovinyl)-L-cysteinylglycine, a putative metabolite of DCVG, also produced cell death, which was prevented by 1,10-phenanthroline, phenylalanylglycine, and aminooxyacetic acid, inhibitors of aminopeptidase M, cysteinylglycine dipeptidase, and cysteine conjugate beta-lyase, respectively [11].
• Furthermore, pretreatment of the crude homogenate with aminooxyacetic acid and alpha-methyl-trans-3-dehydroglutamate, two inactivators of glutamate decarboxylase which function by entirely different mechanisms, decreased count incorporation ([alpha-3H]acetylenic gamma-aminobutyric acid) to the same extent as the activity was decreased [12].
• Alanine synthesis and release were decreased by aminooxyacetic acid, an inhibitor of alanine aminotransferase [13].

Chemical compound and disease context of Aminooxyacetic acid

• Furthermore, we investigated the effect of GABA receptor agonists, muscimol and baclofen, or a GABA transaminase inhibitor, aminooxyacetic acid (AOAA), on these amnesia models [7].
• Biochemical analyses of hearts undergoing ischemia showed aminooxyacetic acid to limit lactate production, impair glutamate utilization, prevent alanine production, and limit succinate accumulation (p less than 0.05) [5].
• At these doses, AOAA, muscimol and THIP reduced motor activity [14].
• Prior treatment of the cells with aminooxyacetic acid (AOAA), an inhibitor of the enzyme cysteine conjugate beta-lyase, afforded complete protection against the toxicity at concentrations of PCBC up to 100 microM and DCVC up to 500 microM [15].
• First, the toxicity of the model conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC) is blocked both in vivo and in isolated, renal proximal tubular cells by aminooxyacetic acid, an inhibitor of PLP-dependent enzymes [16].

Biological context of Aminooxyacetic acid

• Studies in rodents using mitochondrial respiratory chain toxins, such as aminooxyacetic acid, 1-methyl-4-phenylpyridinium ion, malonic acid, and 3-nitropropionic acid, suggest that these agents do induce CNS degeneration by a process involving an excitotoxic mechanism [17].
• Measurements of lactate washout kinetics demonstrated that t1/2 followed the order: 3-NP approximately MPP+ >> AOAA approximately malonate, which parallels the expected lifetimes of the neurotoxins based on their mechanisms of action [18].
• Aminooxyacetic acid, a potent inhibitor of the mitochondrial malate-aspartate shunt, was used to assess the role of mitochondrial energy metabolism in damaged brain of rats of different age groups [19].
• Chronic administration of aminooxyacetic acid inhibits both basal and stress-induced transgene expression [20].
• Entry into the cycle was not affected by the transaminase inhibitor aminooxyacetic acid, indicating that deamination is the major route for 2-oxoglutarate formation from glutamate [21].

Anatomical context of Aminooxyacetic acid

• Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS inhibitor aminooxyacetic acid [22].
• The process was effectively inhibited by the transaminase inhibitor aminooxyacetic acid (IC50, approximately 25 microM), and showed pronounced regional distribution (hippocampus greater than cortical areas greater than thalamus much greater than cerebellum) [23].
• A hypothesis was, however, formulated that explained the convulsant-cum-anticonvulsant action of aminooxyacetic acid on the basis of compartmentation of GABA within the nerve endings [24].
• The effects of aminooxyacetic acid (AOAA), a transaminase inhibitor, and 2-oxoglutarate, a precursor to glutamate by the activity of aspartate aminotransferase (AAT), on slices of rat medulla oblongata, cerebellum, cerebral cortex, and hippocampus were studied [25].
• Although degradation activity of small intestinal contents for cysteine conjugates was very low, degradation activity of the contents of the cecum and large intestine was high and was inhibited by an inhibitor of cysteine conjugate beta-lyase (beta-lyase) activity, aminooxyacetic acid [26].

Associations of Aminooxyacetic acid with other chemical compounds

• Pyridoxal phosphate (PLP) activates the enzyme and aminooxyacetic acid inhibits it, the same as these agents activate or inhibit GAD from several nervous tissue sources [27].
• Concomitant increases in serum growth hormone and hypothalamic somatostatin in rats after injection of gamma-aminobutyric acid, aminooxyacetic acid, or gamma-hydroxybutyric acid [28].
• Time- and concentration-dependent uptake of S-(1,2-dichlorovinyl)-L-cysteine (DCVC) and S-(1,2-dichlorovinyl)-L-homocysteine (DCVHC) into cells were observed; higher concentrations were accumulated in the presence of aminooxyacetic acid (AOAA), an inhibitor of cysteine conjugate beta-lyase, indicating that AOAA does not inhibit transport [29].
• Activation of GABA system was achieved by raising the brain GABA concentration with aminooxyacetic acid (AOAA) or gabaculine which inhibits GABA-transaminase the enzyme responsible for the catabolism of GABA [30].
• The cytotoxicity of BCDFG was blocked by the gamma-glutamyltransferase inhibitor acivicin, and the cytotoxicity of both BCDFG and BCDFC was blocked by the cysteine conjugate beta-lyase inhibitor aminooxyacetic acid [31].

Gene context of Aminooxyacetic acid

• Pharmacological studies reported here show that aminooxyacetic acid improves the behavioral abnormalities of affected spd/spd mice in the same way it improves the behavior of affected spa/spa mice [32].
• Aminooxyacetic acid at 20 mg produced a significant increase in both serum GH and hypothalamic SRIF [28].
• Crayfish glutamic acid decarboxylase (GAD), like the homologous enzymes from other species, is inhibited by carbonyl-trapping agents (e.g. aminooxyacetic acid; AOAA) and sulfhydryl reagents (e.g. 5,5'-dithiobis-(2-nitrobenzoic acid); DTNB) [33].
• Failure of aminooxyacetic acid therapy in Huntington disease [34].
• To evaluate the effects of the gamma-aminobutyric acid (GABA)ergic system on PRL secretion during sexual development in female rats, aminooxyacetic acid (an inhibitor of GABA-transaminase which increases the hypothalamic GABA concentration) was administered to 12- to 16- and 30-day-old female rats [35].

Analytical, diagnostic and therapeutic context of Aminooxyacetic acid

• The effect of castration on GABA turnover in 13 microdissected brain regions was investigated by measuring regional GABA concentrations before and 30 min after injection of aminooxyacetic acid in intact rats or 2 or 6 days postcastration [36].
• This damage can be reproduced in rats by a focal microinjection of the indirect excitotoxin aminooxyacetic acid into the EC (Neurosci. Lett., 147: 185, 1992) [37].
• The present study was designed to examine the neuropathological consequences of an intra-entorhinal aminooxyacetic acid injection at various time-points with a sensitive silver staining method for the visualization of damaged neurons [38].
• Control studies in nonischemic hearts showed that coronary perfusion with aminooxyacetic acid for 5 minutes did not impair myocardial performance [5].
• Effect of aminooxyacetic acid on extracellular level of D-serine in rat striatum: an in vivo microdialysis study [39].

References