Disease relevance of C00956

• In control retinas, a brief period of iontophoretic application of L-alpha-aminoadipic acid resulted in a slight activation of the spontaneous spike firing of ganglion cells but a slight decrease in the rate of light-induced firing [1].
• Intracerebral administration of L-alpha-aminoadipic acid (L-AAA) at 500 mg/kg body weight to rats caused a complex behavioral change with sporadic wet-dog shakes [2].
• N-Acetylisopenicillin N was isolated from the culture broth of Streptomyces tokunonensis sp. nov., and identified from 1H NMR spectroscopy and release of L-alpha-aminoadipic acid by acid hydrolysis [3].

High impact information on C00956

• DL- and L-alpha-aminoadipic acid (alpha-AA) are specific gliotoxins in vitro (Huck, S., F. Grass, and M. E. Hatten (1984) Neuroscience 12: 783-796) [4].
• Voltage-clamp studies of GLT1-expressing oocytes showed that, as in cortical neurons, glutamate transport was not inhibited by L-alpha-aminoadipate [5].
• In slices from adult cerebral cortex, veratridine, quisqualate, and L-alpha-aminoadipate decreased kynurenate synthesis substantially [6].
• 5. Pre-incubation of hippocampal slices with either of the selective glial toxins L-alpha-aminoadipic acid (L-AA) or fluorocitrate (FC) blocked mGluR-mediated potentiation of cAMP accumulation [7].
• 2-Aminoadipic acid (3), which shows a complex excitatory amino acid synaptic pharmacology, was an agonist at mGlu6 as well as mGlu2 [8].

Biological context of C00956

• Acid hydrolysis of the compound gave ethylamine and 2-aminoadipic acid [9].
• Anomalous "saturation kinetics" occurring in the reaction of L-alpha-aminoadipate with pig heart aspartate aminotransferase [10].
• Induction of cell death by L-alpha-aminoadipic acid exposure in cultured rat astrocytes: relationship to protein synthesis [11].
• We have employed the analysis of spontaneous forward mutations that confer the ability to utilize L-alpha-aminoadipate as a nitrogen source (alpha-Aa+) to discern the events that contribute to mitotic segregation of spontaneous recessive mutations by diploid cells. alpha-Aa- diploid cells yield alpha-Aa+ mutants at a rate of 7.8 +/- 3.6 x 10(-9) [12].
• Now, we show that this protein is a new type of lysine oxidase which catalyzes the oxidative deamination of free l-lysine into 6-semialdehyde 2-aminoadipic acid, ammonia and hydrogen peroxide [13].

Anatomical context of C00956

• Uptake, release, and metabolism of D- and L-alpha-aminoadipate by rat cerebral cortex [14].
• When these compounds were examined for their ability to inhibit [3H]NAAG binding to membranes of rat forebrain, the relative order of potency was L-alpha-aminoadipate = D-alpha-aminoadipate greater than L-AP4 greater than L-serine-O-phosphate greater than D-AP4 much greater than D,L-AP3 [15].
• The presence of 0.21 mM DL-alpha-aminoadipic acid or 0.10 mM L-alpha-aminoadipic acid for 40 h caused karyopyknosis in 50% of the astrocytes [16].
• The effects of L-alpha-aminoadipic acid on the levels of extracellular kynurenic acid were now studied by microdialysis in the dorsal hippocampus of freely moving rats [17].
• Effect of D, L-alpha-aminoadipate on the mediobasal hypothalamus and endocrine function in the rat [18].

Associations of C00956 with other chemical compounds

• By contrast, L-alpha-aminoadipate was significantly more potent in the cerebellum than in the cerebral cortex and hippocampus as an antagonist of both L-glutamate and L-aspartate [19].
• Catabolism of lysine in Penicillium chrysogenum leads to formation of 2-aminoadipic acid, a precursor of penicillin biosynthesis [20].
• In addition to L-alpha-aminoadipate, a previously identified gliotoxin, L-homocysteate, L-serine-O-sulfate, L-alpha-amino-4-phosphonobutyrate and L-alpha-amino-3-phosphono-propionate were also found to induce a sequence of degenerative events that led to the lysis of the astrocytes [21].

Gene context of C00956

• We examined whether damage to the glia limitans (GL), via exposure to the gliotoxin l-alpha-aminoadipic acid (l-alphaAAA), alters hypercapnia-induced pial arteriolar dilation in vivo [22].
• 3. L-alpha Aminoadipate was a competitive inhibitor of both glutamine synthetase, and gamma-glutamylcysteine synthetase, with Ki values of 209 microM and 7 mM respectively [23].
• A high dose of DL-alpha-aminoadipic acid (16 mumol) induced as long lasting a suppression in the glutamine synthetase and electroretinographic b-wave activities as 8 mumol L-alpha-aminoadipic acid [24].
• This uptake is increased if the potassium concentration is elevated from 3.45 to 12.0 mM in culture medium, but not in the presence of CSE Differential effects of the glial inhibitor L-alpha-aminoadipic acid (L-alpha-AA) were observed at high concentrations in the presence of CSF, compared with standard incubation conditions [25].

Analytical, diagnostic and therapeutic context of C00956

• The release of L-alpha-aminoadipate from the cerebral cortical slices is stimulated by a high concentration of K+ ions in the presence of Ca2+ in the perfusion buffer; the D-isomer displays this property to a lesser degree [14].
• The reaction product of this enzyme has been identified as L-alpha-aminoadipic acid by use of an amino acid analyzer and thin layer chromatography [26].

References