
<ArticleTitle>Oxygen-induced seizures and inhibition of human <prot>glutamate decarboxylase</prot> and porcine <prot>cysteine sulfinic acid decarboxylase</prot> by oxygen and nitric oxide.</ArticleTitle>
<AbstractText>The recombinant forms of the two human isozymes of <prot>glutamate decarboxylase</prot>, <prot>GAD65</prot> and <prot>GAD67</prot>, are potently and reversibly inhibited by molecular oxygen (Ki = 0.46 and 0.29 mM, respectively). Inhibition of the <prot>vesicle-associated glutamate decarboxylase</prot> (<prot>GAD65</prot>) by molecular oxygen is likely to result in incomplete filling of synaptic vesicles with gamma-aminobutyric acid (GABA) and may be a contributing factor in the genesis of oxygen-induced seizures. Under anaerobic conditions, nitric oxide inhibits both <prot>GAD65</prot> and <prot>GAD67</prot> with comparable potency to molecular oxygen (Ki = 0.5 mM). Two forms of porcine <prot>cysteine sulfinic acid decarboxylase</prot> (<prot>CSADI</prot> and <prot>CSADII</prot>) are also sensitive to inhibition by molecular oxygen (Ki = 0.30 and 0.22 mM, respectively) and nitric oxide (Ki = 0.3 and 0.2 mM, respectively). Similar inhibition of <prot>glutamate decarboxylase</prot> and <prot>cysteine sulfinic acid decarboxylase</prot> by two different radical-containing compounds (O2 and NO) is consistent with the notion that these reactions proceed via radical mechanisms.</AbstractText>
