- 作者: Kathleen Davis Todd Foos Jang-Yen Wu John V. Schloss
- 作者服務機構: Departments of Medicinal Chemistry and Molecuar Biosciences, university of Kansas, Lawrence, Kans., USA and Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Kuwait University, Kuwait
- 中文摘要: --
- 英文摘要: The recombinant forms of the two human isozymes ofglutamate decarboxylase, GAD65 and GAD67, are po-tently and reversibly inhibited by molecular oxygen (K =0.46 and 0.29 mM, respectively). Inhibition of the vesicle-associated glutamate decarboxylase (GAD65) by molec-ular oxygen is likely to result in incomplete filling of syn-aptic vesicles with -aminobutyric acid (GABA) and maybe a contributing factor in the genesis of oxygen-inducedseizures. Under anaerobic conditions, nitric oxide inhib-its both GAD65 and GAD67 with comparable potency tomolecular oxygen (K =0.5 mM). Two forms of porcinecysteine sulfinic acid decarboxylase (CSADI and CSADII)are also sensitive to inhibition by molecular oxygen (K =0.30 and 0.22 mM, respectively) and nitric oxide (K =0.3and 0.2 mM, respectively). Similar inhibition of gluta-mate decarboxylase and cysteine sulfinic acid decarbox-ylase by two different radical-containing compounds (O and NO) is consistent with the notion that these reactionsproceed via radical mechanisms.
- 中文關鍵字: --
- 英文關鍵字: Aminobutyric acid. Glutamate decarboxylase. GAD65. GAD67. Nitric oxide. Oxygen. Radical mechanism. GABA