- 作者: Grzegorz A. Czapskia Grace Y. Sunb Joanna B. Strosznaidera
- 作者服務機構: a Department of Cellular signalling, Medical Research Centre, Polish Academy of sciences, Warsaw, Poland; b Department of Biochemistry, University of Missouri, Columbia, Mo., USA
- 中文摘要: --
- 英文摘要: cofactor for NOS. Incubation of brain homogenates re-suited in a time-dependent increase in the levels of lipidperoxidation products, but ethanol did not further en-hance these products. Taken together, these results pro-vide evidence for the role of BH4 but not oxidative stressin the inhibitory effect of ethanol on NMDA-NOS activityin rat hippocampal slices.The ionotropic glutamatergic receptor system, especial-1y the subtype mediated by N-methyl-D-aspartic acid(NMDA), is known to exhibit special sensitivity to theeffect of ethanol. This is due partly to the ability of etha-nol to modulate the production of nitric oxide throughthe NMDA-nitric oxide synthase (NOS) pathway. In thisstudy, we examined the effects of ethanol on basal andNMDA-stimulated NOS activity in rat hippocampal slicesby measuring the conversion of〔 C -arginine into〔 C -citrulline in an incubation system containing the neces-sary cofactors. Stimulation of hippocampal slices withNMDA (100 M) enhanced NOS activity by 43%(n=12).Although ethanol did not alter NOS activity when addedto the incubation system during NMDA stimulation, itdose-dependently inhibited NMDA-NOS activity whenadded to the slices during the 90-min preincubationperiod. Further assay of NOS activity with brain cyto-solic fraction indicated an inhibitory effect of ethanol(200 mM when the assay was carried out in the absenceof exogenous tetrahydrobiopterin(BH4), a redox-active
- 中文關鍵字: --
- 英文關鍵字: Ethanol Nitric oxide synthase, Lipid peroxidation, N-methyl-D-aspartic acid receptor, Hippocampus, Oxidative stress