2-3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline and 2-3-dihydroxybenzoic-acid

2-3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline has been researched along with 2-3-dihydroxybenzoic-acid* in 1 studies

Other Studies

1 other study(ies) available for 2-3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline and 2-3-dihydroxybenzoic-acid

ArticleYear
Characterization of hydroxyl radical generation in the striatum of free-moving rats due to carbon monoxide poisoning, as determined by in vivo microdialysis.
    Brain research, 2004, Aug-06, Volume: 1016, Issue:2

    Carbon monoxide (CO) poisoning caused by CO exposure at 3000 ppm for 40 min resulted in stimulation of hydroxyl radical (*OH) generation (estimated by measuring 2,3-dihydroxybenzoic acid (2,3-DHBA) production from salicylic acid) in the striatum of free-moving rats, as determined by means of brain microdialysis. Pretreatment with a voltage-dependent Na+ channel blocker, tetrodotoxin (TTX), lowered the basal level of 2,3-DHBA and strongly suppressed the increase in 2,3-DHBA induced by CO poisoning. CO poisoning significantly, though only slightly, increased extracellular glutamate in the striatum, and glutamate (Glu) receptor antagonists, such as MK-801 (dizocilpine) and NBQX, failed to suppress the CO-induced increase in 2,3-DHBA. These findings suggest that CO poisoning may induce Na+ influx via the voltage-dependent Na+ channels, resulting in stimulation of *OH generation in rat striatum. This effect may be independent of Glu receptor activation by increased extracellular Glu.

    Topics: Animals; Carbon Monoxide Poisoning; Corpus Striatum; Dizocilpine Maleate; Excitatory Amino Acid Antagonists; Glutamic Acid; Hydroxybenzoates; Hydroxyl Radical; Male; Microdialysis; Quinoxalines; Rats; Rats, Sprague-Dawley; Tetrodotoxin; Wakefulness

2004