Hydroxyl radical production in the brain after CO hypoxia in rats.

摘要: Abstract Reactive oxygen species (ROS) have been implicated in the pathogenesis of neuronal injury after carbon monoxide (CO) poisoning. Severe CO poisoning is treated with hyperbaric (HBO), which eliminates quickly from hemoglobin and body tissue stores, but has a potential to increase ROS generation. In this study, effects HBO on generation highly reactive hydroxyl radical (HO·) brain rats was investigated using nonenzymatic hydroxylation salicylic acid 2,3 dihydroxybenzoic (2,3-DHBA) as probe. control studies, concentrations 2,3-DHBA mitochondria postmitochondrial supematant (cytosol) were similar air-exposed animals. After poisoning, concentration increased not cytosol. exposure administration at 1.5 atmospheres absolute (ATA), decrease production detected mitochondria. 2.5 ATA, both The oxidant scavenger dimethylthiourea (DMTU) monoamine oxidase (MAO) inhibitor pargyline, administered poisoned diminished subcellular compartments. These findings indicate that HOḃ can be either or accelerated severe depending partial pressure employed during therapy.