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2 3 dihydroxybenzoic acid/crise épileptique
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Formation of free hydroxyl radicals after pentylenetetrazol-induced seizure and kindling.
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The present study indicates that free radicals have been implicated in pentylenetetrazol (PTZ)-induced seizure and kindling. In our experiments we used a method in which free hydroxyl radicals (* OH) are trapped by systemically applied salicylate in vivo, resulting in the stable and quantifiable
Hydroxyl radicals detected via brain microdialysis in rats breathing air and during hyperbaric oxygen convulsions.
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Microdialysis was done on 300-400 g, awake, male rats with microdialysis probes inserted through guide cannulas into the striatum (Bregma co-ordinates A 0.5, L 2.9, D -4.0 for guide cannulas implanted 5 days previously). Rats were exposed to hyperbaric oxygen (HBO; 6 atm absolute, 5 atm gauge
The role of superoxide dismutase and alpha-tocopherol in the development of seizures and kindling induced by pentylenetetrazol - influence of the radical scavenger alpha-phenyl-N-tert-butyl nitrone.
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Previous experiments have shown that the generation of free hydroxyl radicals in rat brain homogenates is increased following pentylenetetrazol (PTZ) kindling. The present study was performed in order to evaluate the involvement of endogeneous radical defence systems as the superoxide dismutase
Inhibition of brain glutamate decarboxylase by 4,5-dihydroxyisophthalic acid and related compounds.
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Hydroxybenzoic and phthalic acids and their related compounds were tested for inhibitory activity to brain glutamate decarboxylase. Of mono-, di-, and trihydroxybenzoic acids, gallic acid was the most inhibitory, giving 50% inhibition at a concentration of 0.17 mM. Dihydroxybenzoic acids were less
Free radical production during ethanol intoxication, dependence, and withdrawal.
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Indices of free radical production and cell damage were examined in male Sprague-Dawley rats chronically exposed to either ethanol (ETOH) or water vapor. In experiment 1, rats experienced either 1 or 11 cycles of ETOH exposure and withdrawal. Brain tissue was harvested 12 hr after ETOH exposure, and
Effect of hyperbaric oxygen treatment on nitric oxide and oxygen free radicals in rat brain.
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Oxygen (O(2)) at high pressures acts as a neurotoxic agent leading to convulsions. The mechanism of this neurotoxicity is not known; however, oxygen free radicals and nitric oxide (NO) have been suggested as contributors. This study was designed to follow the formation of oxygen free radicals and NO
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