Regional H2O2 concentration in rat brain after hyperoxic convulsions

Piantadosi, Claude A.; Tatro, Lynn

doi:10.1152/jappl.1990.69.5.1761

Cited by 51 publications

(30 citation statements)

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“…These decreases in catalase activity indicated an increase in the formation of ATZ-H202-catalase complex relative to control studies. At non-rate limiting ATZ concentrations, formation of the complex is pseudo-first order with respect to time and H202 concentration (16,20). Because ATZ was given 30 min before brain harvesting in all animals, the decreases in regional catalase activity were proportional to the rate of H202 reaching the microperoxisome during the 30 min periods of CO hypoxia and reoxygenation.…”

Section: Resultsmentioning

confidence: 97%

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Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.

Zhang¹,

Piantadosi²

1992

J. Clin. Invest.

293

161

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To better understand the mechanisms of tissue injury during and after carbon monoxide (CO) hypoxia, we studied the generation of partially reduced oxygen species (PROS) in the brains of rats subjected to 1% CO for 30 min, and then reoxygenated on air for 0-180 min. By determining H202-dependent inactivation of catalase in the presence of 3-amino-1,2,4-triazole (ATZ), we found increased H202 production in the forebrain after reoxygenation. The localization of catalase to brain microperoxisomes indicated an intracellular site of H202 production; subsequent studies of forebrain mitochondria isolated during and after CO hypoxia implicated nearby mitochondria as the source of H202. In the mitochondria, two periods of PROS production were indicated by decreases in the ratio of reduced to oxidized glutathione (GSH/GSSG). These periods of oxidative stress occurred immediately after CO exposure and 120 min after reoxygenation, as indicated by 50 and 43% decreases in GSH/GSSG, respectively. The glutathione depletion data were supported by studies of hydroxyl radical generation using a salicylate probe. The salicylate hydroxylation products, 2,3 and 2,5-dihydroxybenzoic acid (DHBA), were detected in mitochondria from CO exposed rats in significantly increased amounts during the same time intervals as decreases in GSH / GSSG. The DHBA products were increased 3.4-fold immediately after CO exposure, and threefold after 120 min reoxygenation. Because these indications of oxidative stress were not prominent in the postmitochondrial fraction, we propose that PROS generated in the brain after CO hypoxia originate primarily from mitochondria. These PROS may contribute to COmediated neuronal damage during reoxygenation after severe CO intoxication. (J. Clin. Invest. 1992. 90:1193-1199

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Section: Resultsmentioning

confidence: 97%

“…Residual catalase activity was measured in six brain regions 30 min after the administration of the H202-dependent inhibitor of catalase (ATZ), as previously described ( 16 (20). Three animals did not meet the ATZ criterion for the study, however, three other rats that met the ATZ criterion were added to complete the study.…”

Section: Methodsmentioning

confidence: 99%

Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.

Zhang¹,

Piantadosi²

1992

J. Clin. Invest.

293

161

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“…The AT-mediated inhibition of brain catalase activity was used as a measure of the rate of cerebral H 2 O 2 production (Yusa et al 1987;Piantadosi and Tatro 1990;Zhang and Piantadosi 1991;Simonson et al 1993). Animals (a total of 48, n=6 per group) were administered with AT (1 g/kg) and 1 h later, they were exposed to air or 99.5% O 2 for 30, 45 or 60 min.…”

Section: Methodsmentioning

confidence: 99%

“…Brain H 2 O 2 levels can be experimentally increased by hyperoxia exposure (Yusa et al 1987;Piantadosi and Tatro 1990;Zhang and Piantadosi 1991;Simonson et al 1993) and changes in H 2 O 2 levels could modify the activity of brain catalase as a response of these substrate level modifications. Based on these premises, we used a novel approach to study the regulation of ethanol-induced behaviours by central catalase.…”

Section: Introductionmentioning

confidence: 99%

Ethanol-stimulated behaviour in mice is modulated by brain catalase activity and H 2 O 2 rate of production

2002

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“…Cortical EEG activity in animals increases before the onset of seizure (14,60,63,189), typically preceded by increased Pti O 2 (210) (I. Demchenko and C. A. Piantadosi, personal communication) and increased ROS production (160,171). Important sites in the mCNS involved in the pathogenesis of O 2 seizures have been identified by using c-fos expression (6), increased 2-deoxyglucose uptake (204,(206)(207)(208), and changes in neuronal morphology indicative of lesions and tissue necrosis after extended exposures to hyperoxia (8)(9)(10).…”

Section: Electrophysiological and Neuroanatomic Responses To Hbomentioning

confidence: 99%

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

Dean¹,

Mulkey²,

Garcia³

et al. 2003

Journal of Applied Physiology

175

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III. Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures. J Appl Physiol 95: 883-909, 2003; 10.1152/japplphysiol.00920.2002.-As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired PO 2, PCO2, and N2 partial pressure, has deleterious effects on neuronal function, resulting in O 2 toxicity, CO2 toxicity, N2 narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures Ͻ5 atmospheres absolute (ATA). Here we summarize these methods, the physiologically relevant test pressures, potential research applications, and results of previous research, focusing on the significance of electrophysiological studies at Ͻ5 ATA. Intracellular recordings and tissue PO 2 measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (Յ3 ATA O 2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system. anesthesia; carbon dioxide toxicity; free radicals; high-pressure nervous syndrome; membrane potential; nitrogen narcosis; oxidative stress; oxygen toxicity; polarographic oxygen electrode MOST HUMANS ARE PHYSIOLOGICALLY adapted to live and work near sea level, where ambient pressure is ϳ1 atmosphere absolute (ATA).1 Nonetheless, we exploit a continuum of barometric pressure (PB) ranging from the near vacuum of outer space, which we survive during Space Shuttle extravehicular activity by wearing a 4.3 lb./in.2 absolute (psia) pressure suit (30,300 ft. pressure equivalent, 0.29 ATA) (120, 220), down to the summit of Mt. Everest at 29,029 ft., where PB is 0.31 ATA (221), to ocean depths as great as 2,300 ft. of sea water (fsw), where PB increases to ϳ70 ATA (18). These situations are the pressure extremes of our inhabitable environment, which only relatively few highly trained individuals have ever occupied.Military personnel, medical personnel, and other humans, however, frequently encounter levels of hyperbaric pressure (i.e., Ͼ1 ATA) of lesser degrees in their normal work environments. Examples of moderate hyperbaric environments (e.g., Ͻ5 ATA) include the following: patients and medical attendants undergoing hyperbaric O 2 therapy (HBOT) (38,203); diving with an underwater breathing apparatus for recreational, professional (oil and salvage companies), and combat purposes (89); simulated dry and wet dives for hyperbaric research and dive training (217); and working in the compressed atmosphere of a subterranean environment (117). Abnormal work environments resulting from catastrophic accident...

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Regional H2O2 concentration in rat brain after hyperoxic convulsions

Cited by 51 publications

References 0 publications

Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.

Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.

Ethanol-stimulated behaviour in mice is modulated by brain catalase activity and H 2 O 2 rate of production

Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures

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