Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment

Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stres...

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Veröffentlicht in:Human & experimental toxicology 2007-08, Vol.26 (8), p.645-651
Hauptverfasser: Taskiran, D., Nesil, T., Alkan, K.
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Nesil, T.
Alkan, K.
description Carbon monoxide (CO) is the most common cause of fatal poisoning all over the world. At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. While CO treatment caused a significant decrease in GSH levels in the cortex and striatum in male rats, reduced GSH levels were observed in the cortex and hippocampus in female rats following CO exposure. Taken together, our data suggest a role for mitochondrial oxidative stress in CO toxicity at the cellular level during CO poisoning. Human & Experimental Toxicology (2007) 26, 645—651
doi_str_mv 10.1177/0960327107076882
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At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. 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At the cellular level, a combination of tissue hypoxia and direct cellular damage underlie the pathophysiology of CO toxicity. The purpose of this study was to determine the effect of CO treatment on oxidative stress parameters in mitochondria isolated from male and female rat brains. Mitochondria prepared from frontal cortex, hippocampus and corpus striatum were treated with 0.1% CO at 37°C for 30 minutes; control samples were not exposed to CO. Cytochrome c oxidase activity (COX), lipid peroxidation (thiobarbituric acid reactive species = TBARS), protein oxidation (protein carbonyls) and glutathione (GSH) levels were measured in CO treated and control samples. Our results confirmed previous studies reporting the inhibition of cytochrome c oxidase activity by CO in rat brain. Additionally, protein carbonyl levels in the hippocampus and striatum significantly increased after CO treatment in male rats. While CO treatment caused a significant decrease in GSH levels in the cortex and striatum in male rats, reduced GSH levels were observed in the cortex and hippocampus in female rats following CO exposure. Taken together, our data suggest a role for mitochondrial oxidative stress in CO toxicity at the cellular level during CO poisoning. Human &amp; Experimental Toxicology (2007) 26, 645—651</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>17884952</pmid><doi>10.1177/0960327107076882</doi><tpages>7</tpages></addata></record>
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subjects Animals
Biological and medical sciences
Brain - drug effects
Brain - enzymology
Brain - metabolism
Brain research
Carbon monoxide
Carbon Monoxide - toxicity
Cellular biology
Cerebral Cortex - drug effects
Cerebral Cortex - metabolism
Chemical and industrial products toxicology. Toxic occupational diseases
Corpus Striatum - drug effects
Corpus Striatum - metabolism
Electron Transport Complex IV - metabolism
Female
Gas, fumes
Glutathione - metabolism
Hippocampus - drug effects
Hippocampus - metabolism
In Vitro Techniques
Lipid Peroxidation - drug effects
Male
Medical sciences
Mitochondria - drug effects
Mitochondria - enzymology
Mitochondria - metabolism
Oxidation
Oxidative Stress - drug effects
Protein Carbonylation - drug effects
Rats
Rats, Sprague-Dawley
Rodents
Toxicology
title Mitochondrial oxidative stress in female and male rat brain after ex vivo carbon monoxide treatment
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