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Human & Experimental Toxicology, Vol. 26, No. 8, 645-651 (2007)
DOI: 10.1177/0960327107076882

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

D. Taskiran

Ege University School of Medicine, Department of Physiology and Center for Brain Research, Izmir, Turkey, dilek.taskiran{at}ege.edu.tr

T. Nesil

Ege University, Institute of Natural and Applied Sciences, Department of Biotechnology, Izmir, Turkey

K. Alkan

Ege University School of Science, Department of Biology, zmir, Turkey

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

Key Words: carbon monoxide • cytochrome c oxidase • mitochondria • oxidative stress


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