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

Abstract

<jats:p> 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 &amp; Experimental Toxicology (2007) 26, 645—651 </jats:p>

In utero exposure to transient ischemia-hypoxemia promotes long-term neurodevelopmental abnormalities in male rat offspring

“…Expression of Nrxn1 was differentially regulated in the brain regions of OXT-exposed offspring regardless of the sex of the offspring; Nrxn1 was markedly downregulated in the amygdala but unchanged in the anterior cingulate and the somatosensory cortices of OXT versus control offspring. Because these results do not explain male-specific impairment of social behavior, we speculate that these changes could be due to sex differences in the response to oxidative stress (38,(50)(51)(52)(53)(54). The considerable sex difference in the expression of genes mediating oxidative stress 1 hour after OXT and the presence of persistently altered mitochondrial ETC proteins in the anterior cingulate cortex of only P28 male offspring support this viewpoint.…”

Carbon monoxide modulates cytochrome oxidase activity and oxidative stress in the developing murine brain during isoflurane exposure

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The Effect of Waterpipe Tobacco Smoke Exposure on Learning and Memory Functions in the Rat Model

“…Finally, because the experiments in the current study were carried out in animal models, the clinical implications of these results are yet to be examined using clinical studies. CO exposure is associated with memory impairment (Ryan, 1990; Bastin et al, 2004; Cutajar and Edwards, 2007; Wang et al, 2009), and elevated oxidative stress (Zhang and Piantadosi, 1992; Taskiran et al, 2007; Wang et al, 2009). CO concentrations in waterpipe smoke are substantial and a typical waterpipe use session involves inhalation of many cigarette equivalents of CO (Eissenberg and Shihadeh, 2009; Katurji et al, 2010).…”