Lipid Peroxidation was Involved in the Memory Impairment of Carbon Monoxide-induced Delayed Neuron Damage

Wang, Pin; Zeng, Tao; Zhang, Cuili; Gao, Xu-Cong; Liu, Zhen; Xie, Keqin; Chi, Zhen‐Ming

doi:10.1007/s11064-008-9908-1

Cited by 49 publications

(26 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

Tobacco smoking is a global health hazard that kills about 5 million people annually. Waterpipe smoking is among the most popular methods of tobacco consumption world-wide. In this study, we investigated whether waterpipe smoking impairs learning and memory in the hippocampus, a question of special concern due to the particular popularity of waterpipe use among youth. Additionally, possible molecular targets for expected learning and memory impairment were determined. In this study, rats were exposed to waterpipe smoke (WTS) by whole body exposure 1hr × 5 days/wk, for one month, and outcomes were compared to a control group exposed only to fresh air. Outcomes included spatial learning and memory using the Radial Arm Water Maze (RAWM), and oxidative stress biomarkers (catalase, GPx, SOD, GSH, GSSG, GSH/GSSG ratio). We found that WTS exposure led to impaired short- and long-term memory. This impairment was accompanied by reduced hippocampal activity of catalase, SOD, GPx, GSH, and GSH/GSSG, elevated GSSG, thus, marked changes in oxidative stress biomarkers. In conclusion, there is reason for concern that WTS exposure may impair cognitive ability.

show abstract

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The ability of CO to stimulate GSH-linked antioxidant defenses in animal tissues has been previously reported (47,54). In rat blood, Thom's group measured the twofold increase of GSH:GSSG levels after administering CO in vivo in a manner known to cause brain damage and induce oxidative stress biomarker formation (47).…”

Section: Discussionmentioning

confidence: 97%

Carbon Monoxide Signaling in Human Red Blood Cells: Evidence for Pentose Phosphate Pathway Activation and Protein Deglutathionylation

Metere

Iorio

Scorza

et al. 2014

Antioxidants & Redox Signaling

View full text Add to dashboard Cite

Aims: The biochemistry underlying the physiological, adaptive, and toxic effects of carbon monoxide (CO) is linked to its affinity for reduced transition metals. We investigated CO signaling in the vasculature, where hemoglobin (Hb), the CO most important metal-containing carrier is highly concentrated inside red blood cells (RBCs). Results: By combining NMR, MS, and spectrophotometric techniques, we found that CO treatment of whole blood increases the concentration of reduced glutathione (GSH) in RBC cytosol, which is linked to a significant Hb deglutathionylation. In addition, this process (i) does not activate glycolytic metabolism, (ii) boosts the pentose phosphate pathway (PPP), (iii) increases glutathione reductase activity, and (iv) decreases oxidized glutathione concentration. Moreover, GSH concentration was partially decreased in the presence of 2-deoxyglucose and the PPP antagonist dehydroepiandrosterone. Our MS results show for the first time that, besides Cys93, Hb glutathionylation occurs also at Cys112 of the b-chain, providing a new potential GSH source hitherto unknown. Innovation: This work provides new insights on the signaling and antioxidant-boosting properties of CO in human blood, identifying Hb as a major source of GSH release and the PPP as a metabolic mechanism supporting Hb deglutathionylation. Conclusions: CO-dependent GSH increase is a new RBC process linking a redox-inactive molecule, CO, to GSH redox signaling. This mechanism may be involved in the adaptive responses aimed to counteract stress conditions in mammalian tissues. Antioxid. Redox Signal. 20,[403][404][405][406][407][408][409][410][411][412][413][414][415][416]

show abstract

“…Diminution de l'oedème cérébral L'intoxication au CO initie des processus périvasculaires nécessaires à la physiopathologie de l'atteinte neurologique liée au CO, comprenant un stress oxydatif qui déclenche l'activation de la voie du N-méthyl-D-aspartate (NMDA) et la NO synthase neuronale (nNOS) [35]. Une autre étude a montré que le syndrome postintervallaire pourrait être relié à une augmentation de la peroxydation lipidique et la diminution du statut antioxydant au niveau plasmatique, du cortex cérébral et de l'hippocampe [36].…”

Section: Arguments Expérimentauxunclassified

Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare

et al. 2011

View full text Add to dashboard Cite

Le traitement par oxygénothérapie hyperbare (OHB) lors des intoxications au monoxyde de carbone est utilisé depuis plus de 50 ans. Néanmoins, le protocole à appliquer et le sous-groupe de patients pouvant bénéficier de l'OHB restent débattus. La physiopathologie de l'intoxication au monoxyde de carbone est complexe, expliquant la diversité des tableaux cliniques retrouvés neurologiques (troubles de la conscience et syndrome postintervallaire) mais aussi cardiaques (ischémie à coronaires saines notamment). La physiopathologie fait intervenir une hypoxie ané-mique par formation de carboxyhémoglobine mais aussi une hypoxie hypoxique par blocage de la chaîne respiratoire au niveau de la cytochrome oxydase, un stress oxydatif et des lésions d'ischémie-reperfusion. La carboxyhémoglobine (veineuse ou artérielle) n'est pas à prendre en compte pour le traitement ; le dosage de la troponine Ic au moindre doute est souhaitable. Les bases de traitement par l'OHB reposent d'abord sur des arguments physiopathologiques : détoxifica-tion plus rapide des protéines héminiques, effet antioxydant et amélioration de la physiologie cérébrale (diminution de la pression intracrânienne, diminution de l'oedème et préserva-tion de la zone de pénombre). Les autres arguments sont issus des essais thérapeutiques randomisés. Quatre des cinq études randomisées utilisant une OHB avec une pression supérieure à 2 ATA étaient positives. Deux études à 2 ATA étaient négatives. Ainsi, les recommandations européennes et américaines suggèrent l'utilisation d'OHB à 2,5 ATA au moins dans les situations à risque de séquelles neurologiques (tout signe neurologique objectif y compris perte de connaissance), en cas d'atteinte cardiaque ou de grossesse. Il faut insister sur un traitement par oxygénothérapie à fort débit pendant 8-12 heures en cas de non-indication de l'OHB. Pour citer cette revue : Réanimation 20 (2011). Mots clés Oxygénothérapie hyperbare · Intoxication au monoxyde de carboneAbstract Hyperbaric oxygen (HBO) is used since more than 50 years for carbon monoxide poisoning. However, HBO protocols and indications are still debated. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms. Carboxyhemoglobin formation, cytochrome oxydase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon are among these mechanisms. Venous and arterial carboxyhemoglobin levels are not correlated with the patient's final prognosis and thus not mandatory for indicating the treatment. Conversely, troponin IC measurement is strongly recommended if myocardial involvement is suspected. HBO treatment relies on mechanistic bases: earlier detoxification, anti-oxidant properties, and improvement in cerebral physiology (decrease in intracranial pressure and oedema, and ischemic penumbra preservation). Clinical basis is assessed by the results of the randomized clinical trials (RCTs). Four among the 5 RCTs using > 2 ATA OHB protocols were p...

show abstract

Lipid Peroxidation was Involved in the Memory Impairment of Carbon Monoxide-induced Delayed Neuron Damage

Cited by 49 publications

References 30 publications

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

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

Carbon Monoxide Signaling in Human Red Blood Cells: Evidence for Pentose Phosphate Pathway Activation and Protein Deglutathionylation

Intoxication au monoxyde de carbone et place de l’oxygénothérapie hyperbare

Contact Info

Product

Resources

About