Corrigendum to “Quantification of chloride channel 2 (CLCN2) gene isoforms in normal versus lesion- and epilepsy-associated brain tissue” [Biochim. Biophys. Acta 1772 (2007) 15–20

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• 作者：Matteo Bertelli ; Stefano Cecchin ; Cristina Lapucci ; Paola de Gemmis ; Daniela Danieli ; Emanuele S.G. d'Amore ; Luciano Buttolo ; Filippo Giunta ; Pietro Mortini ; Massimo P ; olfo
• 关键词：Cytochrome oxidase ; Carbon monoxide ; Heart ; Inhibition
• 刊名：Biochimica et Biophysica Acta (BBA)/Molecular Basis of Disease
• 出版年：2007
• 出版时间：September 2007
• 年：2007
• 卷：1772
• 期：9
• 页码：1117
• 全文大小：70 K

文摘

Carbon monoxide (CO) inhalation often leads to cardiac dysfunction, dysrhythmias, ischemia, infarction, and death. However, the underlying mechanism of CO toxicity is poorly understood. We hypothesize that inhaled CO interrupts myocardial oxidative phosphorylation by decreasing the activity of myocardial cytochrome oxidase (CcOX), the terminal oxidase of the electron transport chain. Male C57Bl6 mice were exposed to either 1000 ppm (0.1 % ) CO or air for 3 h. Cardiac ventricles were harvested and mitochondria were isolated. CcOX kinetics and heme aa₃ content were measured. V_max, K_m, and turnover number were determined. Levels of CcOX subunit I message and protein were evaluated. Carboxyhemoglobin (COHb) levels were measured and tissue hypoxia was assessed with immunohistochemistry for pimonidazole hydrochloride. CO significantly decreased myocardial CcOX activity and V_max without altering K_m. Heme aa₃ content and CcOX I protein levels significantly decreased following CO exposure while enzyme turnover number and CcOX I mRNA levels remained unchanged. CO exposure increased COHb levels without evidence of tissue hypoxia as compared to sham and hypoxic controls. Decreased CcOX activity following CO inhalation was likely due to decreased heme aa₃ and CcOX subunit I content. Importantly, myocardial CcOX impairment could underlie CO induced cardiac dysfunction.