کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738657 | 1046721 | 2011 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A carbon monoxide-releasing molecule (CORM-3) uncouples mitochondrial respiration and modulates the production of reactive oxygen species
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کلمات کلیدی
carbonyl cyanide p-trifluoromethoxyphenyl hydrazoneCO-RMCarboxyatractylosideNQRHRPANTFCCPCORM-3CATRCO-releasing molecule6-Ketocholestanol - 6-کاتوکلستانولBSA - BSAbovine serum albumin - آلبومین سرم گاوGDP - تولید ناخالص ملیadenine nucleotide transporter - حمل کننده نوکلئوتیدی آدنelectron transport chain - زنجیره انتقال الکترونETc - و غیرهMitochondrial membrane potential - پتانسیل غشای میتوکندریHorseradish peroxidase - پراکسیداز هوررادیشguanosine 5′-diphosphate - گوانوزین 5'-دی فسفات
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Carbon monoxide (CO), produced during the degradation of heme by the enzyme heme oxygenase, is an important signaling mediator in mammalian cells. Here we show that precise delivery of CO to isolated heart mitochondria using a water-soluble CO-releasing molecule (CORM-3) uncouples respiration. Addition of low-micromolar concentrations of CORM-3 (1-20 μM), but not an inactive compound that does not release CO, significantly increased mitochondrial oxygen consumption rate (State 2 respiration) in a concentration-dependent manner. In contrast, higher concentrations of CORM-3 (100 μM) suppressed ADP-dependent respiration through inhibition of cytochrome c oxidase. The uncoupling effect mediated by CORM-3 was inhibited in the presence of the CO scavenger myoglobin. Moreover, this effect was associated with a gradual decrease in membrane potential (Ï) over time and was partially reversed by malonate, an inhibitor of complex II activity. Similarly, inhibition of uncoupling proteins or blockade of adenine nucleotide transporter attenuated the effect of CORM-3 on both State 2 respiration and ÎÏ. Hydrogen peroxide (H2O2) produced by mitochondria respiring from complex I-linked substrates (pyruvate/malate) was increased by CORM-3. However, respiration initiated via complex II using succinate resulted in a fivefold increase in H2O2 production and this effect was significantly inhibited by CORM-3. These findings disclose a counterintuitive action of CORM-3 suggesting that CO at low levels acts as an important regulator of mitochondrial respiration.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 50, Issue 11, 1 June 2011, Pages 1556-1564
Journal: Free Radical Biology and Medicine - Volume 50, Issue 11, 1 June 2011, Pages 1556-1564
نویسندگان
Luisa Lo Iacono, Jorge Boczkowski, Roland Zini, Issam Salouage, Alain Berdeaux, Roberto Motterlini, Didier Morin,