Reverse electron flow-induced ROS production is attenuated by activation of mitochondrial Ca2+-sensitive K+ channels

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 293, Issue 3, 2007, Pages

  Heinen, André ^a,d   Aldakkak, Mohammed ^a   Stowe, David F ^a,b,c   Rhodes, Samhita S ^a   Riess, Matthias L ^a   Varadarajan, Srinivasan G ^a   Camara, Amadou K S ^a  

^a MEDICAL COLLEGE OF WISCONSIN   (United States)

^b MARQUETTE UNIVERSITY   (United States)

^c Medical College of Wisconsin and Marquette University   (United States)

^d UNIVERSITY OF AMSTERDAM   (Netherlands)

Author keywords

Mitochondria; Potassium channels; Reactive oxygen species

Indexed keywords

1 (2 HYDROXY 5 TRIFLUOROMETHYLPHENYL) 5 TRIFLUOROMETHYL 2(3H) BENZIMIDAZOLONE; CALCIUM ION; HYDROGEN PEROXIDE; PAXILLINE; POTASSIUM CHANNEL; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE DEHYDROGENASE (UBIQUINONE); ROTENONE; SUCCINIC ACID; SUPEROXIDE;

ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DRUG EFFECT; DRUG INHIBITION; ELECTRON TRANSPORT; GUINEA PIG; MEMBRANE POTENTIAL; MITOCHONDRIAL MEMBRANE; MITOCHONDRIAL RESPIRATION; MITOCHONDRION; NONHUMAN; OXIDATION REDUCTION REACTION; OXYGEN CONSUMPTION; PRIORITY JOURNAL;

ANIMALS; BENZIMIDAZOLES; CELL RESPIRATION; GUINEA PIGS; HYDROGEN PEROXIDE; INDOLES; MEMBRANE POTENTIAL, MITOCHONDRIAL; MITOCHONDRIA, HEART; OXIDATION-REDUCTION; POTASSIUM; POTASSIUM CHANNEL BLOCKERS; POTASSIUM CHANNELS, CALCIUM-ACTIVATED; REACTIVE OXYGEN SPECIES;

EID: 34548397692     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00198.2007     Document Type: Article

References (42)

1. Ballinger SW. Mitochondrial dysfunction in cardiovascular disease. Free Radic Biol Med 38: 1278-1295, 2005.
2. Batandier C, Guigas B, Detaille D, El-Mir MY, Fontaine E, Rigoulet M, Leverve XM. The ROS production induced by a reverse-electron flux at respiratory-chain complex 1 is hampered by metformin. J Bioenerg Biomembr 38: 33-42, 2006.
3. Boveris A, Cadenas E. Mitochondrial production of superoxide anions and its relationship to the antimycin insensitive respiration. FEBS Lett 54: 311-314, 1975.
4. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 72: 248-254, 1976.
5. Brand MD, Buckingham JA, Esteves TC, Green K, Lambert AJ, Miwa S, Murphy MP, Pakay JL, Talbot DA, Echtay KS. Mitochondrial superoxide and aging: uncoupling-protein activity and superoxide production. Biochem Soc Symp 71: 203-213, 2004.
6. Brookes PS, Yoon Y, Robotham JL, Anders MW, Sheu SS. Calcium, ATP, and ROS: a mitochondrial love-hate triangle. Am J Physiol Cell Physiol 287: C817-C833, 2004.
7. Cadenas E, Boveris A. Enhancement of hydrogen peroxide formation by protophores and ionophores in antimycin-supplemented mitochondria. Biochem J 188: 31-37, 1980.
8. Cadenas E, Boveris A, Ragan CI, Stoppani AO. Production of superoxide radicals and hydrogen peroxide by NADH-ubiquinone reductase and ubiquinol-cytochrome c reductase from beef-heart mitochondria. Arch Biochem Biophys 180: 248-257, 1977.
9. + channel activity in isolated heart mitochondria. Cardiovasc Res 73: 720-728, 2007.
10. Chance B, Sies H, Boveris A. Hydroperoxide metabolism in mammalian organs. Physiol Rev 59: 527-605, 1979.
11. Chen Q, Camara AK, Stowe DF, Hoppel CL, Lesnefsky EJ. Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion. Am J Physiol Cell Physiol 292: C137-C147, 2007.
12. Chen Q, Vazquez EJ, Moghaddas S, Hoppel CL, Lesnefsky EJ. Production of reactive oxygen species by mitochondria: central role of complex III. J Biol Chem 278: 36027-36031, 2003.
13. + channel openers NS1619 and NS004 as inhibitors of mitochondrial function in glioma cells. Biochem Pharmacol 65: 1827-1834, 2003.
14. Duchen MR. Mitochondria in health and disease: perspectives on a new mitochondrial biology. Mol Aspects Med 25: 365-451, 2004.
15. + cycle. Biochim Biophys Acta 1606: 23-41, 2003.
16. + influx increases respiration and enhances ROS production while maintaining membrane potential. Am J Physiol Cell Physiol 292: C148-C156, 2007.
17. Kaczorowski GJ, Knaus HG, Leonard RJ, McManus OB, Garcia ML. High-conductance calcium-activated potassium channels; structure, pharmacology, and function. J Bioenerg Biomembr 28: 255-267, 1996.
18. Lambert A, Brand MD. Inhibitors of the quinone-binding site allow rapid superoxide production from mitochondrial NADH:ubiquinone oxidoreductase (complex I). J Biol Chem 279: 39414-39420, 2004.
19. Lesnefsky EJ, Moghaddas S, Tandler B, Kerner J, Hoppel CL. Mitochondrial dysfunction in cardiac disease: ischemia-reperfusion, aging, and heart failure. J Mol Cell Cardiol 33: 1065-1089, 2001.
20. Liu Y, Fiskum G, Schubert D. Generation of reactive oxygen species by the mitochondrial electron transport chain. J Neurochem 80: 780-787, 2002.
21. 2 production in pigeon heart mitochondria. FEBS Lett 18: 261-264, 1971.
22. Lowell BB, Shulman GI. Mitochondrial dysfunction and type 2 diabetes. Science 307: 384-387, 2005.
23. Munujos P, Knaus HG, Kaczorowski GJ, Garcia ML. Cross-linking of charybdotoxin to high-conductance calcium-activated potassium channels: identification of the covalently modified toxin residue. Biochemistry 34: 10771-10776, 1995.
24. o are target proteins of reactive oxygen species. Nature 408: 492-495, 2000.
25. + channels and their role in cardioprotection. Circ Res 94: 420-432, 2004.
26. + channels in cardiac mitochondria. Am J Physiol Heart Circ Physiol 289: H1635-H1642, 2005.
27. ATP channels in preconditioning. J Mol Cell Cardiol 35: 569-575, 2003.
28. + channels by a novel benzimidazolone. Eur J Pharmacol 251: 53-59, 1994.
29. Rego AC, Oliveira CR. Mitochondrial dysfunction and reactive oxygen species in excitotoxicity and apoptosis: implications for the pathogenesis of neurodegenerative diseases. Neurochem Res 28: 1563-1574, 2003.
30. Riess ML, Eells JT, Kevin LG, Camara AKS, Henry MM, Stowe DF. Attenuation of mitochondrial respiration by sevoflurane in isolated cardiac mitochondrial is mediated in part by reactive oxygen species. Anesthesiology 100: 498-505, 2004.
31. Riess ML, Kevin LG, McCormick J, Jiang MT, Rhodes SS, Stowe DF. Anesthetic preconditioning: the role of free radicals in sevoflurane-induced attenuation of mitochondrial electron transport in Guinea pig isolated hearts. Anesth Analg 100: 46-53, 2005.
32. + channels in cardiac myocytes: a mechanism of the cardioprotective effect and modulation by protein kinase A. Circulation 111: 198-203, 2005.
33. + channel opening requires superoxide radical generation. Am J Physiol Heart Circ Physiol 290: H434-H440, 2006.
34. Szewczyk A, Skalska J, Glab M, Kulawiak B, Malinska D, Koszela-Piotrowska I, Kunz WS. Mitochondrial potassium channels: from pharmacology to function. Biochim Biophys Acta 1757: 715-720, 2006.
35. Turrens JF. Mitochondrial formation of reactive oxygen species. J Physiol 552: 335-344, 2003.
36. Turrens JF, Alexandre A, Lehninger AL. Ubisemiquinone is the electron donor for superoxide formation by complex III of heart mitochondria. Arch Biochem Biophys 237: 408-414, 1985.
37. Turrens JF, Boveris A. Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. Biochem J 191: 421-427, 1980.
38. m-dependent and -independent production of reactive oxygen species by rat brain mitochondria. J Neurochem 79: 266-277, 2001.
39. Ca channel cloned from myometrium. Receptors Channels 3: 185-199, 1995.
40. + channels: physiological role and pharmacology. Curr Med Chem 10: 649-661, 2003.
41. + channels in the cardiac inner mitochondrial membrane. Science 298: 1029-1033, 2002.
42. Yoshida T, Maulik N, Engelman RM, Ho YS, Das DK. Targeted disruption of the mouse Sod I gene makes the hearts vulnerable to ischemic reperfusion injury. Circ Res 86: 264-269, 2000.