“Double Edge” Effects of Nitric Oxide Free Radical in Cardio-Brain-Vascular Diseases and Health Studied by ESR

doi:10.11938/cjmr20150205

Abstract

Abstract:

Nitric oxide (NO) is a simple gas with free radical properties. It appears as a major signaling molecule in cardiovascular, immune and nervous systems. NO is generated by three isoforms of NO synthase, endothelial NO synthase (eNOS), neuronal NO synthase (nNOS) and inducible NO synthase (iNOS) in different cells. It is known that NO is an important physiological molecule in the regulation of blood pressure, vascular tone, however, excessive NO produced by iNOS results in inhibition of cardiac contractility, impairment of mitochondrial respiration and apoptosis. NO has been shown to influence neurotransmitter release and synaptogenetic processes, modulate the synaptic plasticity, indicating that NO plays an important role in the development, maintenance and regulation of brain circuits, as signaling molecule in mammary and learning. Increasing evidences indicate that excessive NO may damage cardiovascular and neurons and even cause cardiovascular and neurodegenerative diseases. We review the results about the “double edge” effects of NO in cardio-brain-vascular health and diseases and the protective effects of antioxidants in recent years studied by ESR.

Key words: Nitric oxide (NO), free radical, cardio-brain-vascular health and diseases, natural antioxidants

CLC Number:

O482.53

ZHAO Bao-lu. “Double Edge” Effects of Nitric Oxide Free Radical in Cardio-Brain-Vascular Diseases and Health Studied by ESR[J]. Chinese Journal of Magnetic Resonance, 2015, 32(2): 195-207.

References

[1] Ferrari R, Guardigli G, Mele D, et al. Oxidative stress during myocardial ischaemia and heart failure[J]. Curr Pharm Des, 2004, 10: 1 699－1 711.

[2] Zweier J L, Flaherty J T, Weisfeldt M L. Direct measurement of free radical generation following reperfusion of ischemic myocardium[J]. Proc Natl Acad Sci USA, 1987, 84: 1 404－1 407.

[3] Zweier J L, Kuppusamy P, Williams R, et al. Measurement and characterization of postischemic free radical generation in the isolated perfused heart[J]. J Biol Chem, 1989, 261: 18 890－18 895.

[4] Zhao B L, Shen J G, Li M, et al. Synergic effects of NO and oxygen free radicals in ischemia-reperfusion rabbit myocardium[J]. Sci China, 1996, 26: 331－338.

[5] Zhao B L, Xin W J, Yang W D, et al. Direct measurement of active oxygen free radicals from ischemia-reperfusion rabbit myocardium[J]. Chin Sci Bull, 1989, 34: 780－787.

[6] Cheng S, Zhao B L, Xin W J, et al. Myocadium damage during ischemia-reperfusion of rat heart[J]. Chin Circ, 1990, 5: 222－226.

[7] Huang N, Chen Y, Zhao B L, et al. Studies on free radicals generated during ischemia-reperfusion of rat heat[J]. J Chin Med, 1990, 70: 691－694.

[8] Zweier J L, Rayburn B K, Flaherty J T, et al. The effect of superoxide dismutatase on free radical concentration in post ischemic myocardium[J]. Circulation, 1986, 74: 371－380.

[9] Sanders S P, Zweier J L, Kuppusamy P, et al. Hyperoxic sheep pulmonary microvascular endothelial cells generate free radicals via mitochondrial electron transport[J]. J Clin Invest, 1993, 91: 46－52.

[10] Zweier J L, Kuppusamy P. In vivo EPR spectroscopy of free radicals in the heart[J]. Environ Health Persp, 1994, 102(Suppl 10): 45－51.

[11] Kuppusamy P, Chzhan M, Vij K, et al. Three-dimensional spectral-spatial EPR imaging of free radicals in the heart: a technique for imaging tissue metabolism and oxygenation[J]. Proc Natl Acad Sci USA, 1994, 91: 3 388－3 392.

[12] Zhao B L, Shen J G, Li M, et al. Scavenging effect of Chinonin on NO and oxygen free radicals generated from ischemia reperfusion myocadium[J]. Biachem Biophys Acta, 1996, 1 317: 131－137.

[13] Afanas'ev I B. On mechanism of superoxide signaling under physiological and pathophysiological conditions[J]. Med Hypotheses, 2005, 64: 127－129.

[14] Linnane A W, Kios M, Vitetta L. The essential requirement for superoxide radical and nitric oxide formation for normal physiological function and healthy aging[J]. Mitochondrion, 2007, 7: 1－5.

[15] Zhao B L, Jiang W, Zhao Y, et al. Scavenging effect of salvia miltiorriza on free radicals and its protection for myocardial mitochondrial membrane from ischemia-reperfusion injury[J]. Biochem Mol Biol Intern, 1996, 38: 1 171－1 182.

[16] Shen J G, Wang J, Zhao B L, et al. Effects of EGb-761 on nitric oxide, oxygen free radicals, myocardial damage and arrhythmias in ischemia-reperfusion injury in vivo[J]. Biochim Biophys Acta, 1998, 1406: 228－236.

[17] Zou X L, Wan Q, Li M F, et al. Scavenging effect of green tea polyphenols on oxygen free radicals generated from ischemia-reperfused myocardium[J]. Chinese J Magn Reson, 1995, 12(3): 237－244.

[18] Shen J G, Guo X S, Jiang B, et al. Chinonin, a novel drug against cardiomyocyte apoptosis induced by hypoxia and reoxygenation[J]. Biochim Biophys Acta, 2000, 1500: 217－226.

[19] Shen J G, Li M, Xin W J, et al. Effects of Chinonin on nitric oxide free radical, myocardial damage and arrhythmia in ischemia-reperfusion injury in vivo[J]. Appl Magn Reson, 2000, 19: 9－19.

[20] Zhao B L, Zhou W A, Ni Y C, et al. Kinetic scavenging effects of chinonin on NO and oxygen free radicals generated from ischemia reperfusion myocardium and its protection effects on the myocardium[J]. Res Chem Intermed, 2000, 26: 747－762.

[21] Zhao B L, Shen J G, Li M, et al. Study on NO free radicals generated from ischemia-reperfused heart and macrophage[J]. Chinese J Magn Reson, 1997, 14(1): 99－106.

[22] Zhao B L, Shen J G, Tang C, et al. Analysis of EPR spectrum about NO free radicals trapped by DETCFe2+[J]. Chinese J Magn Reson, 1998, 15(3): 307－311.

[23] Zhang D L, Xiong J, Hu J, et al. Improved method to detect nitric oxide in biological syste[J]. Appl Magn Reson, 2001, 20: 345－358.

[24] Zhou G Y, Zhao B L, Hou J W, et al. Detection of nitric oxide in tissue by spin trapping EPR spectropy and triacetylglycerol extraction[J]. Biotech Tech, 1999, 13: 507－511.

[25] Tredici P D. Ginkgos and people — A thousand years of interactions[J]. Arnoldia, 1991, 51: 2－15.

[26] Tosaki A, Droy-Lefaix M T, Pali T, et al. Effects of SOD, catalase, and a novel antiarrhythmic drug, EGB 761, on reperfusion- induced arrhythmias in isolated rat hearts[J]. Free Radic Biol Med, 1993, 14: 361－370.

[27] Haramaki N, Aggarwal S, Kawabata T, et al. Effects of natural antioxidant ginkgo biloba extract (EGB 761) on myocardial ischemia-reperfusion injury[J]. Free Radic Biol Med, 1994, 16: 789－794.

[28] Shen J G, Zhao B L, Li M F, et al. Inhibitory effects of Ginkgo biloba extract (EGB761) on oxygen free radicals, nitric oxide and myocardial injury in isolated ischemic-reperfusion hearts//Proceedings of the International Symposium on

Natural Antioxidants Molecular Mechanisms and Health Effects. Packer L, Traber M G, Xin W, et al. Eds.[C]. Champaign, Illinois: AOCS Press, 1996.

[29] DeFeudis F V. Ginkgo biloba extract (EGb 761): pharmacological activities and clinical application[M]. Elsevier Paris: Amsterdam, 1991.

[30] Varga E, Bodi A, Ferdinandy P, et al. The protective effect of EGb 761 in isolated ischemic/reperfused rat hearts: a link between cardiac function and nitric oxide production[J]. J Cardiovasc Pharm, 1999, 34: 711－717.

[31] Kusmic C, Basta G, Lazzerini G, et al. The effect of Ginkgo biloba in isolated ischemic/reperfused rat heart: a link between vitamin E preservation and prostaglandin biosynthesis[J]. J Cardiovasc Pharm, 2004, 44: 356－362.

[32] Furchgott R, Zawadzki J V. The obligatory role of the endothelium in the relaxation of arterial smooth muscle by acetycholine[J]. Nature, 1980, 288: 373－376.

[33] Zhao B L, Shen J G, Li M, et al. In: Chinonin Can Scavenging No Free Radicals and Protect the Myocardium Against Ischemia-Reperfusion Injury//Proceedings of the International Symposium on Natural Antioxidants Molecular Mechanisms and Health Effects. Packer L, Ttaber M G, Xin W. Eds.[C]. Champaign, Illinois: AOCS Press, 1996.

[34] Zhang D L, Zhao B L. Oral administration of Crataegus extraction protects against ischemia/reperfusion brain damage in the Mongolian gerbils[J]. J Neur Chem, 2004, 90: 211－219.

[35] Zhao Y, Zhao B L. The neuroprotective effect of L-theanine and its inhibition on nicotine dependence[J]. Chinese Sci Bull, 2014, 59: 4 014－4 019.

[36] Di X, Yan J, Zhao Y, et al. L-theanine protect the APP (Swedish mutation) transgenic SH-SY5Y cell against glutamate-induced excitotoxicity via inhibition of the NMDA receptor pathway[J]. Neuroscience, 2010, 168(3): 778－786.

[37] Wu Z F, Zhu Y S, Cao X S, et al. Mitochondrial toxic effects of Aβ through mitofusins in the early pathogenesis of alzheimer’s disease[J]. Mol Neurobiol, 2014, 50: 986－996.

[38] Siamwala J H, Dias P M, Majumder S, et al. L-theanine promotes nitric oxide production in endothelial cells through eNOS phosphorylation[J]. J Nutr Biochem, 2013, 24(3): 595－605.

[39] Hollenberg N K, Schmitz H, Macdonald I, et al. Cocoa, flavanols and cardiovascular risk[J]. Br J Cardiol, 2004, 11(5): 379－386.

[40] Taubert D, Roesen R, Lehmann C, et al. Effects of Low Habitual Cocoa Intake on Blood Pressure and Bioactive Nitric Oxide[J]. A Randomized Controlled Trial JAMA, 2007, 298(1): 49－60.

[41] Zhao B L. No free radical,natural antioxidant and cardio-brain-vascular health//The Second International Chinese Symposium on Free Radical Research[C]. Hong Kong: 2014. 38.