Age changes of antyoxidant system and free-radical processes in rats at formation of postinfarction cardiosclerosis


Estimation of age dependent changes of the lipid peroxidation (LPO) intensity, content of stable metabolites of nitrogen oxides (NO) and antioxidant enzyme activities in rat blood serum in conditions of experimental postinfarction cardiosclerosis (PICS) is carried out. Initiation of the postinfarction remodeling of animals has been carried out with coronary occlusion, definition of LPO and NO metabolites indices has been performed after 45 days. Investigations have been carried out on 40 four and twelve-month-old male Wistar rats with mass 200-250 gand 400 -450 g, accordingly. Statistical analysis of the results was performed using the Mann-Whitney-Wilcoxone criterion. It has been found that already intact animals have age specificity of indices under consideration. The expressed activity of LPO processes on the background of reduction of endogenous fermentative antioxidant (SOD and catalase) activity as well as nitrite concentration in blood serum is characteristic for PICS of 4-month-old animals. PICS of 12 month-old rats is accompanied with suppression of the LPO processes on the back- ground of reduction of the antioxidant enzyme intensity and increase of NO metabolites production. The following conclusions have been drawn. Process of ontogenesis is characterized by imbalance between pro-and antioxidant processes in rat blood. Increase in catalase activity and concentration of the TBC-active products at simultaneous decrease of SOD activity and content of diene conjugates has been noted. The organism of young animals responds with persistent increase of LPO processes and decrease of SOD and catalase activity on formation of postinfartion cardioslerosis. The less expressed increase of lipid peroxidation activation and decrease of catalase activity has been noted in the organism of old animals within 45 day after PICS formation.

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Rebrova, T. , Afanasiev, S. , Putrova, O. , Batalov, R. and Popov, S. (2013) Age changes of antyoxidant system and free-radical processes in rats at formation of postinfarction cardiosclerosis. Advances in Aging Research, 2, 51-56. doi: 10.4236/aar.2013.21007.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] Vladimirov, Yu.A. (2000) Free radicals in biological systems. Soros Educational Journal, 12, 13-19.
[2] Chen, Q., Moghaddas, S., Hoppel, C.L., et al. (2008) Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria. American Journal of Physiology, 294, 460-466. HUdoi:10.1152/ajpcell.00211.2007U
[3] Cave, A.C., Brewer, A.C., Narayanapanicker, A., et al. (2006) NADPH oxidases in cardiovascular health and di sease. Antioxidants & Redox Signaling, 8, 691-728. HUdoi:10.1089/ars.2006.8.691U
[4] Sato, E., Mokudai, T., Niwano, Y., et al. (2011) Kinetic analysis of reactive oxygen species generated by the in vitro reconstituted NADPH oxidase and xanthine oxidase systems. The Journal of Biochemistry, 150, 173-181. HUdoi:10.1093/jb/mvr051U
[5] Dr?ge, W. (2002) Free radicals in the physiological control of cell function. Physiological Reviews, 82, 47-95.
[6] Valko, M., Leibfritz, D., Moncol, J., et al. (2007) Free radicals and antioxidants in normal physiological functions and human disease. The International Journal of Bio chemistry & Cell Biology, 39, 44-84. HUdoi:10.1016/j.biocel.2006.07.001U
[7] Karageuzyan, K.G. (2005) Oxidative stress in the mole cular mechanism of pathogenesis at different diseased states of organism in clinics and experiment. Current Drug Targets—Inflammation & Allergy, 4, 85-98. HUdoi:10.2174/1568010053622939U
[8] Prabhakar, N.R. (2011) Sensory plasticity of the carotid body: Role of reactive oxygen species and physiological significance. Respiratory Physiology & Neurobiology, 178, 375-380. HUdoi:10.1016/j.resp.2011.05.012U
[9] Anisimov, V.N. (2008) Molecular and physiological mechanisms of aging. Publishing House Nauka, St. Petersburg.
[10] Spiteller, G. (2007) The important role of lipid peroxi dation processes in aging and age dependent diseases. Molecular Biotechnology, 37, 5-12. HUdoi:10.1007/s12033-007-0057-6U
[11] Mirsa, M.K., Sarwat, M., Bhakuni, P., et al. (2009) Oxida tive stress and ischemic myocardial syndromes. Medical Science Monitor, 15, 209-219.
[12] Lankin, V.Z., Tikhaze, A.K. and Belenkov, Yu.N. (2000) Free radical processes in diseases of the cardiovascular system. Kardiologiya, 7, 48-61.
[13] Gomez, A.M., Guatimosim, S., Dilly, K.W., et al. (2001) Heart failure after myocardial infarction: Altered excita tion-contraction coupling. Circulation, 104, 688-693. HUdoi:10.1161/hc3201.092285U
[14] Rebrova, T.Yu., Kondratieva, D.S. and Afanasiev, S.A. (2007) Activity of lipid peroxidatin and functional state of the myocardium in remodeling of rat heart after experimental myocardial infarction. Kardiologiya, 6, 41-45.
[15] Schultz, J.E.J., Hsu, A.K., Nagase, H., et al. (1998) TAN 67, a δ1-opioid receptor agonist, reduces infarct size via activation of Gi/o proteins and KATP channels. American Journal of Physiology, 274, H909-H914.
[16] Korobeinikova, E.N. (1989) Modification of the definition of lipid peroxidation products in the reaction with thiobarbituric acid. Laboratory Work, 7, 8-10.
[17] Bolland, J.L. and Koch, H.P. (1945) The course of antioxidant reaction in polyisoprenes and allied compounds. Part IX. The primary thermal oxidation product of ethyl linoleate. Journal of the Chemical Society, 7, 445. HUdoi:10.1039/jr9450000445U
[18] Karalyuk, M.A., Ivanov, L.I., Mayorov, I.G., et al. (1988) The method for determining the activity of catalase. Laboratory Work, 1, 16-19.
[19] Brusov, O.S., Gerasimov, А.М. and Panchenko, L.F. (1976) The influence of natural inhibitirs of free radical reaction on epinephrine autooxidation. Bulletin of Experimental Biology and Medicine, 1, 33-34.
[20] Slezak, J., Tribulova, N., Ravingerova T., et al. (1992) Myo cardial heterogeneity and regional variations in response to injury. Laboratory Investigation, 67, 322-330.
[21] Barja, G. (1999) Mitochondrial oxygen radical generation and leak: Sites of production in states 4 and 3, organ spe cificity, and relation to aging and longevity. Journal of Bioenergetics and Biomembranes, 31, 347-366. HUdoi:10.1023/A:1005427919188U
[22] Sohal, R.S. and Weindrich, R. (1996) Oxidative stress, caloric restriction and aging. Science, 273, 59-63. HUdoi:10.1126/science.273.5271.59U
[23] Voskresenskii, O.N., Zhutaev, I.A., Bobyrev, V.N., et al. (1982) Antioxidant system ontogenesis and aging. Problems of Medical Khimii, 1, 14-27.
[24] Halliwell, B. (2000) Lipid peroxidation, antioxidants and cardiovascular disease: How should we move forward? Cardiovascular Research, 47, 410-418. HUdoi:10.1016/S0008-6363(00)00097-3U
[25] Lankin, V.Z., Vandyshev, D.B. and Tikhaze, A.K. (1981) Effect of hyperoxia on superoxide dismutase and glutathione peroxidase in the tissues of mice. Doklady of the Academy of Sciences of the USSR, 259, 229-231.
[26] Kogan, A.Kh., Kudrin, A.Kh., Kaktursky, L.V., et al. (1992) Peroxide free radical mechanisms of the pathogenesis of myocardial ischemia and enzyme regulation. Patophysiology, 2, 5-15.
[27] Gudz, T.I., Peshkova, E.G. and Goncharenko, E.N. (1982) Inhibition of superoxide dismutase activity by linolenic acid hydroperoxide. Radiobiology, 22, 674-677.
[28] Lundberg, J.O. and Weitzberg, E. (2005) NO generation from nitrite and its role in vascular control. Arteriosclerosis, Thrombosis, and Vascular Biology, 25, 915-922. HUdoi:10.1161/01.ATV.0000161048.72004.c2U
[29] Gutierrez, J., Ballinger, S.W., Darley-Usmar, V.M., et al. (2006) Free radicals, mitochondria, and oxidized lipids: The emerging role in signal transduction in vascular cells. Circulation Research, 99, 924-932. HUdoi:10.1161/01.RES.0000248212.86638.e9U
[30] Beltrán, B., Mathur, A., Duchen, M.R., et al. (2000) The effect of nitric oxide on cell respiration: A key to understanding its role in cell survival or death. Proceedings of the National Academy of Sciences of the United States of America, 97, 14602-14607. HUdoi:10.1073/pnas.97.26.14602U
[31] Zweier, J.L., Fertmann, J. and Wei, G. (2001) Nitric oxide and peroxynitrite in postischemic myocardium. Antioxidants & Redox Signaling, 3, 11-22. HUdoi:10.1089/152308601750100443U
[32] O’Donnel, V.B. and Freeman, B.A. (2001) Interactions between nitric oxide and lipid oxidation pathways: Implications for vascular disease. Circulation Research, 88, 12-21. HUdoi:10.1161/01.RES.88.1.12U
[33] Yang, B.C. and Mehta, J.L. (1997) Inhibition of nitric oxide does not affect reperfusion-induced myocardial injury, but it prevents lipid peroxidation in the isolated rat heart. Life Sciences, 61, 229-236. HUdoi:10.1016/S0024-3205(97)00378-0U
[34] Brown, G.C. (1995) Reversible binding and inhibition of catalase by nitric oxide. European Journal of Biochemistry, 232, 188-191. HUdoi:10.1111/j.1432-1033.1995.tb20798.xU
[35] Rebrova, T.Yu., Maslov, L.N., Lishmanov, A.Yu. and Tam, S.V. (2001) Stimulation of μ and δ-opite receptors and tolerance of isolate heart to oxidative stress: The role of NO-syntase. Biochemistry (Moscow), 66, 422-428. HUdoi:10.1023/A:1010253530026U

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