Age-related features of activity of free radical oxidation in erythrocyte membranes and blood plasma in postinfarction cardiosclerosis in rats

Abstract

Aim. To determine the presence of lipid and protein peroxidation products in erythrocyte membranes and blood plasma in rats of different ages in an intact state and with developed postinfarction cardiosclerosis.

Methods. In rats aged 4, 12, 24 months postinfarction cardiosclerosis was modeled by coronary occlusion. In blood plasma and erythrocyte membranes, products reacting with thiobarbituric acid and carbonyl derivatives of protein amino acid residues were determined.

Results. In erythrocyte membranes of intact animals aged 12 months, a decrease of the content of thiobarbituric acid-reacting products was revealed in comparison with 4 month-old animals, and in 24 months-old animals the index significantly exceeded the values of young subjects. In the blood plasma of intact animals aged 12 and 24 months, an increased content of thiobarbituric acid-reacting products with respect to rats aged 4 months was revealed. In postinfarction cardiosclerosis, an increase in the accumulation of thiobarbituric acid-reacting products was observed in erythrocyte membranes of 4 and 24 months-old animals. In blood plasma, an increase of this parameter was noted only in the group of 4 months-old animals with postinfarction cardiosclerosis. In erythrocyte membranes of intact rats of all age groups, no differences in the level of carbonyl derivatives of protein amino acid residues were observed, and in blood plasma it significantly increased with age. In 4 and 12 months-old animals with postinfarction cardiosclerosis, significant increase of carbonyl derivatives of protein amino acid residues was mostly pronounced in erythrocyte membranes. In 24 months-old animals with postinfarction cardiosclerosis, this parameter in the membranes and blood plasma was stable.

Conclusion. The intensity of processes of cell membrane and blood lipid peroxidation has pronounced age-dependent features that persist in postinfarction cardiosclerosis; proteins of erythrocyte membranes of intact animals are subject to peroxide modification to a lesser degree than blood plasma proteins; in postinfarction cardiosclerosis formation in 4 and 12 months-old animals, carbonyl derivatives of protein amino acid residues are more intensively accumulated in erythrocyte membranes compared to blood plasma.

Keywords

lipid peroxidation / carbonyl derivatives of proteins / erythrocyte membranes / postinfarction cardiosclerosis

References

[1] Anisimov V.N. Molekulyarnye i fiziologicheskie mekhanizmy stareniya. (Molecular and physiological mechanisms of aging.) Saint Petersburg: Nauka. 2003; 468 р. (In Russ.)

[2] Анисимов В.Н. Молекулярные и физиологические механизмы старения. СПб.: Наука. 2003; 468 с.

[3] Dubinina E.E. Produkty metabolizma kisloroda v funktsional’noy aktivnosti kletok (zhizn’ i smert’, sozidanie i razrushenie). Fiziologicheskie i kliniko-biokhimicheskie aspekty. (Products of oxygen metabolism in the functional activity of cells (life and death, creation and destruction). Physiological and clinical-biochemical aspects.) Saint Petersburg: Meditsinskaya Pressa. 2006; 400 р. (In Russ.)

[4] Дубинина Е.Е. Продукты метаболизма кислорода в функциональной активности клеток (жизнь и смерть, созидание и разрушение). Физиологические и клинико-биохимические аспекты. СПб.: Медицинская пресса. 2006; 400 с.

[5] Valko M., Leibfritz D., Moncol J. et al. Free radicals and antioxidants in normal physiological functions and human disease. Intern. J. Biochem. Cell Biol. 2007; 39: 44–84. DOI: 10.1016/j.biocel.2006.07.001.

[6] Valko M., Leibfritz D., Moncol J. et al. Free radicals and antioxidants in normal physiological functions and human disease. Intern. J. Biochem. Cell Biol. 2007; 39: 44-84. DOI: 10.1016/j.biocel.2006.07.001.

[7] Mirsa M.K., Sarwat M., Bhakuni P. et al. Oxidative stress and ischemic myocardial syndromes. Med. Sci. Monitor. 2009; 15: 209–219. PMID: 19789524.

[8] Mirsa M.K., Sarwat M., Bhakuni P. et al. Oxidative stress and ischemic myocardial syndromes. Med. Sci. Monitor. 2009; 15: 209-219. PMID: 19789524.

[9] Rebrova T.Yu., Kondrat’eva D.S., Afanas’ev S.A. et al. Activity of lipid peroxidation and functional state of the myocardium in remodeling of rat heart after experimental myocardial infarction. Kardiologiia. 2007; 6: 41–45. (In Russ.)

[10] Реброва Т.Ю., Кондратьева Д.С., Афанасьев С.А. и др. Активность перекисного окисления липидов и функциональное состояние миокарда при ремоделировании сердца крыс после экспериментального инфаркта. Кардиология. 2007; 6: 41-45.

[11] Rebrova T.Yu., Afanas’ev S.A., Medvedeva O.D. et al. Age-related features of microviscosity of erythrocyte membranes in experimental cardiosclerosis. Uspekhi gerontologii. 2012; 25 (4): 644–647. (In Russ.)

[12] Реброва Т.Ю., Афанасьев С.А., Медведева О.Д. и др. Возраст-зависимые особенности микровязкости мембран эритроцитов при экспериментальном кардиосклерозе. Успехи геронтол. 2012; 25 (4): 644-647.

[13] Levine R.L., Garlana D., Oliver C.N. et al. Determination of carbonyl content in oxidatively modified proteins. Methods in Enzymol. 1990; 186: 464–478. DOI: 10.1016/0076-6879(90)86141-H.

[14] Levine R.L., Garlana D., Oliver C.N. et al. Determination of carbonyl content in oxidatively modified proteins. Methods in Enzymol. 1990; 186: 464-478. DOI: 10.1016/0076-6879(90)86141-H.

[15] Оnishi S.T., Barr J.K. A simplified method of quantitating protein using the biuret and phenol reagents. Annal. Biochem. 1978; 86 (1): 193–200. DOI: 10.1016/0003-2697(78)90334-2.

[16] Оnishi S.T., Barr J.K. A simplified method of quantitating protein using the biuret and phenol reagents. Annal. Biochem. 1978; 86 (1): 193-200. DOI: 10.1016/0003-2697(78)90334-2.

[17] Dubinina E.E., Pustygina A.V. Free radical processes in aging, neurodegenerative diseases and other pathological states. Biomeditsinskaya khimiya. 2007; 53: 351–372. (In Russ.)

[18] Дубинина Е.Е., Пустыгина А.В. Cвободнорадикальные процессы при старении, нейродегенеративных заболеваниях и других патологических состояниях. Биомед. химия. 2007; 53: 351-372.

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Rebrova T.Y., Afanas’ev S.A.