Effect of hypoxia tolerance on the relation between indicators of free radical oxidation of lipides and proteins in murine kidneys during the post-resuscitation period

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Aim. Study of the relationship between the parameters of free radical oxidation of proteins and lipids in the murine kidneys in the post-resuscitation period after stopping the systemic circulation, depending on their resistance to hypoxia. Methods. The systemic circulation was stopped by intra-thoracic clamping of the neurovascular bundle for 5 minutes, performed under general ether anesthesia in male noninbred white rats, divided after testing into two groups based on resistance to hypoxia. The observation period lasted for 35 days. In the homogenates of kidney tissues, the content of products reactive to tiobarbituric acid, carbonylated proteins, the formation of metal-catalyzed carbonylated proteins and bitirozin were determined. Results. The characteristic manifestation of oxidative stress in the recovery period after stopping blood circulation and resuscitation was found to be reciprocity of the relationship between the levels of lipoperoxidation and oxidative modification of proteins. Highly resistant to hypoxia animals were characterized by high resistance of proteins of kidney tissue to free radical oxidation against the background of high levels of lipid peroxidation. On the contrary, in animals non-resistant to hypoxia, against the background of relatively low values of lipoperoxidation, high levels of oxidative modification of proteins, both initial and induced, were recorded. Conclusion. In post-resuscitation period in highly resistant to hypoxia animals, marked activation of lipoperoxidation occurs accompanied by a transient increase in the carbonylation of proteins in the early observation period; for low-resistant to hypoxia animals high intensity of carbonyl stress against the background of the relative «preservation» of lipid structures of the cell is characteristic, which persists throughout the post-resuscitation period, which can make a significant contribution to kidney damage, increasing the risk of renal failure.

G A Bayburina

Bashkir State Medical University Ufa, Russia

E A Nurgaleeva

Bashkir State Medical University Ufa, Russia

E F Agletdinov

Bashkir State Medical University Ufa, Russia

A F Samigullina

Bashkir State Medical University Ufa, Russia

  • Curtis J.M., Hahn W.S., Long E.K. et al. Protein carbonylation and metabolic control systems. Trends Endocrinol. Metab. 2012; 23 (8): 399-406. doi: 10.1016/j.tem.2012.05.008.
  • Губский Ю.И., Беленичев И.Ф., Левицкий Е.Л. и др. Токсикологические последствия окислительной модификации белков при различных патологических состояниях. Совр. пробл. токсикол. 2005; 3: 20-26.
  • Лукьянова Л.Д. Сигнальная функция митохондрий при гипоксии и адаптации. Патогенез. 2008; 6 (3): 4-12.
  • Грек O.P., Ефремов А.В., Шарапов В.И. Гипобарическая гипоксия и метаболизм ксенобиотиков. М.: ГЭОТАР-Медиа. 2007; 120 с.
  • Lash L.H., Cummings B.S. Mechanisms of toxicant-induced acute kidney injury. Comprehensive toxicology - renal toxicology. Oxford: Elsevier. 2010; 81-116.
  • Sabbahy E.M., Vaidya V.S. Ischemic kidney injury and mechanisms of tissue repair. Wiley Interdiscip. Rev. Syst. Biol. Med. 2011; 3 (5): 606-618. doi: 10.1002/wsbm.133.
  • Rodriguez F., Bonacasa B., Fenoy F.J., Salom M.G. Reactive oxygen and nitrogen species in the renal ischemia/reperfusion injury. Curr. Pharm. Des. 2013; 19 (15): 2776-2794.
  • Байбурина Г.А., Нургалеева Е.А., Шибкова Д.З. и др. Способ определения степени устойчивости к гипобарической гипоксии мелких лабораторных животных. Патент на изобретение РФ №2563059. Бюлл. №26 от 20.09.2015.
  • Корпачёв В.Г., Лысенков С.П., Телль Л.З. Моделирование клинической смерти и постреанимационной болезни у крыс. Патол. физиол. и эксперим. терап. 1982; 3: 78-80.
  • 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; 397 с.
  • Арутюнян А.В., Дубинина Е.Е., Зыбина Н.Н. Методы оценки свободнорадикального окисления и антиоксидантной системы организма. Методические рекомендации. СПб.: Фолиант. 2000; 104 с.
  • Зенков Н.К., Ланкин В.З., Меньщикова Е.Б. Окислительный стресс. Биохимический и патофизиологический аспекты. М.: МАИК «Наука/Интерпериодика». 2001; 343 с.
  • Tsvetkov A.S., Samsonov S.A., Akhmanova A. et al. Microtubule-binding proteins CLASP1 and CLASP2 interact with actin filaments. Cell. Motil. Cytoskeleton. 2007; 64: 519-530. doi: 10.1002/cm.20201.
  • Miyata T., De Strihou C., Kurokawa K. Alterations in nonenzymatic biochemistry in uremia: origin and significance of «carbonyl stress» in long-term uremic complications. Kidney Int. 1999; 55 (2): 389-399. doi: 10.1046/j.1523-1755.1999.00302.x.


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