Affiliation:
1. Siberian State Medical University, Tomsk
Abstract
Currently, diabetes ranks third in relation to medical and social significance after cardiovascular diseases and cancer and is the leading cause of blindness; it greatly increases the risk of myocardial infarction, coronary heart disease, nephropathy and hypertension in patients with this disorder; therefore clinical and experimental studies aimed at investigation of diabetes emergence and development mechanisms are urgent.The aim of the study was to investigate the status of oxidative modification of proteins and glutathionedependent antioxidant defense system in adipocytes of rats with alloxan diabetes under conditions of oxidative stress.Material and methods. Development of type 1 diabetes was induced in rats by alloxan administration (90 mg/kg of body mass). Adipocytes were obtained from epididymal adipose tissue of rats. The level of carbonyl derivatives of proteins, oxidized tryptophan, bityrosine, general, reduced, oxygenated and protein-bound glutathione, as well as glutathione peroxidase activity in adipocytes of rats was determined.Results. In adipocytes of rats with alloxan diabetes, concentration of carbonyl derivatives of proteins, bityrosine and oxidized tryptophan increased on the background of redox-potential of glutathione system and glutathione peroxidase activity decrease.Conclusion. The obtained data indicate the activation of free-radical oxidation of proteins and reduction of antioxidant defense under conditions of oxidative stress in the adipose tissue of rats with alloxan diabetes; this process plays an important role in pathogenesis of diabetes and its complications development.
Publisher
Siberian State Medical University
Reference18 articles.
1. Suntsov Yu.I., Bolotskaya L.L., Maslova O.V., Kazakov I.V. Diabetes Mellitus, 2011, no. 1, pp. 15–18 (in Russian).
2. Dubininа Ye.Ye. Products of metabolism of oxygen in the functional activity of cells (life and death, creation and destruction). Physiological and clinical-biochemical aspects. St. Petersburg, Medical press Publ., 2006. 400 р. (in Russian).
3. Lushchak V.I. Biochemistry, 2007, vol. 72, no. 8, рр. 995–1015 (in Russian).
4. Menshchikova Ye.B., Zenkov N.K., Lankin V.Z., Bondar I.A., Trufakin V.A. Oxidative stress: Pathological conditions and diseases. Novosibirsk, ART Publ., 2008. 284 р.
5. Furukawa S., Fujita T., Shimabukuro M. Increased oxidative stress in obesity and its impact on metabolic syndrome. Clin. Invest., 2004, Dec., vol. 114, no. 12, pp. 1752–1761. doi:10.1172/JCI200421625.
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