Scientific journal
European Journal of Natural History
ISSN 2073-4972

ACTION INHIBITOR PROTEIN HEAT SHOCK 27 ON THE ACTIVITY OF GLUTATHIONE PEROXIDASE AND CATALASE IN TUMOR CELLS

Nosareva O.L., Stepovaya E.A., Ryazantseva N.V., Konovalova E.V., Vesnina O.N., Orlov D.S., Fedosenko I.I., Naumova A.I.

Normally, the accumulation of free radicals in the cells prevents the antioxidant system. With the accumulation of reactive oxygen species formed by oxidative stress, often accompanied by increased levels of heat shock proteins. They are involved in the formation of the correct three-dimensional conformation of newly synthesized polypeptides in the maintenance of functional activity of intracellular proteins and elimination of damaged proteins. Tumor same transformation is accompanied by increased synthesis of heat shock protein 27, as well as the accumulation of oxidation-modified metabolites.

The material for the study is based on the tumor cell line Jurkat (T-lymphoblastic leukemia), obtained from a bank of cell cultures Institute of Cytology RAS (St. Petersburg). Cells were cultured in the way the suspension medium containing 90% RPMI-1640, 10% fetal calf serum («Biolot», St. Petersburg), inactivated at 56 °C for 30 min. Cells were maintained in logarithmic growth phase culture of continuous passages every 2-3 days. Assessment of cell viability were performed using trypan blue. Assessment of the activity of glutathione peroxidase and catalase was performed by spektrofotomitricheskim.

The results of this study showed that the addition of dexamethasone and an inhibitor of heat shock protein - KRIBB3, we received an increase in activity as glutathione peroxidase, and catalase. But in the case of co-added to the incubation medium, an inhibitor of heat shock protein 27, and dexamethasone, we recorded a decrease in the activity of both enzymes.

 


The work was submitted to International Scientific Conference «Fundamental and applied research in medicine», Russia ( Sochi), 27 Septem- ber - 1 October, 2012, came to the editorial office on 28.06.2012.