ROLE OF SODIUM CHANNELS IN THE DEVELOPMENT OF OXIDATIVE STRESS IN ISCHEMIA/REPERFUSION MODEL

Abstract

Ischemic and reperfusion injury is a critical condition, as it is necessary to control cell death and maintain tissue function. Restoration of nutrient and oxygen flow causes secondary damage to ischemic cells and is called reperfusion injury. Reperfusion injury causes, on the one hand, fluctuations in ion concentration inside cells, in particular sodium ions, due to changes in the conductivity of voltage-dependent ion channels, and, on the other hand, activation of the antioxidant system as a response to oxidative stress, in which the key role is given to reactive oxygen species and nitric oxide. Thus, the effect of ion channel inhibitors on the progression of oxidative stress, apoptosis and necrosis during reperfusion is of particular interest.
 The aim of the study is to examine the impact of sodium channels on oxidative stress under ischemic and reperfusion injury and sodium channel blockers action.
 Materials and Methods. The authors studied the influence of the synthesized peptide toxin, an inhibitor of voltage-gated sodium channels, under modelled ischemia/reperfusion in CHO-K1 culture on the level of apoptosis, necrosis, and oxidative stress (concentration of reactive oxygen species, nitric oxide, and glutathione) using fluorescent dyes and fluorescence microplate reader.
 Results. Data obtained indicate a decreased level of apoptosis and necrosis, and a control level of nitric oxide under toxin at a nanomolar concentration. At the same time, the concentrations of reactive oxygen species and glutathione did not change. Thus, the inhibitor toxin acted as a protective agent by preventing a decrease in the nitric oxide concentration, which favorably affected the survival of the cell culture during reperfusion after ischemia.