The influences of various factors on blood lead to the formation of extra reactive oxygen species (ROS), resulting in the disruption of morphology and functions of red blood cells (RBCs). This study considers the mechanisms of the mechanochemical synergism of OH• free radicals, which are most active in the initiation of lipid peroxidation (LPO) in RBC membranes, and H2O2 molecules, the largest typical diffusion path. Using kinetic models of differential equations describing CH2O2t and COH•t, we discuss two levels of mechanochemical synergism that occur simultaneously: (1) synergism that ensures the delivery of highly active free radicals OH• to RBC membranes and (2) a positive feedback system between H2O2 and OH•, resulting in the partial restoration of spent molecules. As a result of these ROS synergisms, the efficiency of LPO in RBC membranes sharply increases. In blood, the appearance of OH• free radicals is due to the interaction of H2O2 molecules with free iron ions (Fe2+) which arise as a result of heme degradation. We experimentally established the quantitative dependences of COH• CH2O2 using the methods of spectrophotometry and nonlinear curve fitting. This study extends the analysis of the influence of ROS mechanisms in RBC suspensions.
Keywords: Fenton reaction; RBC membranes; ROS; hydrogen peroxide; hydroxyl radical; kinetic model; mechanochemical synergism.