Adaptation of Erythrocytes: The Role of Hemoglobin, Nitric Oxide, and Methylglyoxal

All living systems are characterized by fundamental properties such as the ability to adaptation and self-regulation. Mammalian nonnuclear erythrocytes also have the ability to adapt to external effects, but their regulatory capabilities are limited by cytoplasmic mechanisms, including phase transitions of proteins and membranes. This is one of the most ancient mechanisms of adaptation of living systems to external and internal conditions. Erythrocytes under changes in plasma composition, aging, and energy depletion, undergo a reversible morpho-functional transformation, the transition from a discocyte to an echinocyte. The metabolic shifts occurring in this case correspond to a complex of universal changes that take place during erythrocyte transition to metabolic depression. As a rule, echinocytosis is considered as a pathological process preceding eryptosis and hemolysis. However, it can be also considered as the first stage of the implementation of a universal program of passive cell adaptation, the ultimate goal of which is to transfer the system to a state of suspended animation. The energy status of an erythrocyte is determined by the equilibrium of soluble and membrane-bound hemoglobin (Hb) forms. Compounds with pronounced electrophilic properties—nitric oxide and methylglyoxal—affecting this equilibrium can induce cell’s transition from one metabolic state to another. The mechanism of their action is largely related to the modification of thiol groups of membrane and cytoskeleton proteins, including reactive SH-groups of Hb. It seems relevant to consider their effect on the state of Hb and erythrocytes.