Oxidative stress in the intracellular zinc signaling system: <i>in vitro</i> investigation on human erythrocytes
It was demonstrated the existence of specific receptors on the surface of red blood cells and intracellular stores responsible for maintaining zinc homeostasis using intracellular and extracellular zinc chelators - TPEN and DTPA. At the same time, it was shown that rise the cytosolic pool of labile Zn<sup>2+</sup> over 100 nM leads to the initiation of apoptotic processes. The intracellular molecular mechanisms leading to Zn<sup>2+</sup> release from cellular stores determine the cytotoxic zinc effects. Moreover, an inverse relationship between the intracellular labile zinc pool and esterase activity of red blood cells under modeling oxidative stress using H<sub>2</sub>O<sub>2</sub> in vitro was revealed. It indicates the direct participation of Zn<sup>2+</sup> in triggering eryptosis and that “prooxidants/antioxidants” imbalance in favor of the former acts as a trigger of this process. At the same time, an increase in the expression level of cytosolic thiol-containing metallothioneins was detected, both in red blood cells depleted by Zn<sup>2+</sup> and in cells after the oxidative stress induction. These indicate the functioning of metallothioneins as an adjuvant antioxidant in the protective system of red blood cells under oxidative stress.