The stress hormones (cortisol, adrenaline, noradrenaline) can bind to erythrocyte membranes with high affinity. The binding mechanism involves hydrogen bonds, hydrophobic and, to a less extent, electrostatic interactions. Active groups of the hormones (amino, imino, keto and hydroxy groups) interact simultaneously with CO and NH groups both of proteins and phospholipids. This leads to the formation of complex protein-lipid domains that distort the surface of erythrocyte membrane. Water dipoles are displaced from the domains to adjacent regions and facilitate membrane loosening. These processes underlie the structural phase transitions that occur in membrane upon its interaction with the stress hormones. At that, microviscosity of membranes strongly increases in the regions of protein-lipid and lipid-lipid interactions. A loss of plastic properties by erythrocyte membranes hampers their movement in small capillaries and promotes the development of tissue hypoxia. Biological membranes in extreme conditions behave like liquid crystalline structures, whose failure mechanics is identical to destruction of solid crystal in the fields of external action.
|Журнал||International Journal of Terraspace Science and Engineering|
|Состояние||Опубликовано - 2010|
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