[Various hormonal and metabolic disorders in liver cytosol during compensated and decompensated experimental stress].
Alterations of glucocorticoid-receptor interactions in liver cytosol and their importance in cell metabolic impairments were studied under various conditions of experimental stress. The experimental stress caused by acute peritonitis developed in rat males of Wistar strain. The alterations in steroid-receptor interactions, observed in liver cells under the stress conditions, might be responsible for adaptation of the cells and affect distinctly the metabolic reactions, inhibiting the early exhaustion of energy substrates in a cell (the stress compensated form). In severe stress reaction an excess of endogenous corticosterone, accumulated in hepatocyte cytosol, might deteriorate the cell metabolism by means of hormonal-receptor system, as a result of which exhaustion of energy potential led to death (decompensated form of the stress).
D000208:Acute Disease; D000818:Animals; D001665:Binding Sites; D003345:Corticosterone / Q000097:blood; D003600:Cytosol / Q000378:metabolism*; D008099:Liver / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D010538:Peritonitis / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D011965:Receptors, Glucocorticoid / Q000502:physiology*; D011987:Receptors, Steroid / Q000502:physiology*; D013312:Stress, Physiological / Q000378:metabolism* / Q000503:physiopathology; D014444:Tyrosine Transaminase / Q000378:metabolism
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; C028697:dexamethasone receptor; D014444:Tyrosine Transaminase; D003345:Corticosterone
O nekotorykh gormonal'nykh i metabolicheskikh narusheniiakh v tsitozole pecheni pri kompensirovannom i dekompensirovannom techenii éksperimental'nogo stressa.