The osmotic resistance, and zeta potential responses of human erythrocytes to transmembrane modification of Ca2+ fluxes in the presence of the imposed low rate radiation field of 90Sr.

PURPOSE: To investigate the effects of the imposed low dose rate ionizing field on membrane stability of human erythrocytes under modulation of transmembrane exchange of Ca(2+). MATERIALS AND METHODS: Osmotic resistance of human erythrocytes was determined by a measure of haemoglobin released from erythrocytes when placed in a medium containing serial dilutions of Krebs isotonic buffer. The zeta potential as indicator of surface membrane potential was calculated from value of the cellular electrophoretic mobility. The irradiation of erythrocyte suspensions carried out by applying suitable aliquots of (90)Sr in incubation media. RESULTS: Irradiation of human erythrocytes by (90)Sr (1.5-15.0 µGy·h(-1)) induced a reversible increase of hyposmotic hemolysis and negative charge value on the outer membrane surface as well as changed responses these parameters to modification of Ca(2+) fluxes with calcimycin and nitrendipine. CONCLUSIONS: Findings indicate that the low dose rate radionuclides ((90)Sr) field modifies both Ca(2+)-mediated, and Ca(2+)-independent cellular signalling regulating mechanical stability of erythrocyte membrane. A direction of that modification presumably depends on the initial structure of membranes, and it is determined by the quality and quantitative parameters of changes in membrane structure caused by concrete operable factors.

Ultra-low dose beta-irradiation induces constriction of rabbit carotid arteries via the endothelium.

PURPOSE: To investigate the action of ultra-low dose beta-radiation (ULDBR) on isolated segments of blood vessels. MATERIALS AND METHODS: We used the pharmacological model of isolated rabbit carotid arteries with intact or mechanically removed endothelium. Specific vascular responses to beta-irradiation were registered after addition of (90)Sr in the concentration range between 12 and 96 microCi l(-1) to the organ bath containing physiological salt solution (PSS). RESULTS: Intact vascular rings, preconstricted with 20 mM K(+)-PSS, developed an additional constriction upon the addition of (90)Sr depending on the absorbed radiation dose (21.5, 42.9, 85.8, and 171.6 microGy) and the dose rate (51.5, 103.0, 206.0 and 412.0 microGy h(-1)). The vasoconstriction due to (90)Sr was absent in the endothelium-denuded vascular segments indicating the endothelium dependent action of ULDBR. Irradiation did not alter the endothelium dependent relaxation of rabbit carotid arteries induced by acetylcholine. The endothelium dependent responses to ULDBR were abolished after increasing the extra-cellular K(+) to 40 mM. CONCLUSIONS: ULDBR acts on rabbit carotid arteries as a pharmacological signalling agent because ULDBR effects were completely reversible. ULDBR-mediated contractile responses of the vessels are endothelium dependent. The resistance of acetylcholine endothelium-dependent relaxation of rabbit carotid arteries to ULDBR indicates that the polyphosphoinositide-nitric oxide (NO) signalling cascade is not impaired by ULDBR in endothelial cells.