Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.


青野 要 岡山大学医学部附属病院中央放射線部
山本 道夫 岡山大学医学部放射線医学教室
飯田 荘介 岡山大学医学部放射線医学教室
内海 耕慥 岡山大学医学部癌源研究所生化学部門
90_1297.pdf 1.56 MB
In relation to the mechanism by which hemolysis was induced in radiated human erythrocytes in vitro, several inducements of membrane lipid peroxidation and protective effects of V.E and SOD were investigated. Results obtained were as follows: (1) K(+)-release from erythrocytes was accelerated by radiation prior to hemolysis. These accelerated hemolysis and K(+)-release were protected remarkably by V.E and evidently by SOD. (2) Mitochondrial Fe(2+) induced and Fe(3+)-O(2) generating system -ADP induced lipid peroxidation, and microsomal O(2) generating system -induced lipid peroxidation were also protected by V.E and SOD. (3) Radiation of X-ray or (60)Co γ-ray accelerated lipid peroxidation of liver homogenate, microsome and liposome. Some of these accelerated lipid peroxidations were protected effectively by V.E and SOD. These results suggest that O(2) and/or OH. generation by radiation induces of membrane lipid peroxidation, which leads deterioration of membrane resulting in the change of ion permeability and then hemolysis.