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Hypochlorous Acid-Induced Lysis of Human Erythrocytes. Inhibition of Cellular Damage by the Isoflavonoid Genistein-8-C-glucoside

L. B. Zavodnik1, I. B. Zavodnik1*, E. A. Lapshina1, A. P. Shkodich1, M. Bryszewska2, and V. U. Buko1

1Institute of Biochemistry, National Academy of Sciences of Belarus, Grodno, 230017 Belarus; E-mail: zavodnik@biochem.belpak.grodno.by

2Institute of Biophysics, University of Lodz, Lodz 90-237, Poland

* To whom correspondence should be addressed.

Received October 25, 1999; Revision received March 20, 2000
Erythrocyte damage induced by hypochlorous acid (HOCl) results in cell lysis developing with time after the oxidant is removed (post-hemolysis). The apparent rate constant of post-hemolysis depends on time of incubation in the presence of HOCl and concentration of this oxidant. HOCl-dependent damage of erythrocyte membranes is associated with uncompetitive inhibition of the membrane-bound acetylcholinesterase. Genistein-8-C-glucoside is an isoflavonoid isolated from the flowers of Lupinus luteus L.; in aqueous solution, genistein-8-C-glucoside (0.5-2 mM) efficiently inhibited HOCl-induced damage to erythrocytes similar to the known HOCl scavengers taurine and reduced glutathione. This bioflavonoid can protect the erythrocyte membrane (and to a lesser extent, intraerythrocytic components) by interacting with the reactive chlorine species including hypochlorous acid and membrane-bound chloroamines formed in the reaction of HOCl with erythrocyte membrane proteins.
KEY WORDS: human erythrocytes, hemolysis, hypochlorous acid, genistein, acetylcholinesterase