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Antibiotic effects on SO 4 2− uptake in human erythrocytes
Author(s) -
Casella S.,
Pace M.,
Romano P.,
Romano L.,
Romano O.,
Geraci A.,
Crupi M.
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1430
Subject(s) - glutathione , efflux , band 3 , oxidative stress , red blood cell , chemistry , haemolysis , biochemistry , red cell , oxidative phosphorylation , intracellular , antibiotics , thiol , redox , cotransporter , cell , oxidizing agent , erythrocyte deformability , biophysics , membrane , biology , sodium , erythrocyte membrane , medicine , enzyme , immunology , inorganic chemistry , organic chemistry
The erythrocyte is a cell highly exposed to oxygen pressure that, in turn, provokes oxidative stress involving loss of SH‐groups, cell shrinkage by activation of K + –Cl − cotransport (KCC) and membrane destabilization which plays an important role in the premature haemolysis of red blood cells (RBCs). Oxidative stress provoked by chemicals frequently occurs in human erythrocytes. The aim of this study was to test whether the antibiotics alter the redox state and investigate their influences on band 3 protein that is involved in the facilitated electro neutral exchange of Cl − for HCO 3 −across the membrane of mammalian erythrocytes. Normal erythrocytes were treated with some antibiotics and thiol oxidizing agent N ‐ethylmaleimide (NEM) and tested for sulphate uptake, K + efflux and for glutathione (GSH) concentration as an index of oxidative stress. The rate constant of SO 4 =uptake measured in erythrocytes treated with antibiotics as well as NEM was decreased with respect to control cells as a result of band 3 SH‐groups oxidation or the stress‐induced K + ‐Cl − symport‐mediated cell shrinkage. In fact, this hypothesis was verified by increased K + efflux and decreased GSH values measured in treated erythrocytes compared to controls. Copyright © 2007 John Wiley & Sons, Ltd.