The cell membrane as a biosensor of oxidative stress induced by radiation exposure: a multiparameter investigation.
The role of biological membranes as a target in biological radiation damage remains unclear. The present study investigates how the biochemical and biophysical properties of a simple biological model, i.e. human erythrocyte membranes, are altered after exposure to relatively low doses of (60)Co gamma rays. Lipid peroxidation increased in the hours after radiation exposure, based on measurements of MDA and on the lipid peroxidation index after parinaric acid incorporation. Protein carbonyl content also increased rapidly after radiation exposure. An imbalance between the radiation-mediated oxidative damages and the antioxidant capacity of the erythrocytes was observed in the hours after radiation exposure. Antioxidant enzyme activities, mainly catalase and glutathione peroxidase, were found to decrease after irradiation. The development of a radiation-induced oxidative stress probably explains the reorganization of the fatty acid pattern 72 h after radiation exposure. The phosphatidylethanolamine (PE) fatty acids of the (n-3) and (n-6) series decreased, while the PE saturated fatty acid content increased. All these modifications may be involved in the variation of the biophysical properties of the membranes that we noted after radiation exposure. Specifically, we observed that the lipid compartment of the membrane became more fluid while the lipid-protein membrane interface became more rigid. Taken together, these findings reinforce our understanding that the cell membrane is a significant biological target of radiation. Thus the role of the biological membrane in the expression and course of cell damage after radiation exposure must be considered.
Benderitter
M
M
Département de Protection de la santé de l'Homme et de Dosimétrie, IRSN, BP no 17, F-92262 Fontenay-aux-Roses cedex, France. marc.benderitter@irsn.fr
Vincent-Genod
L
L
Pouget
J P
JP
Voisin
P
P
D000328:Adult; D000578:Amidines / Q000494:pharmacology; D015374:Biosensing Techniques; D001798:Blood Proteins / Q000737:chemistry / Q000528:radiation effects; D002374:Catalase / Q000097:blood; D002474:Cell-Free System; D004307:Dose-Response Relationship, Radiation; D004910:Erythrocyte Membrane / Q000528:radiation effects*; D004912:Erythrocytes / Q000201:enzymology / Q000528:radiation effects; D005227:Fatty Acids / Q000032:analysis / Q000528:radiation effects; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology; D005454:Fluorescence Polarization; D005720:Gamma Rays / Q000009:adverse effects*; D005979:Glutathione Peroxidase / Q000097:blood; D006801:Humans; D015227:Lipid Peroxidation / Q000528:radiation effects; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008560:Membrane Fluidity / Q000528:radiation effects; D008563:Membrane Lipids / Q000528:radiation effects; D008565:Membrane Proteins / Q000737:chemistry / Q000528:radiation effects; D016877:Oxidants / Q000494:pharmacology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000528:radiation effects*; D010743:Phospholipids / Q000032:analysis / Q000528:radiation effects; D010799:Phycoerythrin / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
D000578:Amidines; D001798:Blood Proteins; D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D008563:Membrane Lipids; D008565:Membrane Proteins; D016877:Oxidants; D010743:Phospholipids; D017392:Thiobarbituric Acid Reactive Substances; D010799:Phycoerythrin; D008315:Malondialdehyde; C046728:2,2'-azobis(2-amidinopropane); D002374:Catalase; D005979:Glutathione Peroxidase; C013641:parinaric acid