ROLE OF ANTIOXIDANTS ON THE ERYTHROCYTES RESISTANCE TO LIPID-PEROXIDATION AFTER ACUTE IRON OVERLOAD IN RATS

Citation
M. Galleano et S. Puntarulo, ROLE OF ANTIOXIDANTS ON THE ERYTHROCYTES RESISTANCE TO LIPID-PEROXIDATION AFTER ACUTE IRON OVERLOAD IN RATS, Biochimica et biophysica acta. Molecular basis of disease, 1271(2-3), 1995, pp. 321-326
Citations number
39
ISSN journal
09254439
Volume
1271
Issue
2-3
Year of publication
1995
Pages
321 - 326
Database
ISI
SICI code
0925-4439(1995)1271:2-3<321:ROAOTE>2.0.ZU;2-E
Abstract
Iron overload was developed in rats by ip injection of iron-dextran. I ron concentration in plasma increased 12-fold after 20 h of iron suppl ementation and unsaturated iron binding capacity (UIBC) drastically de creased in iron overloaded compared to control rats (69 +/- 36 and 177 +/- 19 mu g/dl, respectively). Lipid peroxidation in plasma increased by 285% and plasma alpha-tocapherol content decreased by 40% after 20 h of iron overload. alpha-Tocopherol supplementation decreased by 30% the measured increase in TEARS content in plasma after iron injection . On the other hand, both iron and TEARS content in erythrocytes were not significantly different in control and iron loaded rats. However, red blood cells from iron treated rats exposed to pro-oxidant conditio ns showed a significant increase in TEARS content as compared to contr ol erythrocytes. alpha-Tocopherol pretreatment prevented this increase . Moreover, red blood cells from iron loaded rats showed a higher cont ent of TEARS after incubation with plasma from iron-dextran injected r ats than after incubation with plasma from control animals. This measu red increase was partially prevented by cr-tocopherol supplementation. Neither the activity of antioxidant enzymes nor the content of alpha- tocopherol in red blood cells were affected by iron overload. Total th iols content was significantly lower (30%) in erythrocytes isolated fr om iron treated rats. The data presented here suggest that free radica l generation catalyzed by metal ions may lead to consumption of thiols . The decrease in thiols content in erythrocytes could afford an appro priate degree of protection and avoid other oxidative damage to these cells.