Contribution of antioxidant enzymes to the adaptive response to ionizing radiation of human lymphoblasts

Citation
A. Bravard et al., Contribution of antioxidant enzymes to the adaptive response to ionizing radiation of human lymphoblasts, INT J RAD B, 75(5), 1999, pp. 639-645
Citations number
34
Categorie Soggetti
Experimental Biology
Journal title
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
ISSN journal
09553002 → ACNP
Volume
75
Issue
5
Year of publication
1999
Pages
639 - 645
Database
ISI
SICI code
0955-3002(199905)75:5<639:COAETT>2.0.ZU;2-S
Abstract
Purpose: To investigate whether the adaptive response to ionizing radiation triggered by a low-dose pre-exposure could be due to the activation of the antioxidant defence system. Materials and methods: Human lymphoblastoid AHH-1 cells were irradiated wit h a 0.02 Gy gamma-radiation and 6 h later were exposed to a 3 Gy challenge dose according to a protocol allowing mutagenic adaptation. Controls includ ed cells left unirradiated or exposed to a single dose (0.02 Gy or 3 Gy). T he activities of the main cellular antioxidant enzymes (AOE) - copper-zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), catalas e (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), glu tathione reductase (GSR) and glucose 6-phosphate dehydrogenase (G6PD)- were evaluated at different times after treatment. The levels of SOD2 and CAT p roteins were also analysed using the immune Western blot method. Results: Compared with non-irradiated controls, the effect of 3 Gy alone wa s shown to increase GPX and CAT activities at 20 h after irradiation. Pre-e xposure of cells did not change these late alterations. Soon after irradiat ion the activities of SOD2, CST, GPX and CAT were slightly higher in adapte d than in nonadapted cells. Conclusion: The data suggest that the increased activities of some AOE obse rved soon after the challenge dose would result in a rapid scavenging of ra dicals and consequently less damage in adapted cells. Due to the moderate a lterations of these AGE, the activation of antioxidant defences would only partly contribute to the protective mechanism underlying the radioadaptatio n of AHH-1 lymphoblasts.