Title of article :
Oxidative and genotoxic damage after radio-iodine therapy of Graves hyperthyroidism
Author/Authors :
Ballardin، M. نويسنده , , Barsacchi، R. نويسنده , , Bodei، L. نويسنده , , Caraccio، N. نويسنده , , Cristofani، R. نويسنده , , martino، F. Di نويسنده , , Ferdeghini، M. نويسنده , , Kusmic، C. نويسنده , , Madeddu، G. نويسنده , , Monzani، F. نويسنده , , Rossi، A. M. نويسنده , , Sbrana، I. نويسنده , , Spanu، A. نويسنده , , Traino، C. نويسنده , , Barale، R. نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2004
Pages :
-208
From page :
209
To page :
0
Abstract :
Purpose: To evaluate genetic damage and oxidative stress following a single therapeutic dose of 131I in Gravesʹ disease patients monitored up to 180 days after treatment. Materials and methods: Genetic damage induction was estimated as the increase in micronuclei in peripheral lymphocytes of patients. As indicators of radiogenic oxidative stress, vitamin E and lipoperoxide levels were assessed in the plasma of patients, as well as the release of plasmic clastogenic factors measured by the induction of micronuclei in vitro in peripheral lymphocytes of a healthy donor. Results: Vitamin E depletion lasted at least 3 days and the basal level was restored within 7 days. No statistically significant variations were observed in lipoperoxide plasma levels. A sharp increase of micronuclei in the peripheral lymphocytes of patients was correlated (p<0.001) with the release of clastogenic factor in the plasma. The highest micronucleus value was negatively correlated (p<0.03) with the lowest vitamin E level observed in each patient. Conclusions: Micronuclei induction was the direct consequence not only of the energy deposition of 131I on the genetic material, but also of oxidative stress, likely via the release of clastogenic factor.
Keywords :
chymosin , bovine osteopontin , Colostrum
Journal title :
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
Serial Year :
2004
Journal title :
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
Record number :
114893
Link To Document :
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