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Enhanced oxidative damage in cystic fibrosis patients
Author(s) -
Domínguez C.,
Gartner S.,
Liñán S.,
Cobos N.,
Moreno A.
Publication year - 1998
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520080125
Subject(s) - malondialdehyde , lipid peroxidation , oxidative stress , superoxide dismutase , glutathione reductase , chemistry , antioxidant , medicine , vitamin e , glutathione , endocrinology , vitamin c , exacerbation , biochemistry , glutathione peroxidase , enzyme
Abstract Antioxidant depletion and increased free radical production by inflammatory cells have been described in cystic fibrosis (CF) patients. To evaluate oxidative damage intensity, we measured plasma concentrations of malondialdehyde, hydroperoxides and protein carbonyl groups as markers of oxidative injury to lipids and proteins in a group of 101 CF patients free of acute exacerbation, and in 43–112 controls. Moreover, we estimated antioxidant function by measuring activities of erythrocyte superoxide dismutase, glutathione reductase and vitamin E concentrations. In CF patients, malondialdehyde and hydroperoxide plasma levels were significantly higher than in controls ( p < 0.001). Increased lipid peroxidation was documented by these two markers. Parallel rises in protein carbonyls in plasma of CF patients were observed ( p < 0.0001). These patients presented biochemical but not clinical vitamin E deficiency. Glutathione reductase and superoxide dismutase activities were significantly higher than in controls. These results show a serious imbalance in CF patients between oxidant—antioxidant status leading to oxidative stress.