1. Altered antioxidant status and increased lipid peroxidation in children with cystic fibrosis.
- Author
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Portal BC, Richard MJ, Faure HS, Hadjian AJ, and Favier AE
- Subjects
- Adolescent, Adult, Carotenoids blood, Child, Cholesterol blood, Cystic Fibrosis blood, Cystic Fibrosis physiopathology, Fatty Acids, Unsaturated blood, Female, Glutathione Peroxidase blood, Humans, Malabsorption Syndromes blood, Malabsorption Syndromes metabolism, Malabsorption Syndromes physiopathology, Male, Oxidative Stress, Reactive Oxygen Species, Selenium metabolism, Superoxide Dismutase blood, Thiobarbituric Acid Reactive Substances metabolism, Vitamin A blood, Vitamin E blood, Vitamins metabolism, Zinc blood, beta Carotene, Cystic Fibrosis metabolism, Lipid Metabolism, Lipid Peroxidation physiology, Vitamins blood
- Abstract
Cystic fibrosis often combines an infectious pathology with a syndrome of malabsorption, both potentially capable of favoring the deleterious effects of reactive oxygen species. This study was a simultaneous evaluation of the main antioxidant systems dependent on micronutrients and of lipid peroxidation products in 27 children with cystic fibrosis and 17 healthy children. Plasma of cystic fibrosis patients showed very low concentrations of beta-carotene (0.30 +/- 0.2 vs 1.63 +/- 0.5 mumol/g cholesterol, P < 0.0001) and a lower activity of selenium-dependent glutathione peroxidase (263.6 +/- 42 vs 296.9 +/- 57 U/L, P = 0.028). In parallel, the higher plasma concentrations of organic hydroperoxides (171.5 +/- 54.4 vs 122.6 +/- 23.3 mumol/L, P = 0.001) and of thiobarbituric acid reactants (2.9 +/- 0.6 vs 2.4 +/- 0.3 mumol/L, P = 0.004) reflected oxidative stress in this pathology. In addition, in these patients the major substrates of lipoperoxidation were significantly lower, whether they be linoleic acid (2.26 +/- 0.8 vs 3.60 +/- 0.9 mmol/L, P < 0.0001) or arachidonic acid (0.55 +/- 0.2 vs 0.74 +/- 0.2 mmol/L, P = 0.006). These results suggested that nutritional deficiencies resulting from malabsorption could considerably amplify disorders related to toxicity of reactive oxygen species. These nutritional deficits could also be aggravated by the destruction of antioxidant compounds by the inflammatory process.
- Published
- 1995
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