Altered antioxidant status and increased lipid peroxidation in children with cystic fibrosis
| Autor: | Henri Faure, Marie-Jeanne Richard, Arthur J Hadjian, Alain Favier, Beatrice Portal |
|---|---|
| Rok vydání: | 1995 |
| Předmět: |
Adult
Male medicine.medical_specialty Antioxidant Adolescent Cystic Fibrosis medicine.medical_treatment Linoleic acid Medicine (miscellaneous) Biology medicine.disease_cause Cystic fibrosis Thiobarbituric Acid Reactive Substances Lipid peroxidation chemistry.chemical_compound Selenium Malabsorption Syndromes Internal medicine medicine Humans Vitamin E Child Vitamin A chemistry.chemical_classification Glutathione Peroxidase Nutrition and Dietetics Cholesterol Superoxide Dismutase Glutathione peroxidase Glutathione Vitamins medicine.disease Lipid Metabolism beta Carotene Carotenoids Oxidative Stress Zinc Endocrinology chemistry Fatty Acids Unsaturated Female Lipid Peroxidation Reactive Oxygen Species Oxidative stress |
| Zdroj: | The American journal of clinical nutrition. 61(4) |
| ISSN: | 0002-9165 |
| Popis: | 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 micronutnients 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 �3-canotene (0.30 ± 0.2 vs 1.63 ± 0.5 �amol/g cholesterol, P < 0.0001) and a lower activity of sele- niurn-dependent glutathione penoxidase (263.6 ± 42 vs 296.9 ± 57 UIL, P = 0.028). In parallel, the higher plasma concen- trations of organic hydnoperoxides (171.5 ± 54.4 vs 122.6 ± 23.3 p.mol/L, P 0.001) and of thiobarbitunic acid reactants (2.9 ± 0.6 vs 2.4 ± 0.3 �.amolfL, 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 anachidonic acid (0.55 ± 0.2 vs 0.74 ± 0.2 mmolfL, 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. Am J Clin Nutr 1995;61: 843-7. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|