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囊性纤维化患儿抗氧化状态改变及脂质过氧化增加。

Altered antioxidant status and increased lipid peroxidation in children with cystic fibrosis.

作者信息

Portal B C, Richard M J, Faure H S, Hadjian A J, Favier A E

机构信息

Laboratoire de Biochimie, UFR des Sciences Pharmaceutiques et Biologiques, Domaine de la Merci, La Tronche, France.

出版信息

Am J Clin Nutr. 1995 Apr;61(4):843-7. doi: 10.1093/ajcn/61.4.843.

DOI:10.1093/ajcn/61.4.843
PMID:7702029
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.

摘要

囊性纤维化常将感染性病理状态与吸收不良综合征合并,二者均可能促使活性氧产生有害作用。本研究同时评估了27例囊性纤维化患儿和17例健康儿童中主要的依赖微量营养素的抗氧化系统及脂质过氧化产物。囊性纤维化患者血浆中β-胡萝卜素浓度极低(0.30±0.2 vs 1.63±0.5μmol/g胆固醇,P<0.0001),硒依赖性谷胱甘肽过氧化物酶活性较低(263.6±42 vs 296.9±57 U/L,P=0.028)。同时,血浆中有机氢过氧化物(171.5±54.4 vs 122.6±23.3μmol/L,P=0.001)和硫代巴比妥酸反应物(2.9±0.6 vs 2.4±0.3μmol/L,P=0.004)浓度较高,反映了该病理状态下的氧化应激。此外,这些患者中脂质过氧化的主要底物显著降低,无论是亚油酸(2.26±0.8 vs 3.60±0.9 mmol/L,P<0.0001)还是花生四烯酸(0.55±0.2 vs 0.74±0.2 mmol/L,P=0.006)。这些结果表明,吸收不良导致的营养缺乏可能会显著加剧与活性氧毒性相关的紊乱。炎症过程对抗氧化化合物的破坏也可能加重这些营养缺乏。

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