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膳食碳水化合物与铜营养对大鼠组织脂质过氧化的相互作用。

Interaction between dietary carbohydrate and copper nutriture on lipid peroxidation in rat tissues.

机构信息

Georgetown University School of Medicine, 20007, Washington, DC.

出版信息

Biol Trace Elem Res. 1984 Oct;6(5):379-91. doi: 10.1007/BF02989255.

Abstract

The effects of the interactions between dietary carbohydrates and copper deficiency on superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and their roles in peroxidative pathways were investigated. Weanling rats were fed diets deficient in copper and containing either 62% starch, fructose, or glucose. Decreased activity of SOD was noted in all rats fed the copper-deficient diets regardless of the nature of dietary carbohydrate. However, the decreased activity was more pronouced in rats fed fructose. Feeding the fructose diets decreased the activity of GSH-Px by 25 and 50% in the copper-supplemented and copper-deficient rats, respectively, compared to enzyme activities in rats fed similar diets containing either starch or glucose. The decreased SOD and GSH-Px activities in rats fed the fructose diet deficient in copper were associated with increased tissue per-oxidation and decreased hepatic adenosine triphosphate (ATP). When the fructose in the diet of copper-deficient rats was replaced with either starch or glucose, tissue SOD and GSH-Px activities were increased and these increases in enzyme activity were associated with a tendency toward reduced mitochondrial peroxidation when compared to the corre-sponding values for rats fed fructose throughout the experiment Dietary fructose aggrevated the symptoms associated with copper deficiency, but starch or glucose ameliorated them. The protective effects were more pronounced with starch than with glucose.

摘要

研究了膳食碳水化合物与铜缺乏之间的相互作用对超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性的影响及其在过氧化途径中的作用。我们用缺乏铜的饮食喂养断奶大鼠,这些饮食中分别含有 62%的淀粉、果糖或葡萄糖。无论饮食中碳水化合物的性质如何,所有喂食铜缺乏饮食的大鼠的 SOD 活性均降低。然而,喂食果糖的大鼠中 SOD 活性的降低更为明显。与喂食含有淀粉或葡萄糖的类似饮食的大鼠相比,分别补充铜和缺乏铜的大鼠喂食果糖饮食时,GSH-Px 的活性分别降低了 25%和 50%。缺乏铜的大鼠喂食果糖饮食时 SOD 和 GSH-Px 活性降低与组织过氧化增加和肝三磷酸腺苷(ATP)减少有关。当铜缺乏大鼠饮食中的果糖被淀粉或葡萄糖替代时,组织 SOD 和 GSH-Px 活性增加,与整个实验期间喂食果糖的大鼠相比,这些酶活性的增加与线粒体过氧化减少的趋势有关。饮食中的果糖加重了与铜缺乏相关的症状,但淀粉或葡萄糖可改善这些症状。淀粉的保护作用比葡萄糖更为明显。

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