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果糖和应激对大鼠肾脏铜代谢和抗氧化酶功能的影响。

Effects of Fructose and Stress on Rat Renal Copper Metabolism and Antioxidant Enzymes Function.

机构信息

Department of Biochemistry, Institute for Biological Research "Siniša Stanković", National Institute of Republic of Serbia, University of Belgrade, 142 Despot Stefan Blvd, 11060 Belgrade, Serbia.

Department of Life Sciences, Institute for Multidisciplinary Research, University of Belgrade, 142 Despot Stefan Blvd, 11060 Belgrade, Serbia.

出版信息

Int J Mol Sci. 2022 Aug 12;23(16):9023. doi: 10.3390/ijms23169023.

DOI:10.3390/ijms23169023
PMID:36012287
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9409054/
Abstract

The effects of a fructose-rich diet and chronic stress on copper metabolism in the kidneys are still understudied. We investigated whether fructose and/or chronic unpredictable stress modulate copper metabolism in a way that affects redox homeostasis, thus contributing to progression of metabolic disturbances in the kidney. We determined protein level of copper transporters, chaperones, and cuproenzymes including cytochrome c oxidase, as well as antioxidant enzymes function in the kidneys of male Wistar rats subjected to 20% liquid fructose supplementation and/or chronic stress. Liquid fructose supplementation increased level of copper chaperone of superoxide dismutase and decreased metallothionein level, while rendering the level of copper importer and copper chaperones involved in copper delivery to mitochondria and trans Golgi network unaffected. Stress had no effect on renal copper metabolism. The activity and expression of renal antioxidant enzymes remained unaltered in all experimental groups. In conclusion, fructose, independently of stress, decreased renal copper level, and modulated renal copper metabolism as to preserve vital cellular function including mitochondrial energy production and antioxidative defense, at the expense of intracellular copper storage.

摘要

富含果糖的饮食和慢性应激对肾脏铜代谢的影响仍研究不足。我们研究了果糖和/或慢性不可预测应激是否以影响氧化还原平衡的方式调节铜代谢,从而导致肾脏代谢紊乱的进展。我们测定了雄性 Wistar 大鼠肾脏中铜转运蛋白、伴侣蛋白和铜酶(包括细胞色素 c 氧化酶)的蛋白水平,以及抗氧化酶的功能,这些大鼠接受了 20%液体果糖补充和/或慢性应激。液体果糖补充增加了超氧化物歧化酶的铜伴侣蛋白水平,降低了金属硫蛋白水平,而不影响铜的内体和铜伴侣蛋白向线粒体和反高尔基网络的铜传递。应激对肾脏铜代谢没有影响。所有实验组的肾脏抗氧化酶的活性和表达都没有改变。总之,果糖(不依赖于应激)降低了肾脏的铜水平,并调节了肾脏的铜代谢,以维持重要的细胞功能,包括线粒体能量产生和抗氧化防御,而牺牲了细胞内的铜储存。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/afd02a2b3ca7/ijms-23-09023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/8027ae27d7b3/ijms-23-09023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/fa61bb822e09/ijms-23-09023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/afd02a2b3ca7/ijms-23-09023-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/8027ae27d7b3/ijms-23-09023-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/fa61bb822e09/ijms-23-09023-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a98c/9409054/afd02a2b3ca7/ijms-23-09023-g003.jpg

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