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大剂量维生素 E 可改善衰老大鼠海马和前额皮质中线粒体功能障碍。

High doses of vitamin E improve mitochondrial dysfunction in rat hippocampus and frontal cortex upon aging.

机构信息

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Cádiz, Cádiz, Spain.

出版信息

Am J Physiol Regul Integr Comp Physiol. 2011 Apr;300(4):R827-34. doi: 10.1152/ajpregu.00525.2010. Epub 2010 Nov 24.

DOI:10.1152/ajpregu.00525.2010
PMID:21106913
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3075077/
Abstract

Rat aging from 4 to 12 mo was accompanied by hippocampus and frontal cortex mitochondrial dysfunction, with decreases of 23 to 53% in tissue and mitochondrial respiration and in the activities of complexes I and IV and of mitochondrial nitric oxide synthase (mtNOS) (P < 0.02). In aged rats, the two brain areas showed mitochondria with higher content (35-78%) of oxidation products of phospholipids and proteins and with higher (59-95%) rates of O(2)(-) and H(2)O(2) production (P < 0.02). Dietary supplementation with vitamin E (2.0 or 5.0 g/kg of food) from 9 to 12 mo of rat age, restored in a dose-dependent manner, the decreases in tissue and mitochondrial respiration (to 90-96%) and complexes I and IV and mtNOS activities (to 86-88%) of the values of 4-mo-old rats (P < 0.02). Vitamin E prevented, by 73-80%, the increases in oxidation products, and by 62-68%, the increases in O(2)(-) and H(2)O(2) production (P < 0.05). High resolution histochemistry of cytochrome oxidase in the hippocampal CA1 region showed higher staining in vitamin E-treated rats than in control animals. Aging decreased (19%) hippocampus mitochondrial mass, an effect that was restored by vitamin E. High doses of vitamin E seem to sustain mitochondrial biogenesis in synaptic areas.

摘要

大鼠从 4 月龄到 12 月龄的衰老伴随着海马体和前额皮质线粒体功能障碍,组织和线粒体呼吸以及复合物 I 和 IV 的活性以及线粒体一氧化氮合酶(mtNOS)的活性降低 23%至 53%(P<0.02)。在衰老的大鼠中,两个脑区的线粒体显示出更高的磷脂和蛋白质氧化产物含量(35-78%),并且具有更高的(59-95%)O2(-)和 H2O2 产生速率(P<0.02)。从 9 月龄到 12 月龄,饮食中补充维生素 E(2.0 或 5.0 g/kg 食物)以剂量依赖性方式恢复了组织和线粒体呼吸(至 4 月龄大鼠的 90-96%)以及复合物 I 和 IV 和 mtNOS 活性(至 86-88%)的降低(P<0.02)。维生素 E 以 73-80%的比例阻止了氧化产物的增加,并以 62-68%的比例阻止了 O2(-)和 H2O2 产生的增加(P<0.05)。海马 CA1 区细胞色素氧化酶的高分辨率组织化学显示,维生素 E 处理的大鼠比对照动物的染色更高。衰老降低了(19%)海马体线粒体质量,这一效应被维生素 E 所恢复。高剂量的维生素 E 似乎维持了突触区的线粒体生物发生。

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