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在经历快速发展的严重低氧环境的老年大鼠的心脏左心室中,氧化还原平衡受损。

Impaired redox homeostasis in the heart left ventricles of aged rats experiencing fast-developing severe hypobaric hypoxia.

机构信息

Graduate Studies, Çankaya University, Çukurambar Mah. Öğretmenler Cad. No: 14, 06530, Ankara, Turkey.

Department of Physical Education and Sport, Ardahan University, Çamlıçatak Mevkii, 75000, Merkez, Ardahan, Turkey.

出版信息

Biogerontology. 2019 Oct;20(5):711-722. doi: 10.1007/s10522-019-09826-1. Epub 2019 Jul 30.

DOI:10.1007/s10522-019-09826-1
PMID:31363871
Abstract

Despite its rare occurrence, humans and animals have been prone to getting fast developing severe hypobaric hypoxia. Understanding the redox homeostasis related response of an aging heart to this type of hypoxia are crucially important, since the metabolism of myocardial tissue depends on the redox status of proteins. Rodents can tolerate hypoxic stress better than human subjects. This study was aimed at investigating the effects of fast developing severe hypobaric hypoxia on redox status biomarkers; such as, advanced oxidation protein products (AOPP), lipid hydroperoxides (LHPs), protein carbonyl groups (PCO), protein thiol groups (P-SH), and total thiol groups (T-SH) on the myocardial left ventricles of young and aged Wistar rats. The rats were gradually ascended and exposed to an 8000-meter hypobaric hypoxia. While AOPP levels showed no difference, the TSH and PSH concentrations decreased, and the PCO and LHP increased in both of the hypoxic groups than the controls. The TSH and PSH were lower, and AOPP, PCO and LHP were found to be higher in the elderly hypoxic groups than in the young ones. The significant outcome of the study represents that an 8000-meter hypobaric hypoxia could be considered as a severe hypoxic stress, but not life-treating for the rats and would affect both the young and aged left ventricles similarly in respect to impaired redox status. However, if the percentage increases are taken into consideration, it seems that the higher rate of protein oxidation occurs in young hearts; meanwhile aged hearts are more prone to T-SH oxidation.

摘要

尽管这种情况很少发生,但人类和动物也容易受到快速发展的严重低氧缺氧的影响。了解衰老心脏对这种缺氧的氧化还原平衡相关反应至关重要,因为心肌组织的代谢依赖于蛋白质的氧化还原状态。啮齿动物比人类更能耐受缺氧应激。本研究旨在探讨快速发展的严重低氧缺氧对氧化还原状态生物标志物的影响;如,高级氧化蛋白产物(AOPP)、脂质过氧化物(LHPs)、蛋白羰基(PCO)、蛋白巯基(P-SH)和总巯基(T-SH)对年轻和老年 Wistar 大鼠左心室的影响。大鼠逐渐上升并暴露于 8000 米的低氧环境中。虽然 AOPP 水平没有差异,但 TSH 和 PSH 浓度降低,而 PCO 和 LHP 在缺氧组中均高于对照组。老年缺氧组的 TSH 和 PSH 较低,而 AOPP、PCO 和 LHP 较高。研究的显著结果表明,8000 米的低氧环境可以被认为是一种严重的低氧应激,但对大鼠没有生命威胁,并且会对年轻和老年左心室的氧化还原状态产生类似的影响。然而,如果考虑到百分比的增加,似乎在年轻心脏中发生的蛋白质氧化的比率更高;同时,老年心脏更容易发生 T-SH 氧化。

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