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从蛰伏中觉醒会增加冬眠的十三线地松鼠 () 的氧化损伤。

Arousal from Torpor Increases Oxidative Damage in the Hibernating Thirteen-Lined Ground Squirrel ().

出版信息

Physiol Biochem Zool. 2022 May-Jun;95(3):229-238. doi: 10.1086/719931.

DOI:10.1086/719931
PMID:35443147
Abstract

AbstractDuring hibernation, especially during arousal from torpor to interbout euthermia (IBE), blood flow changes drastically. In nonhibernating mammals, similar changes during ischemia/reperfusion lead to oxidative damage. We hypothesized that suppression of mitochondrial metabolism during hibernation protects against such damage. We compared markers of oxidative damage and total antioxidant capacity in eight tissues among summer, torpid, and IBE thirteen-lined ground squirrels. Overall, summer tissue had less lipid and protein oxidative damage than tissue from the hibernation season, but DNA damage (in four tissues) and total antioxidant capacity (in all eight tissues) were similar among all groups. During torpor, when mitochondrial metabolism is suppressed, lipid damage in heart, brown adipose tissue, and small intestine was lower than IBE by as much as fivefold. By contrast, oxidative damage to protein was at least twofold higher in liver and skeletal muscle in torpor compared with IBE. Our findings suggest that arousal from torpor creates oxidative damage similar to ischemia/reperfusion injury but that this damage is repaired during IBE. These differences cannot be explained by changes in antioxidant capacity, so they are likely due to differences is reactive oxygen species production among hibernation states that may relate to the well-characterized reversible suppression of mitochondrial metabolism during torpor.

摘要

摘要 在冬眠期间,特别是从蛰伏状态到间歇清醒期(IBE)期间,血液流量会发生剧烈变化。在非冬眠哺乳动物中,类似的缺血/再灌注期间的变化会导致氧化损伤。我们假设在冬眠期间抑制线粒体代谢可以防止这种损伤。我们比较了夏季、蛰伏和 IBE 十三线地松鼠的 8 种组织中的氧化损伤标志物和总抗氧化能力。总的来说,夏季组织的脂质和蛋白质氧化损伤比冬眠季节的组织少,但所有组的 DNA 损伤(4 种组织)和总抗氧化能力(8 种组织)相似。在蛰伏期间,当线粒体代谢受到抑制时,心脏、棕色脂肪组织和小肠的脂质损伤比 IBE 低多达 5 倍。相比之下,与 IBE 相比,肝脏和骨骼肌中的蛋白质氧化损伤在蛰伏期间至少高出两倍。我们的研究结果表明,从蛰伏中苏醒会产生类似于缺血/再灌注损伤的氧化损伤,但这种损伤在 IBE 期间得到修复。这些差异不能用抗氧化能力的变化来解释,因此它们可能是由于休眠状态下活性氧物种产生的差异引起的,这可能与蛰伏期间线粒体代谢可逆抑制的特征有关。

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