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Cellular Turnover: A Potential Metabolic Rate-Driven Mechanism to Mitigate Accumulation of DNA Damage.
Physiological and Biochemical Zoology ( IF 1.8 ) Pub Date : 2020-02-06 , DOI: 10.1086/707506
Stanisław Bury , Agnieszka Cierniak , Joanna Jakóbik , Edyta T Sadowska , Mariusz Cichoń , Ulf Bauchinger

Oxidative stress, the imbalance of reactive oxygen species and antioxidant capacity, may cause damage to biomolecules pivotal for cellular processes (e.g., DNA). This may impair physiological performance and, therefore, drive life-history variation and aging rate. Because aerobic metabolism is supposed to be the main source of such oxidative risk, the rate of oxygen consumption should be positively associated with the level of damage and/or antioxidants. Empirical support for such relationships remains unclear, and recent considerations suggest even a negative relationship between metabolic rate and oxidative stress. We investigated the relationship between standard metabolic rate (SMR), antioxidants, and damage in blood plasma and erythrocytes for 35 grass snakes (Natrix natrix). Reactive oxygen metabolites (dROMs) and nonenzymatic antioxidants were assessed in plasma, while two measures of DNA damage and the capacity to neutralize H2O2 were measured in erythrocytes. Plasma antioxidants showed no correlation to SMR, and the level of dROMs was positively related to SMR. A negative relationship between antioxidant capacity and SMR was found in erythrocytes, but no association of SMR with either measure of DNA damage was detected. No increase in DNA damage, despite lower antioxidant capacity at high SMR, indicates an upregulation in other defense mechanisms (e.g., damage repair and/or removal). Indeed, we observed a higher frequency of immature red blood cells in individuals with higher SMR, which indicates that highly metabolic individuals had increased erythrocyte turnover, a mechanism of damage removal. Such DNA protection through upregulated cellular turnover might explain the negligible senescence observed in some ectotherm taxa.

中文翻译:

细胞周转:潜在的代谢率驱动机制,减轻DNA损伤的积累。

氧化应激,活性氧物种和抗氧化能力的不平衡,可能导致对细胞过程至关重要的生物分子(例如DNA)的破坏。这可能会损害生理机能,因此会影响生活史变化和衰老率。因为有氧代谢被认为是这种氧化风险的主要来源,所以耗氧率应与损伤和/或抗氧化剂的含量成正比。对这种关系的经验支持尚不清楚,最近的考虑表明,代谢率与氧化应激之间甚至存在负相关关系。我们调查了35条草蛇(Natrix natrix)的标准代谢率(SMR),抗氧化剂与血浆和红细胞损害之间的关系。在血浆中评估了活性氧代谢产物(dROM)和非酶性抗氧化剂,同时在红血球中测量了两种DNA损伤和中和H2O2的能力。血浆抗氧化剂与SMR无相关性,而dROMs水平与SMR正相关。在红细胞中发现抗氧化能力与SMR之间呈负相关,但未检测到SMR与DNA损伤的任何一种相关性。尽管在高SMR时抗氧化能力较低,但DNA损伤没有增加,表明其他防御机制(例如,损伤修复和/或清除)上调。确实,我们观察到SMR较高的个体中未成熟红细胞的频率较高,这表明高代谢个体的红细胞更新率增加,这是损伤消除的一种机制。
更新日期:2020-02-04
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