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运动诱导的DNA损伤:与炎症反应有关系吗?

Exercise-induced DNA damage: is there a relationship with inflammatory responses?

作者信息

Neubauer Oliver, Reichhold Stefanie, Nersesyan Armen, König Daniel, Wagner Karl-Heinz

机构信息

Department of Nutritional Sciences, Faculty of Life Sciences, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.

出版信息

Exerc Immunol Rev. 2008;14:51-72.

Abstract

Both a systemic inflammatory response as well as DNA damage has been observed following exhaustive endurance exercise. Hypothetically, exercise-induced DNA damage might either be a consequence of inflammatory processes or causally involved in inflammation and immunological alterations after strenuous prolonged exercise (e.g. by inducing lymphocyte apoptosis and lymphocytopenia). Nevertheless, up to now only few studies have addressed this issue and there is hardly any evidence regarding a direct relationship between DNA or chromosomal damage and inflammatory responses in the context of exercise. The most conclusive picture that emerges from available data is that reactive oxygen and nitrogen species (RONS) appear to be the key effectors which link inflammation with DNA damage. Considering the time-courses of inflammatory and oxidative stress responses on the one hand and DNA effects on the other the lack of correlations between these responses might also be explained by too short observation periods. This review summarizes and discusses the recent findings on this topic. Furthermore, data from our own study are presented that aimed to verify potential associations between several endpoints of genome stability and inflammatory, immune-endocrine and muscle damage parameters in competitors of an Ironman triathlon until 19 days into recovery. The current results indicate that DNA effects in lymphocytes are not responsible for exercise-induced inflammatory responses. Furthermore, this investigation shows that inflammatory processes, vice versa, do not promote DNA damage, neither directly nor via an increased formation of RONS derived from inflammatory cells. Oxidative DNA damage might have been counteracted by training- and exercise-induced antioxidant responses. However, further studies are needed that combine advanced -omics based techniques (transcriptomics, proteomics) with state-of-the-art biochemical biomarkers to gain more insights into the underlying mechanisms.

摘要

在力竭性耐力运动后,已观察到全身炎症反应以及DNA损伤。据推测,运动诱导的DNA损伤可能是炎症过程的结果,或者在剧烈长时间运动后因果性地参与炎症和免疫改变(例如通过诱导淋巴细胞凋亡和淋巴细胞减少)。然而,到目前为止,只有少数研究涉及这个问题,并且几乎没有证据表明在运动背景下DNA或染色体损伤与炎症反应之间存在直接关系。现有数据得出的最确凿情况是,活性氧和氮物种(RONS)似乎是将炎症与DNA损伤联系起来的关键效应物。考虑到一方面炎症和氧化应激反应的时间进程,另一方面DNA效应,这些反应之间缺乏相关性也可能是由于观察期太短。本综述总结并讨论了关于该主题的最新发现。此外,还展示了我们自己研究的数据,该研究旨在验证铁人三项赛参赛者在恢复至19天期间基因组稳定性的几个终点与炎症、免疫内分泌和肌肉损伤参数之间的潜在关联。目前的结果表明,淋巴细胞中的DNA效应并非运动诱导的炎症反应的原因。此外,这项研究表明,反之,炎症过程既不直接也不通过炎症细胞衍生的RONS形成增加来促进DNA损伤。氧化DNA损伤可能已被训练和运动诱导的抗氧化反应抵消。然而,需要进一步的研究将基于先进“组学”的技术(转录组学、蛋白质组学)与最先进的生化生物标志物相结合,以更深入了解潜在机制。

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