Markers of oxidative stress during post-COVID-19 fatigue: a hypothesis-generating, exploratory pilot study on hospital employees

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Abstract

Introduction

Post-COVID-19 fatigue is common after recovery from COVID-19. Excess formation of reactive oxygen species (ROS) leading to oxidative stress-related mitochondrial dysfunction is referred to as a cause of these chronic fatigue-like symptoms. The present observational pilot study aimed to investigate a possible relationship between the course of ROS formation, subsequent oxidative stress, and post-COVID-19 fatigue.

Method

A total of 21 post-COVID-19 employees of the General Hospital Nuremberg suffering from fatigue-like symptoms were studied during their first consultation (T1: on average 3 months after recovery from COVID-19), which comprised an educational talk on post-COVID-19 symptomatology and individualized outpatient strategies to resume normal activity, and 8 weeks thereafter (T2). Fatigue severity was quantified using the Chalder Fatigue Scale together with a health survey (Patient Health Questionnaire) and self-report on wellbeing (12-Item Short-Form Health Survey). We measured whole blood superoxide anion ( $O_{2}^{• -}$ ) production rate (electron spin resonance, as a surrogate for ROS production) and oxidative stress-induced DNA strand breaks (single cell gel electrophoresis: “tail moment” in the “comet assay”).

Results

Data are presented as mean ± SD or median (interquartile range) depending on the data distribution. Differences between T1 and T2 were tested using a paired Wilcoxon rank sign or t-test. Fatigue intensity decreased from 24 ± 5 at T1 to 18 ± 8 at T2 ( p < 0.05), which coincided with reduced $O_{2}^{• -}$ formation (from 239 ± 55 to 195 ± 59 nmol/s; p < 0.05) and attenuated DNA damage [tail moment from 0.67 (0.36–1.28) to 0.32 (0.23–0.71); p = 0.05].

Discussion

Our pilot study shows that post-COVID-19 fatigue coincides with (i) enhanced $O_{2}^{• -}$ formation and oxidative stress, which are (ii) reduced with attenuation of fatigue symptoms.

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Most cited references 40

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The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection.

J E Ware, C Sherbourne (1992)

A 36-item short-form (SF-36) was constructed to survey health status in the Medical Outcomes Study. The SF-36 was designed for use in clinical practice and research, health policy evaluations, and general population surveys. The SF-36 includes one multi-item scale that assesses eight health concepts: 1) limitations in physical activities because of health problems; 2) limitations in social activities because of physical or emotional problems; 3) limitations in usual role activities because of physical health problems; 4) bodily pain; 5) general mental health (psychological distress and well-being); 6) limitations in usual role activities because of emotional problems; 7) vitality (energy and fatigue); and 8) general health perceptions. The survey was constructed for self-administration by persons 14 years of age and older, and for administration by a trained interviewer in person or by telephone. The history of the development of the SF-36, the origin of specific items, and the logic underlying their selection are summarized. The content and features of the SF-36 are compared with the 20-item Medical Outcomes Study short-form.

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Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release.

Dmitry Zorov, Magdalena Juhaszova, Steven J. Sollott (2014)

Byproducts of normal mitochondrial metabolism and homeostasis include the buildup of potentially damaging levels of reactive oxygen species (ROS), Ca(2+), etc., which must be normalized. Evidence suggests that brief mitochondrial permeability transition pore (mPTP) openings play an important physiological role maintaining healthy mitochondria homeostasis. Adaptive and maladaptive responses to redox stress may involve mitochondrial channels such as mPTP and inner membrane anion channel (IMAC). Their activation causes intra- and intermitochondrial redox-environment changes leading to ROS release. This regenerative cycle of mitochondrial ROS formation and release was named ROS-induced ROS release (RIRR). Brief, reversible mPTP opening-associated ROS release apparently constitutes an adaptive housekeeping function by the timely release from mitochondria of accumulated potentially toxic levels of ROS (and Ca(2+)). At higher ROS levels, longer mPTP openings may release a ROS burst leading to destruction of mitochondria, and if propagated from mitochondrion to mitochondrion, of the cell itself. The destructive function of RIRR may serve a physiological role by removal of unwanted cells or damaged mitochondria, or cause the pathological elimination of vital and essential mitochondria and cells. The adaptive release of sufficient ROS into the vicinity of mitochondria may also activate local pools of redox-sensitive enzymes involved in protective signaling pathways that limit ischemic damage to mitochondria and cells in that area. Maladaptive mPTP- or IMAC-related RIRR may also be playing a role in aging. Because the mechanism of mitochondrial RIRR highlights the central role of mitochondria-formed ROS, we discuss all of the known ROS-producing sites (shown in vitro) and their relevance to the mitochondrial ROS production in vivo. Copyright © 2014 the American Physiological Society.

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Is Open Access

Oxidative Stress: Harms and Benefits for Human Health

Gabriele Pizzino, Natasha Irrera, Mariapaola Cucinotta … (2017)

Oxidative stress is a phenomenon caused by an imbalance between production and accumulation of oxygen reactive species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products. ROS can play, and in fact they do it, several physiological roles (i.e., cell signaling), and they are normally generated as by-products of oxygen metabolism; despite this, environmental stressors (i.e., UV, ionizing radiations, pollutants, and heavy metals) and xenobiotics (i.e., antiblastic drugs) contribute to greatly increase ROS production, therefore causing the imbalance that leads to cell and tissue damage (oxidative stress). Several antioxidants have been exploited in recent years for their actual or supposed beneficial effect against oxidative stress, such as vitamin E, flavonoids, and polyphenols. While we tend to describe oxidative stress just as harmful for human body, it is true as well that it is exploited as a therapeutic approach to treat clinical conditions such as cancer, with a certain degree of clinical success. In this review, we will describe the most recent findings in the oxidative stress field, highlighting both its bad and good sides for human health.

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Author and article information

Contributors

Hanna Hofmann: URI : http://loop.frontiersin.org/people/2421850/overviewRole: Role: Role: Role: Role: Role: Role: Role: Role: Role:

Alexandra Önder: Role: Role: Role: Role: Role: Role:

Juliane Becker: Role: Role:

Michael Gröger: Role: Role: Role: Role:

Markus M. Müller: URI : http://loop.frontiersin.org/people/2370307/overviewRole: Role: Role: Role: Role: Role: Role:

Fabian Zink: URI : http://loop.frontiersin.org/people/811796/overviewRole: Role: Role: Role:

Barbara Stein: URI : http://loop.frontiersin.org/people/475967/overviewRole: Role: Role: Role: Role: Role:

Peter Radermacher: URI : http://loop.frontiersin.org/people/580485/overviewRole: Role: Role: Role: Role: Role:

Christiane Waller: URI : http://loop.frontiersin.org/people/927806/overviewRole: Role: Role: Role: Role: Role: Role:

Journal

Journal ID (nlm-ta): Front Med (Lausanne)

Journal ID (iso-abbrev): Front Med (Lausanne)

Journal ID (publisher-id): Front. Med.

Title: Frontiers in Medicine

Publisher: Frontiers Media S.A.

ISSN (Electronic): 2296-858X

Publication date (Electronic): 04 December 2023

Publication date Collection: 2023

Volume: 10

Electronic Location Identifier: 1305009

Affiliations

[1] ¹Department of Psychosomatic Medicine and Psychotherapy, General Hospital Nuremberg, Paracelsus Medical University , Nuremberg, Germany

[2] ²Anesthesiological Pathophysiology and Process Engineering, University Hospital , Ulm, Germany

Author notes

Edited by: César Fernández-de-las-Peñas, Rey Juan Carlos University, Spain

Reviewed by: Hussein Kadhem Al-Hakeim, University of Kufa, Iraq; Nikolaos Papagiannakis, Eginition Hospital, Greece

*Correspondence: Hanna Hofmann hanna.hofmann@ 123456klinikum-nuernberg.de

†These authors have contributed equally to this work and share first authorship

Article

DOI: 10.3389/fmed.2023.1305009

PMC ID: 10725950

PubMed ID: 38111693

SO-VID: 7a3ed4a3-74a1-479e-b140-5945821e0235

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

History

Date received : 30 September 2023

Date accepted : 13 November 2023

Page count

Figures: 2, Tables: 1, Equations: 0, References: 42, Pages: 8, Words: 5770

Funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by the Verein zur Förderung des Tumorzentrums der Universität Erlangen-Nürnberg e.V. (HH) and the Deutsche Forschungsgemeinschaft (DFG: grant number Project-ID 251293561–Collaborative Research Center (CRC) 1149 Project B03) (PR).

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section-at-acceptance Infectious Diseases: Pathogenesis and Therapy

Keywords: reactive oxygen species (ros),oxidative stress,oxidative dna damage,mitochondrial dysfunction,post-covid-19 fatigue

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Keywords: reactive oxygen species (ros), oxidative stress, oxidative dna damage, mitochondrial dysfunction, post-covid-19 fatigue

Markers of oxidative stress during post-COVID-19 fatigue: a hypothesis-generating, exploratory pilot study on hospital employees

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Abstract

Introduction

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Results

Discussion

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Novel Coronavirus Disease COVID-19

Most cited references 40

The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection.

Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release.

Oxidative Stress: Harms and Benefits for Human Health

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