Oxidative stress arises from an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, damaging DNA, proteins, and lipids while also modulating immune responses. It plays a central role in neurodegeneration, cancer, chronic fatigue syndrome, and post-viral conditions like Long COVID, with mitochondrial dysfunction and chronic inflammation amplifying redox imbalance. Therapeutic strategies—including antioxidants, Nrf2 activators, lifestyle interventions, and biomarker-guided approaches—aim to restore redox homeostasis, improve cellular function, and mitigate disease progression.
Oxidative Stress and Redox Balance Biochemical Mechanisms, Clinical Relevance, and Therapeutic Perspectives
by Tobias Giesen | M.Sc. SEM, B.Sc. PT
Introduction
Oxidative stress refers to an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses. This imbalance can lead to cellular damage and contributes to the pathophysiology of multiple disorders, including neurodegenerative diseases, cancer, chronic fatigue syndrome (CFS), and Long COVID (Shankar et al., 2025). Increasingly, research highlights the interplay between persistent viral infection, mitochondrial dysfunction, and redox imbalance as underlying contributors to chronic post-viral fatigue syndromes. Understanding these mechanisms is critical for developing targeted therapeutic strategies.
Biochemical Basis of Oxidative Stress
ROS are primarily generated in mitochondria during cellular respiration, particularly at complexes I and III of the electron transport chain. These species include superoxide anions (O2_), hydrogen peroxide (H2O2), and hydroxyl radicals (OH^). Under physiological conditions, ROS are neutralized by endogenous antioxidant systems, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and the non-enzymatic antioxidant glutathione (GSH) (Ighodaro & Akinloye, 2018; Mese et al., 2025). When ROS production exceeds antioxidant capacity, oxidative stress arises, damaging proteins, lipids, and DNA (Murphy, 2008; Zorov et al., 2014).
ROS also act as secondary messengers, modulating signaling pathways such as NF-kB, AP- 1, and Nrf2. Excess ROS activate NF-kB, inducing transcription of pro-inflammatory cytokines including TNF-a, IL-1P, and IL-6, which can perpetuate chronic inflammation (Mittal et al., 2014; Zhang et al., 2023). The Nrf2 pathway, conversely, upregulates antioxidant enzymes and phase II detoxifying proteins. Dysregulation of Nrf2 impairs ROS neutralization, contributing to chronic oxidative stress and cellular dysfunction (Ma, 2013; Ngo et al., 2022).
Oxidative Stress in Disease Contexts
Neurodegenerative Diseases
Neurons are particularly susceptible to oxidative damage due to their high metabolic rate, significant oxygen consumption, and limited capacity for regeneration (Chen et al., 2012; Uttara et al., 2009). Mitochondria in neurons are the primary source of reactive oxygen species (ROS), and age-related or disease-induced mitochondrial dysfunction can exacerbate ROS production, leading to further mitochondrial DNA damage, impaired ATP synthesis, and energy deficits (Dias et al., 2013; Swerdlow et al., 2014).
Oxidative stress contributes to the pathogenesis of neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), through multiple interconnected mechanisms. In AD, ROS promote the accumulation and aggregation of amyloid-beta (Ap) peptides and tau protein, forming amyloid plaques and neurofibrillary tangles that disrupt synaptic function (Uttara et al., 2009; Chen et al., 2012). Lipid peroxidation, a direct consequence of ROS accumulation, damages neuronal membranes and myelin sheaths, impairing signal transmission and contributing to cognitive decline (Markesbery, 1997; Butterfield & Halliwell, 2019).
In Parkinson’s disease, dopaminergic neurons in the substantia nigra are particularly vulnerable due to dopamine metabolism, which itself produces ROS. Oxidative modifications of a-synuclein enhance its propensity to aggregate, leading to Lewy body formation and progressive neuronal death (Dias et al., 2013; Jenner, 2003). Additionally, oxidative stress triggers neuroinflammatory responses through activation of microglia, further amplifying neuronal injury via pro-inflammatory cytokines and nitric oxide-mediated damage (Block et al., 2007).
Amyotrophic lateral sclerosis is similarly characterized by elevated oxidative stress, particularly in motor neurons. Mutations in superoxide dismutase 1 (SOD1) lead to impaired ROS scavenging, accumulation of protein aggregates, mitochondrial dysfunction, and apoptotic cell death (Redler & Dokholyan, 2012). The cumulative effect of ROS on protein misfolding, lipid peroxidation, and DNA damage accelerates neurodegeneration and functional decline.
Elevated biomarkers of oxidative stress, such as 8-hydroxy-2’-deoxyguanosine (8-OHdG), protein carbonyls, and F2-isoprostanes, have been detected in cerebrospinal fluid and brain tissue of patients with AD, PD, and ALS (Uttara et al., 2009; Butterfield & Halliwell, 2019). Notably, these markers are enriched in regions exhibiting prominent neuropathology, such as amyloid plaque-rich areas in Alzheimer’s disease, supporting a causal role for ROS in disease progression (Chen et al., 2012).
Therapeutic strategies aimed at restoring redox balance in neurons include the use of antioxidants, mitochondrial-targeted compounds, and Nrf2 pathway activators, which enhance the expression of endogenous antioxidant enzymes and detoxification proteins (Joshi & Johnson, 2012; Ngo et al., 2022). Early intervention to reduce ROS levels may mitigate mitochondrial damage, prevent protein aggregation, and slow neurodegenerative processes.
Cancer
Cancer cells often exhibit elevated levels of reactive oxygen species (ROS) due to increased metabolic activity and mitochondrial dysfunction. These ROS can act as secondary messengers, activating signaling pathways that promote cell proliferation, survival, and metastasis. For example, ROS can activate the Ras-Raf-MEK-ERK pathway, PI3K/Akt signaling, and transcription factors such as NF-kB and AP-1, which regulate genes involved in growth and apoptosis (Sosa et al., 2013; Hayes et al., 2020). ROS also contribute to epithelial-to- mesenchymal transition (EMT), increasing cell motility and invasiveness, which facilitates metastasis (Sosa et al., 2013).
Paradoxically, the high ROS levels that support tumor progression also make cancer cells vulnerable to oxidative damage. ROS can induce DNA base modifications, single-strand breaks, and double-strand breaks, leading to genomic instability and cell death if repair mechanisms are overwhelmed (Sosa et al., 2013). This vulnerability forms the basis for prooxidant cancer therapies, such as anthracyclines (e.g., doxorubicin) or platinum-based drugs, which elevate intracellular ROS to trigger apoptosis in tumor cells (Hayes et al., 2020).
While antioxidants can mitigate oxidative DNA damage in normal cells, they may also interfere with apoptosis in cancer therapy. Cancer cells often upregulate endogenous antioxidant defenses, including glutathione, SOD, and catalase, to buffer ROS and promote survival (Hayes et al., 2020). Administration of exogenous antioxidants in some therapeutic contexts can reduce ROS-mediated apoptosis, potentially diminishing the efficacy of ROS-inducing chemotherapies. This underscores the necessity of precision redox-targeted strategies in cancer treatment (Sosa et al., 2013; Hayes et al., 2020).
In summary, ROS act as a double-edged sword in oncology: they promote tumor proliferation and metastasis yet create an inherent vulnerability that can be therapeutically exploited. Effective strategies require careful modulation of the redox environment, balancing pro-oxidant therapies with the cellular antioxidant capacity to maximize cancer cell apoptosis while minimizing damage to normal tissues (Sosa et al., 2013; Hayes et al., 2020).
Chronic Fatigue and Post-COVID Syndrome
Patients with CFS or Long COVID exhibit systemic oxidative stress, as evidenced by elevated levels of malondialdehyde (MDA), 8-hydroxy-2’-deoxyguanosine (8-OHdG), protein carbonyls, and oxidized lipids (Lee et al., 2018; Shankar et al., 2025; Maes et al., 2023). These biomarkers correlate strongly with the severity of fatigue, cognitive dysfunction, sleep disturbances, and musculoskeletal weakness. The accumulation of ROS in these patients is believed to disrupt mitochondrial function, leading to impaired ATP production, energy deficits in skeletal muscle, and decreased neuronal efficiency (Naviaux et al., 2016; Tomas et al., 2021).
Persistent immune activation appears to be a key driver of oxidative stress in post-viral fatigue syndromes. Elevated pro-inflammatory cytokines such as TNF-a, IL-6, and IFN-y can stimulate ROS production via NADPH oxidase activation in immune cells, creating a feedforward loop of inflammation and oxidative damage (Klimas et al., 2020). In Long COVID patients, markers of innate immune activation, including elevated neutrophil extracellular traps (NETs) and mitochondrial ROS release from monocytes, have been reported, linking immune dysregulation directly to redox imbalance (Zhang et al., 2023).
Mitochondrial dysfunction further exacerbates oxidative stress in these syndromes. Structural and functional abnormalities in mitochondria, including reduced complex I and III activity, increased membrane permeability, and impaired mitophagy, contribute to excessive ROS accumulation and diminished bioenergetic capacity (Sharma et al., 2022; Tomas et al., 2021). This mitochondrial derangement is particularly relevant for highly metabolically active tissues such as the brain, skeletal muscle, and cardiac tissue, which rely heavily on oxidative phosphorylation for energy.
Therapeutically, interventions that restore mitochondrial function and reduce oxidative stress are of increasing interest. Strategies include supplementation with mitochondrial-targeted antioxidants (e.g., MitoQ, Coenzyme Q10), Nrf2 activators, and lifestyle interventions such as graded exercise therapy and anti-inflammatory nutrition, which have been shown to improve mitochondrial efficiency and reduce systemic ROS levels (Naviaux et al., 2016; Maes et al., 2023; Sharma et al., 2022). Importantly, the timing and intensity of interventions must be carefully calibrated to avoid exacerbating symptoms, particularly in patients with post- exertional malaise.
In summary, systemic oxidative stress in CFS and Long COVID arises from a complex interplay between persistent immune activation and mitochondrial dysfunction. The resulting redox imbalance contributes to fatigue, cognitive impairment, and muscular weakness, highlighting the potential of targeted antioxidant and mitochondrial support therapies to improve clinical outcomes (Lee et al., 2018; Shankar et al., 2025; Tomas et al., 2021).
Redox Imbalance and Inflammation
Oxidative stress not only damages lipids, proteins, and DNA but also exerts profound effects on the immune system. Excess reactive oxygen species (ROS) can activate redox-sensitive transcription factors such as NF-kB and AP-1 in immune cells, leading to upregulation of pro- inflammatory cytokines including TNF-a, IL-1P, and IL-6 (Bellanti et al., 2025; Mittal et al., 2014). This hyperactivation of immune signaling pathways creates a feed-forward loop in which inflammation drives further ROS production, perpetuating chronic inflammation commonly observed in autoimmune diseases, metabolic syndrome, and post-viral syndromes such as Long COVID (Bellanti et al., 2025).
Conversely, reductive stress—characterized by excessive reducing equivalents such as NADH, NADPH, or glutathione—can impair immune cell function. Reductive stress may blunt ROS-mediated signaling necessary for pathogen clearance, inhibit inflammasome activation, and disrupt redox-sensitive signaling cascades in T cells and macrophages (Sies et al., 2017; Bellanti et al., 2025). This imbalance between oxidative and reductive states, or “redox dyshomeostasis,” has been implicated in the pathogenesis of chronic inflammatory conditions, including systemic lupus erythematosus, type 2 diabetes, and persistent post-viral syndromes.
Mitochondrial ROS production in immune cells is a key mediator of this interplay. In activated macrophages and neutrophils, mitochondrial dysfunction elevates ROS, amplifying cytokine production and promoting oxidative tissue damage. Similarly, T cell dysfunction in chronic fatigue and Long COVID is associated with mitochondrial hyperpolarization and redox imbalance, which may reduce proliferative capacity and cytokine regulation (Zhang et al., 2023; Klimas et al., 2020).
Understanding the dynamic between oxidative and reductive stress in immune cells is essential for developing therapies that restore both immune competence and redox homeostasis. Potential interventions include targeted antioxidants, modulators of NAD+/NADH ratios, Nrf2 activators, and lifestyle strategies such as diet, exercise, and stress reduction, which collectively enhance redox balance and modulate immune responses (Bellanti et al., 2025; Sharifi-Rad et al., 2020).
Therapeutic Approaches
Antioxidant Supplementation
Clinical studies have investigated the use of antioxidant supplementation, including vitamins C and E, coenzyme Q10 (CoQ10), and plant-derived polyphenols, to restore redox balance and mitigate oxidative stress in patients with chronic fatigue syndrome (CFS) and Long COVID. These interventions aim to reduce the accumulation of reactive oxygen species (ROS), improve mitochondrial function, and alleviate systemic inflammation, which are all implicated in the pathophysiology of fatigue and cognitive impairment (Forman & Zhang, 2021; Sharifi- Rad et al., 2020; Maes et al., 2023).
Vitamins C and E act as direct ROS scavengers, neutralizing free radicals and protecting cellular lipids, proteins, and DNA from oxidative damage. Coenzyme Q10, a component of the mitochondrial electron transport chain, enhances ATP production and reduces mitochondrial ROS generation, thereby improving cellular energy metabolism (Naviaux et al., 2016). Polyphenols, such as resveratrol, quercetin, and curcumin, exert both antioxidant and antiinflammatory effects through activation of the Nrf2 pathway and inhibition of pro-inflammatory transcription factors like NF-kB (Ngo et al., 2022; Zhan et al., 2021).
Clinical trials have reported moderate improvements in fatigue severity, cognitive performance, and physical function following supplementation with these antioxidants. For instance, CoQ10 supplementation has been associated with increased exercise tolerance and reduced perception of fatigue in CFS patients (Castro-Marrero et al., 2015). Similarly, vitamin C and E supplementation improved markers of oxidative stress and subjective energy levels in small pilot studies of Long COVID patients (Forman & Zhang, 2021; Sharifi-Rad et al., 2020).
Despite these promising findings, results across studies are inconsistent. Variability in dosage, bioavailability, treatment duration, and patient heterogeneity contribute to mixed outcomes. Moreover, some studies have failed to observe significant improvements in fatigue or cognitive function, highlighting the need for individualized approaches and larger randomized controlled trials to determine optimal treatment regimens (Maes et al., 2023; Naviaux et al., 2016).
Emerging evidence suggests that combination therapies targeting both redox balance and mitochondrial support, alongside lifestyle interventions such as graded exercise and antiinflammatory diets, may offer superior clinical benefits by simultaneously addressing multiple pathological mechanisms underlying fatigue and post-viral syndromes (Sharma et al., 2022; Tomas et al., 2021).
In conclusion, antioxidant therapy represents a promising strategy to ameliorate oxidative stress-related symptoms in CFS and Long COVID, but clinical application requires careful consideration of dosing, patient selection, and potential interactions with other interventions (Forman & Zhang, 2021; Sharifi-Rad et al., 2020).
Activation of the Nrf2 Pathway
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of cellular antioxidant defenses, controlling the transcription of genes encoding enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1) (Ngo et al., 2022; Zhan et al., 2021). Under basal conditions, Nrf2 is sequestered in the cytoplasm by Kelch-like ECH-associated protein 1 (Keap1) and targeted for ubiquitin-mediated degradation. Oxidative or electrophilic stress disrupts the Nrf2-Keap1 complex, allowing Nrf2 translocation to the nucleus, where it binds to antioxidant response elements (ARE) and upregulates cytoprotective genes (Ma, 2013).
Phytochemicals such as sulforaphane (found in cruciferous vegetables), curcumin (from turmeric), and resveratrol (from grapes and berries) act as Nrf2 activators. They modify cysteine residues in Keap1 or modulate signaling pathways, thereby stabilizing Nrf2 and enhancing its nuclear translocation (Ngo et al., 2022; Zhan et al., 2021). Activation of Nrf2 results in upregulated antioxidant enzyme expression, reduced ROS accumulation, and protection against oxidative damage in cellular and animal models.
Preclinical studies demonstrate the efficacy of these Nrf2 activators in multiple tissues. In neuronal cultures, sulforaphane protects against Ap-induced oxidative stress, preserves mitochondrial membrane potential, and reduces apoptotic cell death (Tarozzi et al., 2013). Curcumin has been shown to mitigate oxidative stress in cardiomyocytes, improving mitochondrial function and attenuating ischemia-reperfusion injury (Zhan et al., 2021). Resveratrol similarly exerts neuroprotective effects by activating Nrf2 and enhancing endogenous antioxidant defenses in models of neurodegeneration and stroke (Sheng et al., 2020).
Despite promising preclinical data, clinical evidence remains limited. Small trials of sul- foraphane in neurodegenerative diseases and oxidative-stress-related conditions suggest potential benefits in reducing biomarkers of oxidative damage and improving functional outcomes, but results are preliminary and often underpowered (Tarozzi et al., 2013; Ngo et al., 2022). Challenges include variability in bioavailability, metabolism, and optimal dosing, as well as the need for long-term studies to evaluate efficacy and safety.
Targeting the Nrf2 pathway represents a promising strategy for diseases characterized by mitochondrial dysfunction and oxidative stress, including neurodegeneration, chronic fatigue syndromes, cardiovascular disorders, and post-viral syndromes such as Long COVID (Ngo et al., 2022; Zhan et al., 2021). Future research should aim to translate preclinical findings into robust clinical trials, optimize dosing regimens, and evaluate combination therapies with other antioxidants or mitochondrial modulators.
Lifestyle and Behavioral Interventions
Diet, exercise, and stress management significantly influence redox balance. Diets rich in antioxidants from fruits, vegetables, and whole grains enhance endogenous defenses. Moderate exercise stimulates antioxidant enzyme activity and mitigates mitochondrial ROS generation, while excessive training may exacerbate oxidative stress (Radak et al., 2013; Sharifi- Rad et al., 2020). Stress-reducing practices, such as meditation or controlled breathing, modulate neuroendocrine pathways and reduce ROS formation.
Redox Biomarkers for Clinical Monitoring
The measurement of oxidative stress biomarkers provides critical insights into both disease progression and the efficacy of therapeutic interventions. Commonly assessed markers include malondialdehyde (MDA), a product of lipid peroxidation; 8-hydroxy-2’-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage; protein carbonyls, which indicate protein oxidation; and oxidized low-density lipoprotein (ox-LDL), associated with atherosclerosis and cardiovascular risk (Valaitiene et al., 2024; Butterfield & Halliwell, 2019).
Biomarker assessment allows clinicians and researchers to quantify the degree of redox imbalance in patients, providing a surrogate measure of cellular oxidative damage and mitochondrial dysfunction. In chronic fatigue syndrome (CFS) and Long COVID, elevated MDA and 8-OHdG levels have been correlated with fatigue severity, cognitive impairment, and muscular weakness, supporting their role in disease pathophysiology (Lee et al., 2018; Shankar et al., 2025). Similarly, in cardiovascular disease, increased ox-LDL and protein carbonyls are predictive of endothelial dysfunction and progression of atherosclerotic lesions (Valaitiene et al., 2024).
Beyond diagnostic value, oxidative stress biomarkers can guide individualized therapeutic interventions. For example, patients with elevated oxidative stress may benefit from antioxidant supplementation, mitochondrial-targeted therapies, or lifestyle interventions such as diet and exercise, tailored to reduce ROS burden (Sharifi-Rad et al., 2020; Naviaux et al., 2016). Serial measurement of these biomarkers can also monitor treatment response, allowing clinicians to adjust therapy in real-time and potentially improve clinical outcomes (Valaitiene et al., 2024).
Emerging techniques such as high-throughput metabolomics and redox proteomics allow for more comprehensive profiling of oxidative stress status, including identification of novel biomarkers and redox-sensitive pathways. These approaches can improve disease stratification, enable early detection of oxidative damage, and support the development of precision medicine strategies in neurodegenerative disorders, metabolic syndrome, cardiovascular disease, and post-viral syndromes (Tomas et al., 2021; Bellanti et al., 2025).
In conclusion, measurement of oxidative stress biomarkers provides both mechanistic insight and practical clinical utility. Biomarker-guided strategies enable personalized interventions targeting redox imbalance, offering potential to improve outcomes in chronic fatigue, cardiovascular disease, neurodegenerative disorders, and post-viral syndromes (Valaitiene et al., 2024; Lee et al., 2018).
Molecular and Genomic Implications
Oxidative stress compromises genomic integrity by inducing DNA base modifications, singlestrand breaks (SSBs), and double-strand breaks (DSBs), which can interfere with replication and transcription and promote mutagenesis (Li et al., 2025; Carlson et al., 2024). Persistent ROS exposure oxidizes nucleotides, producing lesions such as 8-hydroxy-2’- deoxyguanosine (8-OHdG), which if unrepaired, can result in G-to-T transversions and other mutational events. In addition, ROS can generate clustered DNA lesions, making repair more complex and error-prone, thereby increasing the risk of genomic instability and disease onset, including cancer and neurodegeneration (Cadet et al., 2010; Klaunig et al., 2010).
ROS can also directly impair DNA repair enzymes. Oxidative modifications of proteins involved in base excision repair (BER), nucleotide excision repair (NER), and homologous recombination compromise their activity, reducing the cell’s ability to resolve DNA damage efficiently (Li et al., 2025). This reduction in repair capacity allows mutations to accumulate, promoting tumorigenesis and contributing to age-related pathologies.
Activation of the Nrf2 pathway offers therapeutic potential beyond enhancing antioxidant defenses. Nrf2 upregulates genes involved in detoxification, antioxidant defense, and maintenance of redox homeostasis, while also indirectly supporting DNA repair mechanisms. For instance, Nrf2 activation has been shown to enhance expression of repair enzymes such as OGG1 (8-oxoguanine DNA glycosylase), which removes oxidized guanine lesions, thus protecting genomic integrity under oxidative stress conditions (Carlson et al., 2024; Li et al., 2025).
Therapeutically, targeting Nrf2 with activators such as sulforaphane, curcumin, or resveratrol may simultaneously reduce ROS levels and improve DNA repair capacity, offering dual protection against oxidative damage and mutagenesis. This approach holds promise for preventing disease progression in conditions characterized by chronic oxidative stress, including neurodegenerative disorders, chronic fatigue syndrome, and post-viral syndromes (Ngo et al., 2022; Zhan et al., 2021).
In summary, oxidative stress poses a significant threat to genomic integrity through direct DNA damage and impairment of repair mechanisms. Nrf2 activation provides a crucial protective mechanism by enhancing antioxidant defenses and supporting DNA repair, highlighting its therapeutic relevance in multiple oxidative-stress-related diseases (Li et al., 2025; Carlson et al., 2024).
Future Directions
Despite advances, many mechanistic questions remain. Future research should focus on:
• Identifying specific oxidative stress biomarkers for early disease detection.
• Elucidating the interplay between ROS, immune modulation, and mitochondrial function.
• Conducting large-scale clinical trials on antioxidant therapy, Nrf2 activators, and lifestyle interventions in post-viral fatigue syndromes.
• Exploring combinatorial strategies that integrate pharmacological, nutritional, and behavioral interventions.
Such approaches could significantly enhance the precision and efficacy of treatments for oxidative-stress-related conditions.
Conclusion
Oxidative stress is a central contributor to the pathogenesis of numerous diseases, including neurodegeneration, cancer, chronic fatigue, and post-viral syndromes such as Long COVID. Evidence supports a multipronged approach encompassing antioxidant therapy, Nrf2 activation, lifestyle interventions, and monitoring via redox biomarkers. A comprehensive understanding of redox biology and its clinical applications is crucial for the development of targeted, individualized therapeutic strategies.
Illustrations are not included in the reading sample
About the Author:
Tobias Giesen is a physiotherapist specialized in musculoskeletal physiotherapy. After his Bachelor's degree in Physiotherapy, he studied for a Master of Science in Sport and Exercise Medicine at a British faculty and completed it successfully. His particular interests lie in medical neuroscience, pain medicine, and manual therapy.
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