oxidative stress

Overview

Oxidative stress is a fundamental biological process arising from an imbalance between the production of reactive oxygen species (ROS) and the capacity of cellular antioxidant defense systems to neutralize them. Under normal physiological conditions, ROS such as superoxide anions, hydrogen peroxide, and hydroxyl radicals are generated as byproducts of mitochondrial oxidative phosphorylation and serve essential roles in cell signaling, immune defense, and redox homeostasis. However, when ROS generation overwhelms antioxidant mechanisms — including enzymatic defenses such as superoxide dismutase and catalase, as well as non-enzymatic molecules such as glutathione — the resulting oxidative stress damages cellular macromolecules including lipids, proteins, and DNA. Lipid peroxidation, marked biochemically by elevated malondialdehyde (MDA), represents one of the most widely measured consequences of this imbalance.

Oxidative stress is now recognized as a central, upstream driver linking metabolic dysfunction, chronic inflammation, mitochondrial impairment, and cellular senescence across a remarkably broad spectrum of human diseases. It interacts in reciprocal and self-amplifying cycles with nuclear factor kappa B (NF-κB) signaling, the KEAP1/nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, ferroptosis, autophagy, and apoptotic cascades. Rather than functioning as a downstream epiphenomenon, oxidative stress actively shapes disease progression in conditions ranging from neurodegeneration and cardiovascular disease to diabetic complications, cancer, and aging, making it a high-priority therapeutic target across biomedical research.

Focus of Latest Publications

Recent publications have continued to examine oxidative stress as a central biological process across diverse disease contexts, including pseudoexfoliation syndrome, metabolic phenotypes, air pollution exposure in children, neurodegeneration, septic acute kidney injury, and myocardial infarction. Several studies focused on oxidative stress biomarkers and related redox systems, such as thiol-disulfide homeostasis, superoxide dismutase, and markers of lipid, DNA, and inflammatory injury, to better characterize disease-associated oxidative imbalance and its links to ocular, systemic, metabolic, and environmental factors.

In clinical and epidemiologic research, oxidative stress was assessed alongside comorbidities and exposure patterns. In adults, higher ultra-processed food intake was associated with the hypertriglyceridemic waist phenotype in a dose-response manner, while total ultra-processed food intake was not significantly associated with oxidative stress or inflammation biomarkers; however, some food components, including sweets, were linked to lower superoxide dismutase levels. In children from a high air pollution area, urinary biomarkers of oxidative stress and inflammation were positively correlated with metabolites of several volatile organic compounds and polycyclic aromatic hydrocarbons, and specific exposure markers such as crotonaldehyde and naphthalene were significantly associated with 8-Isop, 8-OHdG, prostaglandin E2, and CC16.

Mechanistic and therapeutic studies also highlighted oxidative stress as a target of intervention. Nicotiflorin was reported to improve septic acute kidney injury in mice and renal cells by restoring mitochondrial function and reducing oxidative stress through the PINK1/Parkin pathway, with accompanying changes in ROS, mitochondrial membrane potential, Nrf2, KEAP1, LC3II/LC3I, and p62. A heart-homed nanomedicine designed for rapid mitochondrial rescue after myocardial infarction similarly acted by modulating mitochondrial membrane potential and oxidative stress, leading to reduced cardiomyocyte loss, inflammation, and fibrosis. In neurodegenerative and aging-related research, Broussonetia papyrifera fruit extract was studied for its ability to disrupt the reciprocal amplification between Aβ proteotoxicity and oxidative stress in Alzheimer’s disease models, while broader reviews described natural products, antioxidants, and integrative topical/internal strategies as approaches that may alleviate oxidative stress in aging and longevity contexts.

Overall, these publications reinforce oxidative stress as a convergent mechanism linking environmental exposure, diet, mitochondrial dysfunction, inflammation, and disease progression. The studies collectively used biomarker profiling, cell and animal models, and review-based synthesis to explore how oxidative stress interacts with pathways such as PINK1/Parkin, Nrf2/KEAP1, and autophagy-related signaling, and how modulation of this process may support prevention or treatment across multiple biomedical settings.

Key Publications

NEWJun Assesment of oxidative stress and antioxidant status in pseudoexfoliation syndrome with ocular and systemic comorbidities. (International ophthalmology, 2026, PMID 42371156): "This study aimed to investigate oxidative stress (OS) markers and thiol-disulfide homeostasis (TDH) in patients with pseudoexfoliation (PEX) syndrome and to investigate their associations with ocular and systemic comorbidities."
NEWJun Association of ultra-processed foods (UPFs) with hypertriglyceridemic waist (HTGW) phenotype, oxidative stress, and inflammation in Iranian adults: a cross-sectional study. (Food & function, 2026, PMID 42300027): "Additionally, biomarkers of oxidative stress and inflammation were measured."
Jun Urinary Biomarkers of Exposure and Effect in California Schoolchildren From a High Air Pollution Area. (Environmental and molecular mutagenesis, 2026, PMID 42219792): "This pilot study investigates biomarkers of oxidative stress and inflammation and their association with urinary biomarkers of air pollutant exposure in children."
Apr Integrative Dermatology for Longevity: The Synergy of Topical and Internal Approaches. (Dermatology and therapy, 2026, PMID 41926038): "By targeting key hallmarks of aging, oxidative stress, inflammation, and epigenetic changes, this dual-modality model has the potential to promote skin regeneration, enhance aesthetic and functional outcomes, and contribute to broader health span optimization."
Jun Arthrospira platensis prevents impairment of intestinal smooth muscle relaxation in diet-induced obesity via modulation of nitric oxide, prostanoid and oxidative stress pathways. (Journal of ethnopharmacology, 2026, PMID 41833761): "Arthrospira platensis prevents impairment of intestinal smooth muscle relaxation in diet-induced obesity via modulation of nitric oxide, prostanoid and oxidative stress pathways."
Apr Mechanistic Modulation of Autophagy by Bioactive Natural Products: Implications for Human Aging and Longevity. (Nutrients, 2026, PMID 41830033): "Mechanistically, these compounds regulate autophagy by modulating key signaling pathways, such as AMPK, PI3K/AKT/mTOR, SIRT1, and FOXO, while also alleviating oxidative stress, inflammation, and mitochondrial dysfunction."
Apr Broussonetia papyrifera fruit extract attenuates Alzheimer's pathogenesis via disrupting the vicious cycle of Aβ and oxidative stress in C. elegans and cellular models. (Journal of ethnopharmacology, 2026, PMID 41819509): "This study aimed to investigate whether the ethyl acetate fraction of FB (FBA) could attenuate AD pathogenesis by disrupting the reciprocal exacerbation between Aβ proteotoxicity and oxidative stress."
Apr Efficacy of nicotiflorin in ameliorating septic acute kidney injury: the role of PINK1/parkin in mitochondrial restoration and oxidative stress reduction. (Renal failure, 2026, PMID 41730753): "...whether nicotiflorin restores mitochondrial function and reduces oxidative stress in septic AKI via mediating the PTEN-induced putative protein kinase 1 (PINK1)/Parkin signaling pathway."
Apr Heart-homed nanomedicine induces fast mitochondrial rescue to enhance cardiac function post-myocardial infarction. (Bioactive materials, 2026, PMID 41696142): "By synergistically modulating mitochondrial membrane potential (MMP) and oxidative stress, H-FAME stabilizes mitochondrial function, thereby attenuating cardiomyocyte loss, inflammation, and fibrosis and ultimately promoting functional recovery after MI."