Antioxidants

16 pages, 546 KB

Open AccessSystematic Review

The Role of Antioxidant Minerals in the Pathophysiology and Treatment of Endometriosis—Systematic Review

by Kamila Pokorska-Niewiada, Maciej Ziętek, Iwona Szydłowska, Karina Ryterska and Małgorzata Szczuko

Antioxidants 2025, 14(10), 1238; https://doi.org/10.3390/antiox14101238 (registering DOI) - 15 Oct 2025

Abstract

Endometriosis (EM) is a chronic gynecological disease of women of reproductive age. Due to the lack of a known cause, treatment is limited to reducing symptoms associated with pelvic pain and infertility. The aim was to determine the contribution of minerals and their [...] Read more.

Endometriosis (EM) is a chronic gynecological disease of women of reproductive age. Due to the lack of a known cause, treatment is limited to reducing symptoms associated with pelvic pain and infertility. The aim was to determine the contribution of minerals and their supplementation to the EM. This systematic review was conducted in accordance with the PRISMA guidelines. The literature was searched in four databases: PubMed, Scopus, Web of Science and Google Scholar for the keywords ‘oxidative stress’, ‘supplementation’, ‘trace elements’, ‘metalloestrogens’, ‘antioxidants’, ‘zinc’, ‘copper’, ‘manganese’, “selenium”, ‘Zn/Cu’ and ‘molybdenum’ published by the end of June 2025. It turns out that there are significant differences in the biochemical analysis of elements between women with EM and healthy women. Most studies showed decreased zinc levels in women with EM, and copper and molybdenum were usually in comparable amounts, whereas the results for selenium are inconclusive. The lack of direct clinical trials of antioxidant element supplementation, coupled with evidence of differences in their levels between women with EM and healthy women, warrants further, more detailed analysis. Studies should be expanded to include dose–response analyses and potential threshold effects. This will allow for the assessment of the clinical usefulness of supplementation or dietary enrichment as an adjunctive therapeutic approach in the treatment of EM symptoms. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases, 2nd Edition)

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22 pages, 608 KB

Open AccessReview

The Heme Oxygenase/Biliverdin Reductase System as a Therapeutic Target to Counteract Cellular Senescence in Alzheimer’s Disease

by Cesare Mancuso

Antioxidants 2025, 14(10), 1237; https://doi.org/10.3390/antiox14101237 (registering DOI) - 15 Oct 2025

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disorder involving free radical overload, neuroinflammation, and a deranged cell stress response. In particular, the modulation of the heme oxygenase/biliverdin reductase (HO/BVR) system, a key component of the brain stress response, is currently regarded as a promising [...] Read more.

Alzheimer’s disease (AD) is a neurodegenerative disorder involving free radical overload, neuroinflammation, and a deranged cell stress response. In particular, the modulation of the heme oxygenase/biliverdin reductase (HO/BVR) system, a key component of the brain stress response, is currently regarded as a promising therapeutic approach for AD. Cellular senescence, defined as a process of cell cycle arrest due to oxidative stress, DNA damage, mitochondrial dysfunction, and oncogene activation, has been identified as a pivotal factor in the development of AD. A mounting body of research has demonstrated that the accumulation of senescent cells in the brain can lead to a variety of neurotoxic effects, including synaptic dysfunction, the destruction of the blood–brain barrier, and impaired remyelination. Finally, the release of proinflammatory molecules by senescent cells further exacerbates neurodegeneration. A considerable number of xenobiotics, with well-documented neuroprotective effects through the activation of the HO/BVR system, have been shown to modulate pathways involved in cellular senescence outside the brain. Unfortunately, a direct link between HO/BVR and cellular senescence in AD is yet to be established. This compelling evidence should motivate basic and clinical researchers to address such a significant gap in knowledge and conduct novel studies in this field. Full article

(This article belongs to the Special Issue Oxidative Stress and Its Mitigation in Neurodegenerative Disorders)

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21 pages, 8200 KB

Open AccessArticle

Role of Cell Oxidant Status and Redox State in Controlling Cell Proliferation and Apoptosis in Two Models of Wallerian Degeneration of Rat Sciatic Nerve

by Myrna Alexandra Roberta Dent, Alejandro Martínez-Gómez and Rolando Hernández-Muñoz

Antioxidants 2025, 14(10), 1236; https://doi.org/10.3390/antiox14101236 - 15 Oct 2025

Abstract

After peripheral nerve lesion, the role of reactive oxygen species (ROS) has not been clarified during Wallerian degeneration. The present study examined the participation of oxidant stress after rat sciatic nerve injury induced by two experimental models (crush and transection). Here, biochemical parameters [...] Read more.

After peripheral nerve lesion, the role of reactive oxygen species (ROS) has not been clarified during Wallerian degeneration. The present study examined the participation of oxidant stress after rat sciatic nerve injury induced by two experimental models (crush and transection). Here, biochemical parameters indicative of oxidant stress, nitric oxide (NO) metabolism, cell proliferation, apoptosis, and bioenergetics were determined in injured and contralateral sciatic nerves and caudofemoralis muscle. After crushing, we found two peaks of increased lipid peroxidation (LP) by-products and carbonylation of proteins in crushed nerves. In transected nerves, increases in LP showed similar patterns in both proximal and distal nerve. In both models, NO production was decreased and accompanied by an early increase in cell proliferation. Moreover, caspase-3 activity increased later only in crushed nerves. NAD availability and mitochondrial cytochrome oxidase activity were increased in transected but not in crushed nerves. The contralateral nerves also had changes in these parameters, but in a differential manner depending on the type of nerve lesion. In conclusion, present data suggest that changes in the patterns of LP may play a regulatory role in cell damage and death, somehow exerting a control in the progression of Wallerian degeneration. Full article

(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)

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20 pages, 5831 KB

Open AccessArticle

Androgen-Induced Lactic Acid Accumulation Contributes to the Apoptosis of Ovarian Granulosa Cells in Polycystic Ovary Syndrome Mice

by Bining Zhao, Liting Fan, Mengfei Liu, Haowen Wu, Youyou Zhang, Qiyang Shen and Jihong Kang

Antioxidants 2025, 14(10), 1235; https://doi.org/10.3390/antiox14101235 - 14 Oct 2025

Abstract

Background: Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility. The apoptosis of granulosa cells (GCs) is strongly associated with the impaired follicular development in PCOS. The underlying mechanisms, however, remain incompletely elucidated. A significant increase in circulating lactic acid, an [...] Read more.

Background: Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility. The apoptosis of granulosa cells (GCs) is strongly associated with the impaired follicular development in PCOS. The underlying mechanisms, however, remain incompletely elucidated. A significant increase in circulating lactic acid, an anaerobic respiration product, has been detected in PCOS patients. Yet, alterations in local ovarian lactic acid levels and their impact on GCs remain unknown. Methods: PCOS mouse models were established via 20-day daily subcutaneous dehydroepiandrosterone (DHEA) injections. In vitro experiments utilized DHEA-treated KGN cells to mimic hyperandrogenic conditions. Circulating, ovarian, and cellular lactic acid concentrations were quantified. Intracellular and extracellular pH values were measured using BCECF-AM fluorescent probe and a blood gas analyzer, respectively. Apoptosis was assessed through both flow cytometry and TUNEL assay. The antioxidant N-acetylcysteine (NAC) was used to investigate its effects on lactic acid levels and the subsequent GC apoptosis. Results: High androgen levels caused mitochondrial damage, promoted anaerobic glycolysis and led to lactic acid accumulation, inducing decreased intracellular pH and thus apoptosis of GCs. The antioxidant NAC effectively alleviated oxidative stress, mitigated mitochondrial damage, and decreased lactic acid levels and apoptosis in KGN cells. In PCOS mice, NAC improved ovarian morphology, but it did not affect the estrous cycle of the mice. Conclusions: Hyperandrogenemia-induced mitochondrial dysfunction caused the accumulation of lactic acid and thus apoptosis of ovarian GCs in PCOS mice. NAC enhanced mitochondrial function, consequently decreasing lactic acid concentrations. These findings suggest novel therapeutic targets for PCOS. Full article

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Graphical abstract

19 pages, 1978 KB

Open AccessArticle

Natural Deep Eutectic Solvent (NaDES) Extraction, HPLC-DAD Analysis, and Antioxidant Activity of Chilean Ugni molinae Turcz. Fruits

by Javier Antileo-Laurie, Verónica Olate-Olave, Valentina Fehrmann-Riquelme, Camila Anabalón-Alvarez, Luis Cid-Carrillo, Javier Campanini-Salinas, Carlos Fernández-Galleguillos and Luisa Quesada-Romero

Antioxidants 2025, 14(10), 1234; https://doi.org/10.3390/antiox14101234 - 14 Oct 2025

Abstract

The demand for sustainable methods to extract bioactive compounds from native fruits is increasing. We evaluated the potential of natural deep eutectic solvents (NaDES) combined with ultrasound-assisted extraction (UAE) to recover phenolic compounds from Ugni molinae Turcz. (murta), a Chilean fruit with recognized [...] Read more.

The demand for sustainable methods to extract bioactive compounds from native fruits is increasing. We evaluated the potential of natural deep eutectic solvents (NaDES) combined with ultrasound-assisted extraction (UAE) to recover phenolic compounds from Ugni molinae Turcz. (murta), a Chilean fruit with recognized ethnopharmacological and antioxidant value. Seven choline chloride-based NaDESs (M1–M7) were assessed and compared with conventional methanol: formic acid extraction (M8). The choline chloride: 1,2-propanediol system (1:2, M2) achieved the highest recovery of total phenolics (64.87 mg GAE/g) and flavonoids (35.38 mg QE/g), together with strong antioxidant activity (DPPH IC₅₀: 1.05 µg/mL; ORAC: 40,291 µmol TE/g). When comparing the different NaDES formulations (M1–M8), M8 displayed superior FRAP and ORAC values, although its phenolic and flavonoid yields were lower, reflecting differences in solvent selectivity. HPLC-DAD analysis further revealed that NaDES, particularly M5 (choline chloride: oxalic acid, 1:1), favored the extraction of flavonoid and anthocyanin-type compounds. Multivariate and PCA analyses showed distinct chemical profiles in NaDES extracts, forming two clusters apart from M8. Pearson correlation analysis linked antioxidant capacity with major flavonoids. Overall, NaDES combined with UAE represents an efficient, green strategy for selectively recovering bioactives, supporting applications in foods, nutraceuticals, and health products from Chilean native fruits. Full article

(This article belongs to the Special Issue Antioxidant Research in Chile—2nd Edition)

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24 pages, 1251 KB

Open AccessReview

Nicotinism vs. Glomerulopathies—Smoking as a Risk Factor for Primary Glomerulopathies

by Magdalena Dzięgiel, Aleksandra Maciejowska, Marek Misiak and Katarzyna A. Lisowska

Antioxidants 2025, 14(10), 1233; https://doi.org/10.3390/antiox14101233 - 14 Oct 2025

Abstract

Smoking cigarettes affects the human body on many levels—not only are the lungs and heart targeted, but also other organs, directly and through derived alterations. We decided to parallel the impacts most often described in the literature in the hope of better future [...] Read more.

Smoking cigarettes affects the human body on many levels—not only are the lungs and heart targeted, but also other organs, directly and through derived alterations. We decided to parallel the impacts most often described in the literature in the hope of better future targeting regarding treatment for smoke-induced renal injury. As a result of our research, it is clear that damage is mostly localized directly in vessels and glomeruli. We perceive it as a connected web, where oxidative stress leads to local inflammation, general inflammation in the form of obesity, or inflammation due to nasopharyngeal infection. It later affects other types of tissues: podocytes, epithelium in both glomeruli, renal tubules, and vessels. We mention major molecules proven to participate in kidney damage that tend to be similar in all disease entities depicted in this study: IgA nephropathy, membranous nephropathy, and minimal change disease. Moreover, as nicotine is a major component of both classic cigarettes and electronic cigarettes, we decided to approximate and summarize the information on its impact on primary glomerulopathies. Full article

(This article belongs to the Special Issue Cigarette Smoke and Oxidative Stress)

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27 pages, 2246 KB

Open AccessArticle

Bioactive Compounds, Antioxidant, Antimicrobial and Anticancerogenic Activity in Lacmellea edulis H. Karst., at Different Stages of Maturity

by Elena Coyago-Cruz, Johana Zúñiga-Miranda, Gabriela Méndez, Melany Alomoto, Steven Vélez-Vite, Carlos Barba-Ostria, Rebeca Gonzalez-Pastor and Jorge Heredia-Moya

Antioxidants 2025, 14(10), 1232; https://doi.org/10.3390/antiox14101232 - 14 Oct 2025

Abstract

Lacmellea edulis, traditionally known as chicle, is a species that has received little attention despite its nutraceutical potential. This study aimed to evaluate the physicochemical characteristics (pH, soluble solids, titratable acidity, moisture, ash, and minerals) and the content of bioactive compounds (vitamin [...] Read more.

Lacmellea edulis, traditionally known as chicle, is a species that has received little attention despite its nutraceutical potential. This study aimed to evaluate the physicochemical characteristics (pH, soluble solids, titratable acidity, moisture, ash, and minerals) and the content of bioactive compounds (vitamin C, organic acids, carotenoids, and phenols) of fruits at different stages of ripeness, as well as their antimicrobial (against Candida albicans, Candida tropicalis, Escherichia coli, Staphylococcus aureus, and Streptococcus mutans), antiproliferative and antihaemolytic activity. Bioactive compounds were quantified using liquid chromatography, while biological activities were assessed via spectrophotometric assays. The results revealed a high concentration of ascorbic acid in the ripe pulp (3.0 mg/100 g DW), higher levels of organic acids in the unripe pulp (3947.6 mg/100 g DW), and a high total phenol content in the ripe peel (10,890.9 mg/100 g DW). The peel exhibited the highest antioxidant activity (63.3 mmol ET/100 g DW). Regarding antimicrobial activity, the pulp exhibited the lowest MIC values against E. coli (2.7 mg/mL) and S. mutans (2.6 mg/mL), the peel against S. aureus (21.3 mg/mL) and C. tropicalis (5.3 mg/mL), and the seeds against C. albicans (20.8 mg/mL). Additionally, the peel exhibited the greatest antiproliferative efficacy against cervical (HeLa) and hepatoma (HepG2) cancer cells. None of the evaluated extracts showed significant haemolytic effects, confirming their safety. Overall, L. edulis appears to be a promising source of bioactive metabolites with potential applications in functional foods and pharmaceutical products. Full article

(This article belongs to the Special Issue Plant Polyphenols in Human Health: Emerging Insights for Future Therapeutic Strategies)

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16 pages, 2343 KB

Open AccessArticle

The Vasomotor Impact of Cu/ZnSODs Is Higher in Arterial Smooth Muscle of Early Postnatal Rats Compared to Adult Animals

by Anastasia A. Shvetsova, Valentina S. Shateeva, Dmitry S. Semenovich, Rudolf Schubert and Dina K. Gaynullina

Antioxidants 2025, 14(10), 1231; https://doi.org/10.3390/antiox14101231 - 14 Oct 2025

Abstract

The mechanisms of vascular tone regulation during early postnatal ontogenesis differ considerably from those in adulthood. We tested the hypothesis that the vasomotor influence of superoxide dismutases is higher in arteries of rats shortly after birth compared to adult animals. Saphenous arteries of [...] Read more.

The mechanisms of vascular tone regulation during early postnatal ontogenesis differ considerably from those in adulthood. We tested the hypothesis that the vasomotor influence of superoxide dismutases is higher in arteries of rats shortly after birth compared to adult animals. Saphenous arteries of 10 to 15 day (“young”) and 3 to 4 month (“adult”) old rats were studied using quantitative PCR, spectrophotometry, Western blotting, and isometric myography. Sod3 mRNA was most abundant in both adult and young saphenous arteries. Total SOD activity, Cu/ZnSODs activity, and SOD3 protein content were higher in young compared to adult arteries. H₂O₂ caused vessel contraction, while elimination of H₂O₂ weakened contractile responses of endothelium-denuded young arteries. The Cu/ZnSOD inhibitor DETC had no influence on contraction of adult arteries, but weakened contraction of endothelium-denuded, but not endothelium-intact arteries of young rats. The latter effect was observed in the presence of the NO-synthase inhibitor L-NNA, but not with the soluble guanylate cyclase inhibitor ODQ. DETC had no effect in the presence of sodium nitroprusside. Thus, Cu/ZnSODs promote contraction of saphenous arteries in the early postnatal period, but not in adult age. This influence of Cu/ZnSODs is counteracted by endothelial NO in early postnatal arteries. Full article

(This article belongs to the Special Issue Oxidative Stress in the Newborn)

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23 pages, 4462 KB

Open AccessArticle

Rosiglitazone Ameliorates Adverse Effects of High-Fat Diet in Largemouth Bass (Micropterus salmoides): Modulation of Lipid Metabolism, Antioxidant Capacity, Inflammatory Response, and Gut Microbiota

by Ying Yan, Yanjie Tang, Xiting Chen, Xuan Chen, Muzi Zhang, Dexiang Feng and Ming Li

Antioxidants 2025, 14(10), 1230; https://doi.org/10.3390/antiox14101230 - 14 Oct 2025

Abstract

High-fat (HF) diets are widely used in aquaculture to reduce feed costs, but they often lead to hepatic steatosis, oxidative stress, and reduced environmental tolerance in carnivorous fish. This study evaluated whether dietary rosiglitazone (RO; 10 mg·kg⁻¹) alleviates HF (18% fat) [...] Read more.

High-fat (HF) diets are widely used in aquaculture to reduce feed costs, but they often lead to hepatic steatosis, oxidative stress, and reduced environmental tolerance in carnivorous fish. This study evaluated whether dietary rosiglitazone (RO; 10 mg·kg⁻¹) alleviates HF (18% fat) diet-induced metabolic dysfunctions in juvenile largemouth bass (Micropterus salmoides). Fish were fed a control diet (10% fat), an HF diet (18% fat), or an HF + RO diet for 8 weeks. RO supplementation reversed HF-induced dyslipidemia by lowering plasma triglyceride (TG) and total cholesterol (T-CHO) while elevating high-density lipoprotein cholesterol (HDL-c), and it reduced intraperitoneal fat and whole-body lipid (p < 0.05). RO also mitigated hepatic vacuolization and decreased plasma alanine aminotransferase (ALT) (p < 0.05) and aspartate aminotransferase (AST) (p > 0.05) activities. Antioxidant capacity was enhanced by RO, as indicated by increased glutathione (GSH), catalase (CAT), and total antioxidant capacity (T-AOC), together with reduced malondialdehyde (MDA), and accompanied by upregulation of nrf2, downstream antioxidant genes, and downregulation of keap1 (p < 0.05). Moreover, RO suppressed HF-induced endoplasmic reticulum (ER) stress (grp78, eif2α, chop) and pro-inflammatory genes (tnfα, il-1β, nf-κb), while upregulating il-10 (p < 0.05). Gut microbiota analysis showed RO-mediated enrichment of Firmicutes and short-chain fatty acid-producing genera (Faecalibaculum, Dubosiella). Importantly, RO significantly reduced mortality during a 96 h acute ammonia challenge (p < 0.05). Collectively, these results demonstrate that dietary rosiglitazone mitigates HF diet-induced hepatic oxidative stress and metabolic dysregulation through Nrf2 activation, anti-inflammatory effects, and microbiota modulation, providing a potential strategy to enhance HF feed utilization and environmental stress resilience in carnivorous fish. Further studies on dose optimization and residue safety are warranted. Full article

(This article belongs to the Special Issue Use of Antioxidant Supplementation in Aquaculture: Impact on Growth, Health, and Product Quality)

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28 pages, 1724 KB

Open AccessSystematic Review

Proinflammatory Risk Factors in Patients with Ischemic Stroke: A Systematic Review and Meta-Analysis

by Alexandru Gerdanovics, Ioana Cristina Stănescu, Camelia Manuela Mîrza, Gabriela Bombonica Dogaru, Cristina Ariadna Nicula, Paul-Mihai Boarescu, Cezara-Andreea Gerdanovics and Adriana Elena Bulboacă

Antioxidants 2025, 14(10), 1229; https://doi.org/10.3390/antiox14101229 - 14 Oct 2025

Abstract

Ischemic stroke is a leading cause of disability worldwide, often triggered by atherothrombotic or embolic events. A growing body of evidence highlights the role of neuroinflammation as a central mechanism in post-stroke damage, influenced by modifiable systemic risk factors. Emerging evidence suggests that [...] Read more.

Ischemic stroke is a leading cause of disability worldwide, often triggered by atherothrombotic or embolic events. A growing body of evidence highlights the role of neuroinflammation as a central mechanism in post-stroke damage, influenced by modifiable systemic risk factors. Emerging evidence suggests that oxidative stress mediates the impact of several modifiable risk factors by activating redox-sensitive pathways (such as NF-κB), impairing nitric oxide bioavailability, and promoting matrix metalloproteinase activity that disrupts vascular integrity and contributes to ischemic injury. In this context, our meta-analysis examined major modifiable risk factors for ischemic stroke, with a particular focus on their shared ability to promote oxidative stress and neuroinflammatory cascades. By emphasizing these redox-dependent mechanisms, our work supports the biological plausibility of exploring antioxidant strategies as complementary approaches to mitigate stroke risk. Hypertension, diabetes, dyslipidemia, smoking, atrial fibrillation, and transient ischemic attacks all contribute to oxidative damage through mechanisms such as endothelial dysfunction, vascular inflammation, and excessive free radical exposure. We searched PubMed, PubMed Central, Web of Science, and Scopus for observational studies published within the last five years, identifying 23 studies (691,524 participants) meeting eligibility criteria. Using a random-effects model, we found significant associations between stroke risk and hypertension (OR = 1.58, 95% CI: 1.28–1.94), smoking (OR = 1.61, 95% CI: 1.13–2.28), type 2 diabetes (OR = 1.53, 95% CI: 1.29–1.81), atrial fibrillation (OR = 1.88, 95% CI: 1.28–2.75), and prior transient ischemic attack (OR = 1.62, 95% CI: 1.24–2.11). These risk factors are known to contribute to systemic inflammation, potentially exacerbating neuroinflammatory cascades post-stroke. Despite limitations such as heterogeneity and low certainty of evidence, our findings reinforce the relevance of targeting inflammation-driven risk factors in stroke prevention strategies and future research. Full article

(This article belongs to the Special Issue Oxidative Stress and Inflammation in Neurologic Diseases)

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23 pages, 2203 KB

Open AccessReview

The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress

by Huiying Zhao and Wei Wu

Antioxidants 2025, 14(10), 1228; https://doi.org/10.3390/antiox14101228 - 13 Oct 2025

Abstract

Osteoarthritis (OA) is one of the most common joint diseases worldwide, which is characterized by degenerative changes in articular cartilage and secondary osteophyte formation. Numerous factors influence OA, including aging, obesity, joint injury and chronic overloading. Among them, the senescence of chondrocytes is [...] Read more.

Osteoarthritis (OA) is one of the most common joint diseases worldwide, which is characterized by degenerative changes in articular cartilage and secondary osteophyte formation. Numerous factors influence OA, including aging, obesity, joint injury and chronic overloading. Among them, the senescence of chondrocytes is one of the key factors leading to OA. Chondrocyte senescence can trigger inflammatory responses, extracellular matrix (ECM) degradation, mitochondrial dysfunction and oxidative stress (OS), and autophagy. Sirtuin 6 (SIRT6), as a deacetylase related to aging, can regulate chondrocyte senescence and plays a certain part in OA. SIRT6 regulates the number and membrane integrity of mitochondria, alleviates excessive Reactive Oxygen Species (ROS) in mitochondria and reduces inflammation-mediated mitochondrial damage. In addition, SIRT6 can also regulate the activity of antioxidant enzymes, inhibit excessive ROS induced by inflammatory factors, and alleviate OS. However, as aging progresses, the activity of SIRT6 will decrease. Activating the activity of SIRT6 becomes a potential therapeutic target and has a certain alleviating effect on the development of OA. The supplementation of nicotinamide adenine dinucleotide (NAD+) precursors and SIRT6-specific activators can increase SIRT6, alleviate chondrocyte senescence, and reduce OA. This paper aims to focus on mitochondrial dysfunction and OS to explore SIRT6’s effects on OA chondrocytes’ senescence under aging and summarize the potential therapeutic targets for activating SIRT6 to provide assistance for the improvement of OA. Full article

(This article belongs to the Special Issue Inflammation and Oxidative Stress in Articular Cartilage)

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14 pages, 1363 KB

Open AccessArticle

Assessment of Antioxidant Potential of Carbon-Based Nanomaterials from Different Sources

by Oladoyin Grace Famutimi, Sam Masha, Rodney Maluleke, Vuyelwa Ncapayi, Thabang Calvin Lebepe, Nande Mgedle, Cynthia Mutendu Kungwa, Olufunto Tolulope Fanoro, Isaac Olusanjo Adewale and Oluwatobi Samuel Oluwafemi

Antioxidants 2025, 14(10), 1227; https://doi.org/10.3390/antiox14101227 - 13 Oct 2025

Abstract

Antioxidants regulate oxidative reactions by impeding, delaying, or inhibiting the oxidation of biomolecules. Concerns regarding the toxicity of synthetic antioxidants have driven the search for safer alternatives. In this study, the antioxidant activities of three nontoxic carbon-based nanomaterials—carbon dots from citric acid precursor [...] Read more.

Antioxidants regulate oxidative reactions by impeding, delaying, or inhibiting the oxidation of biomolecules. Concerns regarding the toxicity of synthetic antioxidants have driven the search for safer alternatives. In this study, the antioxidant activities of three nontoxic carbon-based nanomaterials—carbon dots from citric acid precursor (CB-Ca), iron-doped carbon dots (CB-Fe) and carbon dots derived from Momordica charantia leaves (CB-Mc)—were investigated using 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging, hydrogen peroxide (H₂O₂) scavenging, ferric-reducing antioxidant power, and total antioxidant capacity (TAC) assays. Scavenging activity was carried out at varying concentrations, and half-maximal inhibitory concentration (IC₅₀) was calculated using non-linear regression. Reductive ability and TAC were expressed as mg ascorbic acid equivalents/g nanomaterial. CB-Fe exhibited the most potent DPPH scavenging activity (IC₅₀ = 254.2 ± 37.37 µg/mL), surpassing CB-Mc and CB-Ca by 2- to 3-fold. In contrast, CB-Ca had the highest H₂O₂ scavenging (IC₅₀ = 84.2 ± 11.87 µg/mL), while CB-Mc had the highest TAC of 77.95 mg ascorbic acid Eq/g. CB-Fe also displayed superior ferric ion reducing capacity. The study concluded that each carbon dot type exhibits unique antioxidant profiles and may offer some special advantages in nanomedicine and other applications. Full article

(This article belongs to the Section Natural and Synthetic Antioxidants)

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32 pages, 5594 KB

Open AccessArticle

In Vitro Antioxidant Activity and In Vivo Neuroprotective Effect of Parastrephia quadrangularis in a Drosophila Parkinson’s Disease Model

by Branco Cárdenas, Ayza Cuevas, Duxan Arancibia, Lucas Urrutia, Pedro Zamorano, Adrián Paredes and Rafaella V. Zárate

Antioxidants 2025, 14(10), 1226; https://doi.org/10.3390/antiox14101226 - 12 Oct 2025

Abstract

Oxidative stress (OxS) is a central factor in neurodegenerative diseases (NDs), including Parkinson’s disease (PD). Phenolic compounds, including flavonoids and coumarins, counteract reactive species and modulate key intracellular survival pathways, highlighting their therapeutic potential. Parastrephia quadrangularis (Pq), a plant from the [...] Read more.

Oxidative stress (OxS) is a central factor in neurodegenerative diseases (NDs), including Parkinson’s disease (PD). Phenolic compounds, including flavonoids and coumarins, counteract reactive species and modulate key intracellular survival pathways, highlighting their therapeutic potential. Parastrephia quadrangularis (Pq), a plant from the Atacama Desert traditionally used by Andean communities, contains phenolic compounds with antioxidant, antifungal, and anti-inflammatory activities. However, its neuroprotective potential remains unexplored. Here, a hydroalcoholic extract (HAE) of Pq and four subfractions (MeOH, EtOAc, DCM, and n-hex) were obtained and assessed for in vitro antioxidant activity, with HAE selected for its consistent activity. In SH-SY5Y cells, HAE-Pq lowered basal reactive oxygen species and attenuated hydrogen peroxide-induced OxS. The UHPLC-MS analysis of HAE-Pq unveiled a high abundance of flavonoids, followed by coumarins and phenolic acids, and identified 16 additional metabolites, including jaceidin as the most abundant. In vivo assays using a Drosophila genetic PD model induced by overexpression of human α-synuclein, showed that HAE-Pq was non-toxic and non-aversive and that it delayed the onset of motor defects by one week in female flies. This study provides the first evidence of the neuroprotective potential of Pq, supporting its value as a source of bioactive metabolites relevant to NDs and reinforcing its ethnopharmacological validation. Full article

(This article belongs to the Special Issue Antioxidant Research in Chile—2nd Edition)

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21 pages, 6661 KB

Open AccessArticle

Bioactive Antioxidants from Avocado By-Products: Mechanistic Study and Laboratory-Scale Extraction Optimization

by Ziyao Xin, Yicheng Gao, Leiyu He, Zhilong Xiu and Lihui Sun

Antioxidants 2025, 14(10), 1225; https://doi.org/10.3390/antiox14101225 - 11 Oct 2025

Abstract

This study aimed to develop an environmentally friendly and relatively efficient method for extracting natural antioxidants from avocado by-products while investigating the antioxidant mechanisms of their core bioactive components on multiple dimensions. In vitro antioxidant assays (ABTS, FRAP, SAFR, SFR, ORAC, DPPH) demonstrated [...] Read more.

This study aimed to develop an environmentally friendly and relatively efficient method for extracting natural antioxidants from avocado by-products while investigating the antioxidant mechanisms of their core bioactive components on multiple dimensions. In vitro antioxidant assays (ABTS, FRAP, SAFR, SFR, ORAC, DPPH) demonstrated that flavonoid procyanidin was the primary antioxidant component in avocado seeds, exhibiting the strongest activity (DPPH EC₅₀ = 3.6 µg/mL). The Hill model indicated a positive synergistic effect (n = 3.1). Chemical and molecular mechanism analyses revealed that avocado seeds exert antioxidant activity predominantly through hydrogen atom transfer (HAT) and electron transfer (ET) pathways. The model predictions suggested procyanidins may stably bind to protein targets in the Keap1-Nrf2 pathway and NOX2 via hydrogen bonding, hydrophobic interactions, and π-cation interactions. Furthermore, response surface methodology (RSM) was employed to optimize the extraction process of avocado seed antioxidants in an ethanol-water system. This study underscores the considerable health benefits and antioxidant capacity of avocado by-products, supporting their promising application in functional foods formulations. Full article

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20 pages, 968 KB

Open AccessArticle

Comprehensive Characterization of Bioactive Properties in Extracts from Different Chilean Hop Ecotypes (Humulus lupulus L.): Antioxidant, Antimicrobial and Antitumor Activities

by María C. Betancur, Fernando Salazar, Michael Araya, Anita Behn, Jéssica López, Ana Quesille-Villalobos, José M. Villatoro, Jacqueline Poblete and Angara Zambrano

Antioxidants 2025, 14(10), 1224; https://doi.org/10.3390/antiox14101224 - 11 Oct 2025

Abstract

Chilean hop (Humulus lupulus L.) ecotypes are an under-explored resource with high bioactive potential, offering promising applications in food preservation and health promotion. This study aimed to characterize the chemical composition and evaluate the antioxidant, antimicrobial, and cytotoxic properties of methanolic extracts [...] Read more.

Chilean hop (Humulus lupulus L.) ecotypes are an under-explored resource with high bioactive potential, offering promising applications in food preservation and health promotion. This study aimed to characterize the chemical composition and evaluate the antioxidant, antimicrobial, and cytotoxic properties of methanolic extracts from three native ecotypes—Ranco, La Unión, and Valdivia—to identify their potential as sources of multifunctional bioactive compounds. Each ecotype exhibited a distinct composition of bioactive compounds; Valdivia stood out for its pronounced levels of α- and β-acids and xanthohumol. Antioxidant capacity, assessed by DPPH, FRAP, and ABTS, was strong across extracts, with Valdivia showing the highest values in all the tests carried out. The extracts inhibited multidrug-resistant clinical isolates, notably Enterococcus faecalis and Pseudomonas aeruginosa, and showed dose-dependent cytotoxic effects in H1299 and MCF-7 cell lines, with the La Unión extract particularly active against H1299. Overall, these findings position Chilean hop ecotypes as promising sources of natural antioxidants and antimicrobial agents for functional food and nutraceutical applications. Full article

(This article belongs to the Special Issue Antioxidant Research in Chile—2nd Edition)

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22 pages, 3131 KB

Open AccessArticle

The Role of miR-144/Nrf2 Pathway in Muscle Oxidative Stress Induced by Oxidized Fish Oil in Megalobrama amblycephala, with an Emphasis on Protein Oxidation

by Jie Yang, Xiaochuan Zheng, Qunlan Zhou, Changyou Song, Hongyan Tian, Aimin Wang, Xiangfei Li, Bo Liu and Cunxin Sun

Antioxidants 2025, 14(10), 1223; https://doi.org/10.3390/antiox14101223 - 11 Oct 2025

Abstract

This study investigated the role of miR-144 in mitigating oxidized fish oil (OFO)-induced muscle oxidative stress and quality deterioration in Megalobrama amblycephala. The feeding trial was conducted for 5 weeks, and four experimental diets were formulated, namely NC (fresh fish oil), OF [...] Read more.

This study investigated the role of miR-144 in mitigating oxidized fish oil (OFO)-induced muscle oxidative stress and quality deterioration in Megalobrama amblycephala. The feeding trial was conducted for 5 weeks, and four experimental diets were formulated, namely NC (fresh fish oil), OF (OFO), OF + ago (OFO and miR-144 agomir), and OF + anta (OFO and miR-144 antagomir). Histological results showed that OFO significantly reduced myofiber density (from 758.00 ± 13.69 to 636.57 ± 13.44 N/mm²) and decreased the percentage of myofibers with diameters > 50 μm (from 53.45% to 38.52%). OFO intake significantly increased the content of malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP), and 3-nitrotyrosine (3-NT), and significantly decreased superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity in muscle. OFO treatment significantly up-regulated the expression of inflammatory factors (NF-κB, TNF-α, HO-1, and IL-6), significantly down-regulated NQO1. Moreover, OFO reduced muscle differentiation and maturation by down-regulating the expression of MyoG, MYHC1, and protein synthesis genes (AKT3, TOR, and S6K1), and up-regulating the expression of protein hydrolysis genes (FoxO3a, MuRF1, HSP70, Beclin-1, P62, and ATG8). Moreover, miR-144 agomir exacerbated OFO-induced muscle damage by suppressing Nrf2, whereas miR-144 antagomir mitigated these effects. Silencing miR-144 re-activates Nrf2, alleviating oxidative damage, enhancing protein deposition, and improving muscle quality. These findings suggest that targeting the miR-144/Nrf2 axis could counteract OFO-induced muscle deterioration. Full article

(This article belongs to the Special Issue Natural Antioxidants and Aquatic Animal Health—2nd Edition)

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16 pages, 2871 KB

Open AccessArticle

PK11007 Covalently Inhibits Thioredoxin Reductase 1 to Induce Oxidative Stress and Autophagy Impairment in NSCLC Cells

by Hanziyi Zhou, Shibo Sun, Haowen Liu, Tong Li, Yiran Xu, Rui Yang, Haiyan Liu, Leiyu He, Weiping Xu, Shui Guan and Jianqiang Xu

Antioxidants 2025, 14(10), 1222; https://doi.org/10.3390/antiox14101222 - 11 Oct 2025

Abstract

Selenoprotein thioredoxin reductase 1 (TXNRD1) is frequently upregulated in various cancer cells to sustain cellular redox homeostasis, and its inhibition has emerged as a promising anti-cancer strategy. In this study, we identified PK11007, a thiol-modifying compound previously characterized as a p53 reactivator, as [...] Read more.

Selenoprotein thioredoxin reductase 1 (TXNRD1) is frequently upregulated in various cancer cells to sustain cellular redox homeostasis, and its inhibition has emerged as a promising anti-cancer strategy. In this study, we identified PK11007, a thiol-modifying compound previously characterized as a p53 reactivator, as a potent inhibitor of TXNRD1. PK11007 irreversibly inhibited recombinant TXNRD1 in a time- and dose-dependent manner. Using differential scanning fluorimetry (DSF) and LC–MS/MS analysis, we confirmed that PK11007 covalently modifies the C-terminal redox motif (Cys⁴⁹⁷-Sec⁴⁹⁸) of TXNRD1. In non-small cell lung cancer (NSCLC) H1299 cells, PK11007-induced TXNRD1 inhibition disrupted cellular redox balance, leading to impaired autophagy flux and cell death. Similar autophagy suppression was observed in TXNRD1-knockdown cells, as well as pharmacological inhibition of TXNRD1 by Auranofin (AF) and TXNRD1 inhibitor 1 (TRi-1). Taken together, these findings highlight that oxidative stress contributes to the cytotoxic effects of PK11007 and uncover autophagy disorder as a downstream consequence of TXNRD1 inhibition. Full article

(This article belongs to the Section Antioxidant Enzyme Systems)

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20 pages, 749 KB

Open AccessArticle

Effect of Dietary PUFAs and Antioxidants on Antioxidant and Anti-Inflammatory Functions of HDL in a Cohort of Women

by Gianmarco Mola, Raffaella Riccetti, Domenico Sergi, Alessandro Trentini, Valentina Rosta, Angela Passaro, Juana M. Sanz and Carlo Cervellati

Antioxidants 2025, 14(10), 1221; https://doi.org/10.3390/antiox14101221 - 10 Oct 2025

Abstract

High-density lipoproteins (HDLs) protect against atherosclerosis through their antioxidant, anti-inflammatory, and other beneficial properties. Although interest is increasing in uncovering both physiological and external factors that influence these functions, definitive evidence remains lacking in this area. To fill this gap, we assessed for [...] Read more.

High-density lipoproteins (HDLs) protect against atherosclerosis through their antioxidant, anti-inflammatory, and other beneficial properties. Although interest is increasing in uncovering both physiological and external factors that influence these functions, definitive evidence remains lacking in this area. To fill this gap, we assessed for the first time how intake of saturated and unsaturated fatty acids and dietary antioxidants affects key HDL-associated proteins. We observed that myeloperoxidase (MPO) activity, a marker of HDL oxidation, was inversely correlated with total polyunsaturated fatty acids (PUFAs), omega-3 and omega-6 intake (p < 0.05), polyphenols (p < 0.001), and overall antioxidant capacity (p < 0.05). Levels of lipoprotein-associated phospholipase A2 also decreased with higher antioxidant consumption (p < 0.05). By contrast, glutathione peroxidase 3 (Gpx3) activity, a protective HDL enzyme, increased in tandem with omega-3 and antioxidant intake. Finally, a composite HDL-antioxidant/anti-inflammatory score integrating all measured proteins rose in association with total PUFAs (p < 0.001), omega-6 (p < 0.001), omega-3 (p < 0.01), polyphenols, and total antioxidants (p < 0.05). These findings suggest that higher dietary PUFA, especially omega-6, and antioxidant intake may enhance HDL’s atheroprotective properties. Full article

(This article belongs to the Special Issue Impact of Antioxidant and Anti-Inflammatory Functions of HDL in Diseases—3rd Edition)

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29 pages, 51386 KB

Open AccessArticle

Aspirin Eugenol Ester Alleviates Vascular Endothelial Ferroptosis by Enhancing Antioxidant Ability and Inhibiting the JNK/c-Jun/NCOA4/FTH Signaling Pathway

by Ji Feng, Qi Tao, Zhi-Jie Zhang, Qin-Fang Yu, Ya-Jun Yang and Jian-Yong Li

Antioxidants 2025, 14(10), 1220; https://doi.org/10.3390/antiox14101220 - 10 Oct 2025

Abstract

Oxidative stress occurs within bovine when exposed to harmful stimuli, accompanied by substantial accumulation of reactive oxygen species. Without timely clearance, these reactive oxygen species attack vascular endothelial cells, concurrently inducing extensive production of lipid peroxides within the vascular endothelium, and thereby triggering [...] Read more.

Oxidative stress occurs within bovine when exposed to harmful stimuli, accompanied by substantial accumulation of reactive oxygen species. Without timely clearance, these reactive oxygen species attack vascular endothelial cells, concurrently inducing extensive production of lipid peroxides within the vascular endothelium, and thereby triggering ferroptosis. Aspirin eugenol ester (AEE) showed pharmacological activity against oxidative stress-induced vascular endothelial damage. However, whether it could alleviate vascular endothelial damage by inhibiting ferroptosis remains unclear. This study aimed to evaluate the effects of AEE on vascular endothelial ferroptosis and elucidate its underlying molecular mechanisms. This study established vascular endothelial damage models in vitro and in vivo to explore the ability of AEE to inhibit ferroptosis and oxidative stress by measuring ferroptosis- and oxidative stress-related biomarkers. Transcriptomic and network pharmacology analyses were performed to identify AEE-regulated pathways and key targets. Validation of the pathways were conducted using molecular docking, cellular thermal shift assay, and specific protein agonists/inhibitors. AEE inhibited oxidative stress and ferroptosis in bovine aortic endothelial cells induced by hydrogen peroxide (H₂O₂) or RSL3 via suppressing the upregulation of ferroptosis-related genes and enhancing the expression of antioxidant genes. Transcriptomic and network pharmacology analyses identified JNK as a core target of AEE in regulating ferroptosis. JNK agonists enhanced H₂O₂-induced ferritinophagy; on the contrary, JNK inhibitors alleviated it. AEE suppressed H₂O₂-induced phosphorylation of JNK/c-Jun and ferritinophagy. In a carrageenan-induced rat aortic vascular endothelial damage model, AEE alleviated vascular endothelial damage and ferroptosis-related gene changes, promoted antioxidant gene expression, and inhibited JNK/c-Jun phosphorylation and ferritinophagy. AEE inhibited vascular endothelial ferroptosis by enhancing antioxidant ability, blocking downstream ferritinophagy, and reducing ferrous ion release. Full article

(This article belongs to the Section Aberrant Oxidation of Biomolecules)

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