Journal Description
Antioxidants
Antioxidants
is an international, peer-reviewed, open access journal, published monthly online by MDPI. The International Coenzyme Q10 Association (ICQ10A), Israel Society for Oxygen and Free Radical Research (ISOFRR) and European Academy for Molecular Hydrogen Research (EAMHR) are affiliated with Antioxidants and their members receive discounts on the article processing charge.
- Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
- High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, FSTA, PubAg, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Food Science & Technology) / CiteScore - Q1 (Food Science)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 13.9 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the second half of 2023).
- Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
- Testimonials: See what our editors and authors say about Antioxidants.
- Companion journal: Oxygen.
Impact Factor:
7.0 (2022);
5-Year Impact Factor:
7.3 (2022)
Latest Articles
A Systematic Review of Cardio-Metabolic Properties of Lonicera caerulea L
Antioxidants 2024, 13(6), 694; https://doi.org/10.3390/antiox13060694 - 5 Jun 2024
Abstract
In the light of growing concerns faced by Western societies due to aging, natality decline, and epidemic of cardio-metabolic diseases, both preventable and treatable, new and effective strategical interventions are urgently needed in order to decrease their socio-economical encumbrance. The recent focus of
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In the light of growing concerns faced by Western societies due to aging, natality decline, and epidemic of cardio-metabolic diseases, both preventable and treatable, new and effective strategical interventions are urgently needed in order to decrease their socio-economical encumbrance. The recent focus of research has been redirected towards investigating the potential of haskap (Lonicera caerulea L.) as a novel functional food or superfruit. Therefore, our present review aims to highlight the latest scientific proofs regarding the potential of Lonicera caerulea L. (LC), a perennial fruit-bearing plant rich in polyphenols, in reversing cardio-metabolic dysfunctions. In this regard, a systematic search on two databases (PubMed and Google Scholar) from 1 January 2016 to 1 December 2023 was performed, the keyword combination being Lonicera caerulea L. AND the searched pharmacological action, with the inclusion criteria consisting of in extenso original articles, written in English. The health-enhancing characteristics of haskap berries have been examined through in vitro and in vivo studies from the 35 included original papers. Positive effects regarding cardiovascular diseases and metabolic syndrome have been assigned to the antioxidant activity, hypolipidemic and hypoglycemic effects, as well as to the hepatoprotective and vasoprotective potential. Latest advances regarding LCF mechanisms of action are detailed within this review as well. All these cutting-edge data suggest that this vegetal product would be a good candidate for further clinical studies.
Full article
(This article belongs to the Special Issue Potential Health Benefits of Dietary Antioxidants)
Open AccessArticle
Ergothioneine-Mediated Neuroprotection of Human iPSC-Derived Dopaminergic Neurons
by
Damien Meng-Kiat Leow, Irwin Kee-Mun Cheah, Lucrecia Chen, Yang-Kai Ng, Crystal Jing-Jing Yeo, Barry Halliwell and Wei-Yi Ong
Antioxidants 2024, 13(6), 693; https://doi.org/10.3390/antiox13060693 - 5 Jun 2024
Abstract
Cell death involving oxidative stress and mitochondrial dysfunction is a major cause of dopaminergic neuronal loss in the substantia nigra (SN) of Parkinson’s disease patients. Ergothioneine (ET), a natural dietary compound, has been shown to have cytoprotective functions, but neuroprotective actions against PD
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Cell death involving oxidative stress and mitochondrial dysfunction is a major cause of dopaminergic neuronal loss in the substantia nigra (SN) of Parkinson’s disease patients. Ergothioneine (ET), a natural dietary compound, has been shown to have cytoprotective functions, but neuroprotective actions against PD have not been well established. 6-Hydroxydopamine (6-OHDA) is a widely used neurotoxin to simulate the degeneration of dopaminergic (DA) neurons in Parkinson’s disease. In this study, we investigated the protective effect of ET on 6-OHDA treated iPSC-derived dopaminergic neurons (iDAs) and further confirmed the protective effects in 6-OHDA-treated human neuroblastoma SH-SY5Y cells. In 6-OHDA-treated cells, decreased mitochondrial membrane potential (ΔΨm), increased mitochondrial reactive oxygen species (mROS), reduced cellular ATP levels, and increased total protein carbonylation levels were observed. 6-OHDA treatment also significantly decreased tyrosine hydroxylase levels. These effects were significantly decreased when ET was present. Verapamil hydrochloride (VHCL), a non-specific inhibitor of the ET transporter OCTN1 abrogated ET’s cytoprotective effects, indicative of an intracellular action. These results suggest that ET could be a potential therapeutic for Parkinson’s disease.
Full article
(This article belongs to the Special Issue Reactive Oxygen Species in Different Biological Processes—Second Edition)
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Open AccessSystematic Review
Integration of Antioxidant Activity Assays Data of Stevia Leaf Extracts: A Systematic Review and Meta-Analysis
by
Maria Papaefthimiou, Panagiota I. Kontou, Pantelis G. Bagos and Georgia G. Braliou
Antioxidants 2024, 13(6), 692; https://doi.org/10.3390/antiox13060692 - 4 Jun 2024
Abstract
Stevia rebaudiana Bertoni, a no-calorie natural sweetener, contains a plethora of polyphenols that exert antioxidant properties with potential medicinal significance. Due to the variety of functional groups, polyphenols exhibit varying solubility depending on the nature of the extraction solvents (water, organic, or their
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Stevia rebaudiana Bertoni, a no-calorie natural sweetener, contains a plethora of polyphenols that exert antioxidant properties with potential medicinal significance. Due to the variety of functional groups, polyphenols exhibit varying solubility depending on the nature of the extraction solvents (water, organic, or their mixtures, defined further on as hydroalcoholic extracts). In the present study, we performed a systematic review, following PRISMA guidelines, and meta-analysis, synthesizing all available data from 45 articles encompassing 250 different studies. Our results showed that the total phenolic content (TPC) of hydroalcoholic and aqueous extracts presents higher values (64.77 and 63.73 mg GAE/g) compared to organic extracts (33.39). Total flavonoid content (TFC) was also higher in aqueous and hydroalcoholic extracts; meta-regression analysis revealed that outcomes in different measuring units (mg QE/g, mg CE/g, and mg RUE/g) do not present statistically significant differences and can be synthesized in meta-analysis. Using meta-regression analysis, we showed that outcomes from the chemical-based ABTS, FRAP, and ORAC antioxidant assays for the same extract type can be combined in meta-analysis because they do not differ statistically significantly. Meta-analysis of ABTS, FRAP, and ORAC assays outcomes revealed that the antioxidant activity profile of various extract types follows that of their phenolic and flavonoid content. Using regression meta-analysis, we also presented that outcomes from SOD, CAT, and POX enzymatic antioxidant assays are independent of the assay type (p-value = 0.905) and can be combined. Our study constitutes the first effort to quantitatively and statistically synthesize the research results of individual studies using all methods measuring the antioxidant activity of stevia leaf extracts. Our results, in light of evidence-based practice, uncover the need for a broadly accepted, unified, methodological strategy to perform antioxidant tests, and offer documentation that the use of ethanol:water 1:1 mixtures or pure water can more efficiently extract stevia antioxidant compounds.
Full article
(This article belongs to the Topic Recent Advances in Application of Essential Oil and other Νatural Εxtracts in Food Industry)
Open AccessReview
Facilitating Nitrite-Derived S-Nitrosothiol Formation in the Upper Gastrointestinal Tract in the Therapy of Cardiovascular Diseases
by
Mila Silva-Cunha, Riccardo Lacchini and Jose E. Tanus-Santos
Antioxidants 2024, 13(6), 691; https://doi.org/10.3390/antiox13060691 - 4 Jun 2024
Abstract
Cardiovascular diseases (CVDs) are often associated with impaired nitric oxide (NO) bioavailability, a critical pathophysiological alteration in CVDs and an important target for therapeutic interventions. Recent studies have revealed the potential of inorganic nitrite and nitrate as sources of NO, offering promising alternatives
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Cardiovascular diseases (CVDs) are often associated with impaired nitric oxide (NO) bioavailability, a critical pathophysiological alteration in CVDs and an important target for therapeutic interventions. Recent studies have revealed the potential of inorganic nitrite and nitrate as sources of NO, offering promising alternatives for managing various cardiovascular conditions. It is now becoming clear that taking advantage of enzymatic pathways involved in nitrite reduction to NO is very relevant in new therapeutics. However, recent studies have shown that nitrite may be bioactivated in the acidic gastric environment, where nitrite generates NO and a variety of S-nitrosating compounds that result in increased circulating S-nitrosothiol concentrations and S-nitrosation of tissue pharmacological targets. Moreover, transnitrosation reactions may further nitrosate other targets, resulting in improved cardiovascular function in patients with CVDs. In this review, we comprehensively address the mechanisms and relevant effects of nitrate and nitrite-stimulated gastric S-nitrosothiol formation that may promote S-nitrosation of pharmacological targets in various CVDs. Recently identified interfering factors that may inhibit these mechanisms and prevent the beneficial responses to nitrate and nitrite therapy were also taken into consideration.
Full article
(This article belongs to the Special Issue Prevention of Atherosclerosis and of Low-Density Lipoprotein Oxidation: Role of Dietary Antioxidant Compounds and Altered Redox Pathways. A Commemorative Special Issue in Honour of Professor Stanley Omaye)
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Open AccessArticle
RSM- and ANN-Based Multifrequency Ultrasonic Extraction of Polyphenol-Rich Sargassum horneri Extracts Exerting Antioxidative Activity via the Regulation of MAPK/Nrf2/HO-1 Machinery
by
Ahsan Javed, Md Badrul Alam, Marufa Naznin, Raees Ahmad, Chang Hyung Lee, Sunghwan Kim and Sang-Han Lee
Antioxidants 2024, 13(6), 690; https://doi.org/10.3390/antiox13060690 - 4 Jun 2024
Abstract
Sargassum horneri (SH) is widely consumed as a healthy seaweed food in the Asia–Pacific region. However, the bioactive components contributing to its biological activity remain unknown. Herein, we optimized multifrequency ultrasonic-assisted extraction conditions to achieve higher antioxidant activity using a response surface methodology
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Sargassum horneri (SH) is widely consumed as a healthy seaweed food in the Asia–Pacific region. However, the bioactive components contributing to its biological activity remain unknown. Herein, we optimized multifrequency ultrasonic-assisted extraction conditions to achieve higher antioxidant activity using a response surface methodology and an artificial neural network. High-resolution mass spectrometry (HRMS; negative mode) was used to tentatively identify the secondary metabolites in the optimized SH extract, which were further tested against oxidative stress in RAW264.7 cells. Additionally, the identified compounds were analyzed in silico to determine their binding energies with the Keap1 protein (4L7B). We identified 89 compounds using HRMS, among which 19 metabolites (8 polyphenolics, 2 flavonoids, 2 lignans, 2 terpenes, 2 tannins, 2 sulfolipids, and 1 phospholipid) were putatively reported for the first time in SH. The in vitro results revealed that optimized SH extract inhibited oxidative stress via the Nrf2/MAPKs/HO-1 pathway in a dose-dependent manner. This result was validated by performing in silico simulation, indicating that sargaquinoic acid and glycitein-7-O-glucuronide had the highest binding energies (−9.20 and −9.52 Kcal/mol, respectively) toward Keap1 (4L7B). This study offers a unique approach for the scientific community to identify potential bioactive compounds by optimizing the multivariant extraction processing conditions, which could be used to develop functional and nutraceutical foods.
Full article
(This article belongs to the Topic Research on Extraction Technologies, Analysis Methods and Functional Evaluation of Food Active Components)
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Open AccessCommunication
Oxidative Status, Iron Plasma Levels in Venous Thrombosis Patients
by
Salvatore Santo Signorelli, Andrea Barbagallo, Gea Oliveri Conti, Maria Fiore, Antonio Cristaldi and Margherita Ferrante
Antioxidants 2024, 13(6), 689; https://doi.org/10.3390/antiox13060689 - 3 Jun 2024
Abstract
Exaggerated clot induces venous thrombosis (VTE); oxidative stress (OxS) can to be postulated as additional risk factor. This study evaluates firstly OxS by measuring surrogate biomarkers (malondialdehyde-MDA, 4-hydroxinonenal-4-HNE, superoxide desmutase enzyme (SOD)), secondly the iron (Fe) plasma level and thirdly the hepcidin protein
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Exaggerated clot induces venous thrombosis (VTE); oxidative stress (OxS) can to be postulated as additional risk factor. This study evaluates firstly OxS by measuring surrogate biomarkers (malondialdehyde-MDA, 4-hydroxinonenal-4-HNE, superoxide desmutase enzyme (SOD)), secondly the iron (Fe) plasma level and thirdly the hepcidin protein (Hep) level in patients with VTE. A case control study was performed enrolling twenty hospitalized patients and an equal number of healthy individuals. In VTE patients, the following results were found. The MDA was 8.38 ± 0.5 µM/L, the 4-HNE measured 2.75 ± 0.03 µM/L and the SOD was 0.025 ± 0.01 U/mL. The I was 73.10 ± 10 µg/dL and the He was 4.77 ± 0.52 ng/mL. In the control group, the MDA measured 5.5 ± 0.6 µM/L, the 4-HNE 2.24 ± 0.021 µM/L and the SOD 0.08 ± 0.12 U/mL. The Hep was 2.1 ± 0.55 ng/mL and the Fe was 88.2 ± 9.19 µg/dL. Differences were statistically significant. Results suggest that in VTE there is activated OxS, Fe deregulation and over-production of Hep. Fe deregulation induces OxS, leading both to inflammation in the clot activator and stimulation of the pro-thrombotic status. The study highlights OxS and Fe and their regulation as intriguing indicators for risk of VTE.
Full article
(This article belongs to the Special Issue Iron Metabolism, Oxidative Stress and Cellular Dysfunction)
Open AccessReview
Selenium as a Modulator of Redox Reactions in the Prevention and Treatment of Cardiovascular Diseases
by
Klaudia Leszto, Laura Biskup, Klaudia Korona, Weronika Marcinkowska, Maria Możdżan, Andrzej Węgiel, Ewelina Młynarska, Jacek Rysz and Beata Franczyk
Antioxidants 2024, 13(6), 688; https://doi.org/10.3390/antiox13060688 - 3 Jun 2024
Abstract
Cardiovascular diseases stand as the predominant global cause of mortality, exerting a profound impact on both life expectancy and its quality. Given their immense public health burden, extensive efforts have been dedicated to comprehending the underlying mechanisms and developing strategies for prevention and
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Cardiovascular diseases stand as the predominant global cause of mortality, exerting a profound impact on both life expectancy and its quality. Given their immense public health burden, extensive efforts have been dedicated to comprehending the underlying mechanisms and developing strategies for prevention and treatment. Selenium, a crucial participant in redox reactions, emerges as a notable factor in maintaining myocardial cell homeostasis and influencing the progression of cardiovascular disorders. Some disorders, such as Keshan disease, are directly linked with its environmental deficiency. Nevertheless, the precise extent of its impact on the cardiovascular system remains unclear, marked by contradictory findings in the existing literature. High selenium levels have been associated with an increased risk of developing hypertension, while lower concentrations have been linked to heart failure and atrial fibrillation. Although some trials have shown its potential effectiveness in specific groups of patients, large cohort supplementation attempts have generally yielded unsatisfactory outcomes. Consequently, there persists a significant need for further research aimed at delineating specific patient cohorts and groups of diseases that would benefit from selenium supplementation.
Full article
(This article belongs to the Special Issue Antioxidant Therapy for Cardiovascular Diseases)
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Open AccessReview
Role of Uremic Toxins, Oxidative Stress, and Renal Fibrosis in Chronic Kidney Disease
by
Weronika Frąk, Bartłomiej Dąbek, Marta Balcerczyk-Lis, Jakub Motor, Ewa Radzioch, Ewelina Młynarska, Jacek Rysz and Beata Franczyk
Antioxidants 2024, 13(6), 687; https://doi.org/10.3390/antiox13060687 - 3 Jun 2024
Abstract
Affecting millions of people worldwide, chronic kidney disease is a serious medical problem. It results in a decrease in glomerular filtration rate below 60 mL/min/1.73 m, albuminuria, abnormalities in urine sediment and pathologies detected by imaging studies lasting a minimum of 3 months.
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Affecting millions of people worldwide, chronic kidney disease is a serious medical problem. It results in a decrease in glomerular filtration rate below 60 mL/min/1.73 m, albuminuria, abnormalities in urine sediment and pathologies detected by imaging studies lasting a minimum of 3 months. Patients with CKD develop uremia, and as a result of the accumulation of uremic toxins in the body, patients can be expected to suffer from a number of medical consequences such as progression of CKD with renal fibrosis, development of atherosclerosis or increased incidence of cardiovascular events. Another key element in the pathogenesis of CKD is oxidative stress, resulting from an imbalance between the production of antioxidants and the production of reactive oxygen species. Oxidative stress contributes to damage to cellular proteins, lipids and DNA and increases inflammation, perpetuating kidney dysfunction. Additionally, renal fibrogenesis involving the accumulation of fibrous tissue in the kidneys occurs. In our review, we also included examples of forms of therapy for CKD. To improve the condition of CKD patients, pharmacotherapy can be used, as described in our review. Among the drugs that improve the prognosis of patients with CKD, we can include: GLP-1 analogues, SGLT2 inhibitors, Finerenone monoclonal antibody—Canakinumab and Sacubitril/Valsartan.
Full article
(This article belongs to the Special Issue Oxidative Stress in Renal Health)
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Open AccessReview
Artesunate Exerts Organ- and Tissue-Protective Effects by Regulating Oxidative Stress, Inflammation, Autophagy, Apoptosis, and Fibrosis: A Review of Evidence and Mechanisms
by
Mingtao Zhu, Yu Wang, Jianwei Han, Yanping Sun, Shuang Wang, Bingyou Yang, Qiuhong Wang and Haixue Kuang
Antioxidants 2024, 13(6), 686; https://doi.org/10.3390/antiox13060686 - 3 Jun 2024
Abstract
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The human body comprises numerous organs and tissues operating in synchrony, it facilitates metabolism, circulation, and overall organismal function. Consequently, the well-being of our organs and tissues significantly influences our overall health. In recent years, research on the protective effects of artesunate (AS)
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The human body comprises numerous organs and tissues operating in synchrony, it facilitates metabolism, circulation, and overall organismal function. Consequently, the well-being of our organs and tissues significantly influences our overall health. In recent years, research on the protective effects of artesunate (AS) on various organ functions, including the heart, liver, brain, lungs, kidneys, gastrointestinal tract, bones, and others has witnessed significant advancements. Findings from in vivo and in vitro studies suggest that AS may emerge as a newfound guardian against organ damage. Its protective mechanisms primarily entail the inhibition of inflammatory factors and affect anti-fibrotic, anti-aging, immune-enhancing, modulation of stem cells, apoptosis, metabolic homeostasis, and autophagy properties. Moreover, AS is attracting a high level of interest because of its obvious antioxidant activities, including the activation of Nrf2 and HO-1 signaling pathways, inhibiting the release of reactive oxygen species, and interfering with the expression of genes and proteins associated with oxidative stress. This review comprehensively outlines the recent strides made by AS in alleviating organismal injuries stemming from various causes and protecting organs, aiming to serve as a reference for further in-depth research and utilization of AS.
Full article
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Open AccessArticle
Neuroinflammation and Lysosomal Abnormalities Characterise the Essential Role for Oxidation Resistance 1 in the Developing and Adult Cerebellum
by
Eboni M. V. Bucknor, Errin Johnson, Stephanie Efthymiou, Javeria R. Alvi, Tipu Sultan, Henry Houlden, Reza Maroofian, Ehsan G. Karimiani, Mattéa J. Finelli and Peter L. Oliver
Antioxidants 2024, 13(6), 685; https://doi.org/10.3390/antiox13060685 - 3 Jun 2024
Abstract
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Loss-of-function mutations in the TLDc family of proteins cause a range of severe childhood-onset neurological disorders with common clinical features that include cerebellar neurodegeneration, ataxia and epilepsy. Of these proteins, oxidation resistance 1 (OXR1) has been implicated in multiple cellular pathways related to
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Loss-of-function mutations in the TLDc family of proteins cause a range of severe childhood-onset neurological disorders with common clinical features that include cerebellar neurodegeneration, ataxia and epilepsy. Of these proteins, oxidation resistance 1 (OXR1) has been implicated in multiple cellular pathways related to antioxidant function, transcriptional regulation and cellular survival; yet how this relates to the specific neuropathological features in disease remains unclear. Here, we investigate a range of loss-of-function mouse model systems and reveal that constitutive deletion of Oxr1 leads to a rapid and striking neuroinflammatory response prior to neurodegeneration that is associated with lysosomal pathology. We go on to show that neuroinflammation and cell death in Oxr1 knockouts can be completely rescued by the neuronal expression of Oxr1, suggesting that the phenotype is driven by the cell-intrinsic defects of neuronal cells lacking the gene. Next, we generate a ubiquitous, adult inducible knockout of Oxr1 that surprisingly displays rapid-onset ataxia and cerebellar neurodegeneration, establishing for the first time that the distinctive pathology associated with the loss of Oxr1 occurs irrespective of developmental stage. Finally, we describe two new homozygous human pathogenic variants in OXR1 that cause neurodevelopmental delay, including a novel stop-gain mutation. We also compare functionally two missense human pathogenic mutations in OXR1, including one newly described here, that cause different clinical phenotypes but demonstrate partially retained neuroprotective activity against oxidative stress. Together, these data highlight the essential role of Oxr1 in modulating neuroinflammatory and lysosomal pathways in the mammalian brain and support the hypothesis that OXR1 protein dosage may be critical for pathological outcomes in disease.
Full article
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Open AccessArticle
Arctigenin from Fructus arctii Exhibits Antiaging Effects via Autophagy Induction, Antioxidative Stress, and Increase in Telomerase Activity in Yeast
by
Siqi Chen, Yajing Li, Enchan Wu, Qing Li, Lan Xiang and Jianhua Qi
Antioxidants 2024, 13(6), 684; https://doi.org/10.3390/antiox13060684 - 2 Jun 2024
Abstract
Aging is often accompanied by irreversible decline in body function, which causes a large number of age-related diseases and brings a huge economic burden to society and families. Many traditional Chinese medicines have been known to extend lifespan, but it has still been
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Aging is often accompanied by irreversible decline in body function, which causes a large number of age-related diseases and brings a huge economic burden to society and families. Many traditional Chinese medicines have been known to extend lifespan, but it has still been a challenge to isolate a single active molecule from them and verify the mechanism of anti-aging action. Drugs that inhibit senescence-associated secretory phenotypes (SASPs) are called “senomorphics”. In this study, arctigenin (ATG), a senomorphic, was screened from the Chinese medicine Fructus arctii using K6001 yeast replicative lifespan. Autophagy, oxidative stress, and telomerase activity are key mechanisms related to aging. We found that ATG may act through multiple mechanisms to become an effective anti-aging molecule. In exploring the effect of ATG on autophagy, it was clearly observed that ATG significantly enhanced autophagy in yeast. We further verified that ATG can enhance autophagy by targeting protein phosphatase 2A (PP2A), leading to an increased lifespan. Meanwhile, we evaluated the antioxidant capacity of ATG and found that ATG increased the activities of the antioxidant enzymes, thereby reducing reactive oxygen species (ROS) and malondialdehyde (MDA) levels to improve the survival of yeast under oxidative stress. In addition, ATG was able to increase telomerase activity by enhancing the expression of EST1, EST2, and EST3 genes in yeast. In conclusion, ATG exerts anti-aging effects through induction of autophagy, antioxidative stress, and enhancement of telomerase activity in yeast, which is recognized as a potential molecule with promising anti-aging effects, deserving in-depth research in the future.
Full article
(This article belongs to the Collection Advances in Antioxidant Ingredients from Natural Products)
Open AccessArticle
Formulation and Physical–Chemical Analysis of Functional Muffin Made with Inulin, Moringa, and Cacao Adapted for Elderly People with Parkinson’s Disease
by
Paula García-Milla, Rocío Peñalver and Gema Nieto
Antioxidants 2024, 13(6), 683; https://doi.org/10.3390/antiox13060683 - 31 May 2024
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder that affects people’s health. Constipation is probably one of the most prominent gastrointestinal symptoms (non-motor symptoms) of PD with devastating consequences. The aim of this research work is to formulate a functional food product, supplemented with
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Parkinson’s disease (PD) is a neurodegenerative disorder that affects people’s health. Constipation is probably one of the most prominent gastrointestinal symptoms (non-motor symptoms) of PD with devastating consequences. The aim of this research work is to formulate a functional food product, supplemented with inulin, cocoa, and Moringa, which can be an adjuvant in the treatment of constipation. The product was prepared according to a muffin or “Chilean cake” recipe; this basic muffin was prepared with additions of inulin (MI), inulin + cacao (MIC), and inulin + Moringa (MIM). A physical–chemical analysis of the macronutrients and an antioxidant capacity assessment of the samples were conducted, as well as a sensory evaluation performed by a group of people suffering from Parkinson’s disease. A statistically significant difference was observed in the soluble (p = 0.0023) and insoluble (p = 0.0015) fiber values between the control samples and all samples. Furthermore, inulin + cacao improved the antioxidant capacity and folate intake compared to the control. Inulin alone has been shown to have antioxidant capacity according to ABTS (262.5728 ± 34.74 μmol TE/g) and DPPH (9.092518 ± 10.43 μmol TE/g) assays. A sensory evaluation showed a preference for the product with inulin and for the product with inulin + cacao, with a 78% purchase intention being reported by the subjects who evaluated the products. The incorporation of inulin and cacao improved the nutritional value of the muffins; the dietary fiber, antioxidant capacity and folate content are some of the features that stood out. A bakery product enriched with inulin, cocoa and Moringa could serve as a nutritional strategy to enhance nutritional value, thus helping in the treatment of constipation.
Full article
(This article belongs to the Special Issue Natural Products: Biological, Antioxidant Properties and Health Effects—3rd Edition)
Open AccessArticle
Palm Kernel Cake Extracts Obtained from the Combination of Bacterial Fermentation and Enzymic Hydrolysis Promote Swine Small Intestine IPEC-J2 Cell Proliferation and Alleviate LPS-Induced Inflammation In Vitro
by
Hui Zeng, Jingna Miao, Jinghong Liao, Zhiyuan Sui, Meixin Hou and Suqin Hang
Antioxidants 2024, 13(6), 682; https://doi.org/10.3390/antiox13060682 - 31 May 2024
Abstract
Co-fermentation with bacteria and enzymes can reduce sugar content in palm kernel cake (PKC); however, the chemical changes and their effects on cell functionality are unclear. This study investigated the active components in pre-treated PKC extracts and their effects on pig small intestine
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Co-fermentation with bacteria and enzymes can reduce sugar content in palm kernel cake (PKC); however, the chemical changes and their effects on cell functionality are unclear. This study investigated the active components in pre-treated PKC extracts and their effects on pig small intestine IPEC-J2 cell proliferation and LPS-induced inflammation. The extracts contained 60.75% sugar, 36.80% mannose, 1.75% polyphenols and 0.59% flavone, as determined by chemical analyses, suggesting that the extracts were palm kernel cake oligosaccharides (PKCOS). Then, we found that 1000 µg/mL PKCOS counteracted the decrease in cell viability (CCK8 kit) caused by LPS induction by 5 µg/mL LPS (p < 0.05). Mechanistic studies conducted by RNA-seq and qPCR analyses suggested PKCOS promoted cell proliferation through the upregulation of TNF-α, PI3KAP1, MAP3K5 and Fos in the PI3K/MAPK signalling pathway; alleviated inflammation caused by LPS via the downregulation of the target genes Casp3 and TNF-α in association with apoptosis; and regulated the expression of the antioxidant genes SOD1, SOD2 and GPX4 to exert positive antioxidant effects (p < 0.05). Furthermore, PKCOS upregulated SLC5A1 (encoding SLGT1), HK and MPI in the glycolytic pathway (p < 0.05), suggesting cell survival. In summary, PKCOS has positive effects on promoting swine intestine cell proliferation against inflammation.
Full article
Open AccessReview
Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers
by
Sandra I. Anjo, Zhicheng He, Zohaib Hussain, Aruba Farooq, Alan McIntyre, Charles A. Laughton, Andreia Neves Carvalho and Mattéa J. Finelli
Antioxidants 2024, 13(6), 681; https://doi.org/10.3390/antiox13060681 - 31 May 2024
Abstract
Oxidation–reduction post-translational modifications (redox-PTMs) are chemical alterations to amino acids of proteins. Redox-PTMs participate in the regulation of protein conformation, localization and function, acting as signalling effectors that impact many essential biochemical processes in the cells. Crucially, the dysregulation of redox-PTMs of proteins
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Oxidation–reduction post-translational modifications (redox-PTMs) are chemical alterations to amino acids of proteins. Redox-PTMs participate in the regulation of protein conformation, localization and function, acting as signalling effectors that impact many essential biochemical processes in the cells. Crucially, the dysregulation of redox-PTMs of proteins has been implicated in the pathophysiology of numerous human diseases, including neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. This review aims to highlight the current gaps in knowledge in the field of redox-PTMs biology and to explore new methodological advances in proteomics and computational modelling that will pave the way for a better understanding of the role and therapeutic potential of redox-PTMs of proteins in neurodegenerative diseases. Here, we summarize the main types of redox-PTMs of proteins while providing examples of their occurrence in neurodegenerative diseases and an overview of the state-of-the-art methods used for their detection. We explore the potential of novel computational modelling approaches as essential tools to obtain insights into the precise role of redox-PTMs in regulating protein structure and function. We also discuss the complex crosstalk between various PTMs that occur in living cells. Finally, we argue that redox-PTMs of proteins could be used in the future as diagnosis and prognosis biomarkers for neurodegenerative diseases.
Full article
(This article belongs to the Special Issue Protein Oxidative Modification in Brain function, Brain Ageing and Neurological Diseases)
Open AccessArticle
Co-Microencapsulation of Cushuro (Nostoc sphaericum) Polysaccharide with Sacha Inchi Oil (Plukenetia huayllabambana) and Natural Antioxidant Extracts
by
Nancy Chasquibol, Axel Sotelo, Mateo Tapia, Rafael Alarcón, Francisco Goycoolea and María del Carmen Perez-Camino
Antioxidants 2024, 13(6), 680; https://doi.org/10.3390/antiox13060680 - 31 May 2024
Abstract
Cushuro (Nostoc sphaericum) polysaccharide was used to co-microencapsulate sacha inchi oil, natural antioxidant extracts from the oleoresin of charapita chili peppers (Capsicum frutescens L.) and grape orujo (Vitis vinifera L.). Encapsulation efficiency, moisture, particle size, morphology, oxidative stability, shelf-life,
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Cushuro (Nostoc sphaericum) polysaccharide was used to co-microencapsulate sacha inchi oil, natural antioxidant extracts from the oleoresin of charapita chili peppers (Capsicum frutescens L.) and grape orujo (Vitis vinifera L.). Encapsulation efficiency, moisture, particle size, morphology, oxidative stability, shelf-life, solubility, essential fatty acid profile, sterol content and antioxidant capacity were evaluated. The formulations with grape orujo extract showed higher oxidative stability (4908 ± 184 h), antioxidant capacity (4835.33 ± 40.02 µg Trolox/g ms), higher phenolic contents (960.11 ± 53.59 µg AGE/g ms) and a smaller particle size (7.55 µm) than the other formulations, as well as good solubility and a low moisture content. Therefore, grape orujo extracts can be used as natural antioxidants. The fatty acid composition (ω-3) remained quite stable in all the formulations carried out, which also occurred for sterols and tocopherols. In combination with gum arabic, grape orujo extract offered oxidative protection to sacha inchi oil during the first week of storage.
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(This article belongs to the Section Extraction and Industrial Applications of Antioxidants)
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Lovastatin-Induced Mitochondrial Oxidative Stress Leads to the Release of mtDNA to Promote Apoptosis by Activating cGAS-STING Pathway in Human Colorectal Cancer Cells
by
Xiaoming Huang, Ning Liang, Fuming Zhang, Wanjun Lin and Wenzhe Ma
Antioxidants 2024, 13(6), 679; https://doi.org/10.3390/antiox13060679 - 31 May 2024
Abstract
Statins are 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibitors widely used in the treatment of hyperlipidemia. The inhibition of HMG-CoA reductase in the mevalonate pathway leads to the suppression of cell proliferation and induction of apoptosis. The cyclic GMP-AMP synthase (cGAS) stimulator of the interferon
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Statins are 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase inhibitors widely used in the treatment of hyperlipidemia. The inhibition of HMG-CoA reductase in the mevalonate pathway leads to the suppression of cell proliferation and induction of apoptosis. The cyclic GMP-AMP synthase (cGAS) stimulator of the interferon genes (STING) signaling pathway has been suggested to not only facilitate inflammatory responses and the production of type I interferons (IFN), but also activate other cellular processes, such as apoptosis. It has not been studied, however, whether cGAS-STING activation is involved in the apoptosis induced by statin treatment in human colorectal cancer cells. In this study, we reported that lovastatin impaired mitochondrial function, including the depolarization of mitochondrial membrane potential, reduction of oxygen consumption, mitochondrial DNA (mtDNA) integrity, and mtDNA abundance in human colorectal cancer HCT116 cells. The mitochondrial dysfunction markedly induced ROS production in mitochondria, whereas the defect in mitochondria respiration or depletion of mitochondria eliminated reactive oxygen species (ROS) production. The ROS-induced oxidative DNA damage by lovastatin treatment was attenuated by mitochondrial-targeted antioxidant mitoquinone (mitoQ). Upon DNA damage, mtDNA was released into the cytosol and bound to DNA sensor cGAS, thus activating the cGAS-STING signaling pathway to trigger a type I interferon response. This effect was not activated by nuclear DNA (nuDNA) or mitochondrial RNA, as the depletion of mitochondria compromised this effect, but not the knockdown of retinoic acid-inducible gene-1/melanoma differentiation-associated protein 5 (RIG-I/MDA5) adaptor or mitochondrial antiviral signaling protein (MAVS). Moreover, lovastatin-induced apoptosis was partly dependent on the cGAS-STING signaling pathway in HCT116 cells as the knockdown of cGAS or STING expression rescued cell viability and mitigated apoptosis. Similarly, the knockdown of cGAS or STING also attenuated the antitumor effect of lovastatin in the HCT116 xenograft model in vivo. Our findings suggest that lovastatin-induced apoptosis is at least partly mediated through the cGAS-STING signaling pathway by triggering mtDNA accumulation in the cytosol in human colorectal cancer HCT116 cells.
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(This article belongs to the Section ROS, RNS and RSS)
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The Coming Age of Antisense Oligos for the Treatment of Hepatic Ischemia/Reperfusion (IRI) and Other Liver Disorders: Role of Oxidative Stress and Potential Antioxidant Effect
by
Siyuan Yao, Aanchal Kasargod, Richard Chiu, Taylor R. Torgerson, Jerzy W. Kupiec-Weglinski and Kenneth J. Dery
Antioxidants 2024, 13(6), 678; https://doi.org/10.3390/antiox13060678 - 31 May 2024
Abstract
Imbalances in the redox state of the liver arise during metabolic processes, inflammatory injuries, and proliferative liver disorders. Acute exposure to intracellular reactive oxygen species (ROS) results from high levels of oxidative stress (OxS) that occur in response to hepatic ischemia/reperfusion injury (IRI)
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Imbalances in the redox state of the liver arise during metabolic processes, inflammatory injuries, and proliferative liver disorders. Acute exposure to intracellular reactive oxygen species (ROS) results from high levels of oxidative stress (OxS) that occur in response to hepatic ischemia/reperfusion injury (IRI) and metabolic diseases of the liver. Antisense oligonucleotides (ASOs) are an emerging class of gene expression modulators that target RNA molecules by Watson–Crick binding specificity, leading to RNA degradation, splicing modulation, and/or translation interference. Here, we review ASO inhibitor/activator strategies to modulate transcription and translation that control the expression of enzymes, transcription factors, and intracellular sensors of DNA damage. Several small-interfering RNA (siRNA) drugs with N-acetyl galactosamine moieties for the liver have recently been approved. Preclinical studies using short-activating RNAs (saRNAs), phosphorodiamidate morpholino oligomers (PMOs), and locked nucleic acids (LNAs) are at the forefront of proof-in-concept therapeutics. Future research targeting intracellular OxS-related pathways in the liver may help realize the promise of precision medicine, revolutionizing the customary approach to caring for and treating individuals afflicted with liver-specific conditions.
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(This article belongs to the Special Issue New Strategies in Preventing Inflammatory and/or Oxidative-Stress-Induced Damages in Ischemia–Reperfusion Injury)
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TNFα Induces DNA and Histone Hypomethylation and Pulmonary Artery Smooth Muscle Cell Proliferation Partly via Excessive Superoxide Formation
by
Patrick Crosswhite and Zhongjie Sun
Antioxidants 2024, 13(6), 677; https://doi.org/10.3390/antiox13060677 - 31 May 2024
Abstract
Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is
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Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is to investigate whether TNF-α induces PASMC proliferation and explore the potential mechanisms. Methods: PASMCs were isolated from 8-week-old male Sprague-Dawley rats and treated with 0, 20, or 200 ng/mL TNF-α for 24 or 48 h. After treatment, cell number, superoxide production, histone acetylation, DNA methylation, and histone methylation were assessed. Results: TNF-α treatment increased NADPH oxidase activity, superoxide production, and cell numbers compared to untreated controls. TNF-α-induced PASMC proliferation was rescued by a superoxide dismutase mimetic tempol. TNF-α treatment did not affect histone acetylation at either dose but did significantly decrease DNA methylation. DNA methyltransferase 1 activity was unchanged by TNF-α treatment. Further investigation using QRT-RT-PCR revealed that GADD45-α, a potential mediator of DNA demethylation, was increased after TNF-α treatment. RNAi inhibition of GADD45-α alone increased DNA methylation. TNF-α impaired the epigenetic mechanism leading to DNA hypomethylation, which can be abolished by a superoxide scavenger tempol. TNF-α treatment also decreased H3-K4 methylation. TNF-α-induced PASMC proliferation may involve the H3-K4 demethylase enzyme, lysine-specific demethylase 1 (LSD1). Conclusions: TNF-α-induced PASMC proliferation may be partly associated with excessive superoxide formation and histone and DNA methylation.
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(This article belongs to the Special Issue Understanding Oxidative Stress in Cardiovascular Disorders)
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Occupational Exposure to Metal-Based Nanomaterials: A Possible Relationship between Chemical Composition and Oxidative Stress Biomarkers
by
Valeria Bellisario, Giacomo Garzaro, Giulia Squillacioti, Marco Panizzolo, Federica Ghelli, Giuseppe Mariella, Roberto Bono, Irina Guseva Canu and Enrico Bergamaschi
Antioxidants 2024, 13(6), 676; https://doi.org/10.3390/antiox13060676 - 31 May 2024
Abstract
Nanomaterials (NMs) are in high demand for a wide range of practical applications; however, comprehensively understanding the toxicity of these materials is a complex challenge, due to the limited availability of epidemiological evidence on the human health effects arising from workplace exposures. The
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Nanomaterials (NMs) are in high demand for a wide range of practical applications; however, comprehensively understanding the toxicity of these materials is a complex challenge, due to the limited availability of epidemiological evidence on the human health effects arising from workplace exposures. The aim of this work is to assess whether and how urinary metal concentrations could be reliable and useful in NM biomonitoring. In the framework of “NanoExplore Project” [EU LIFE17 Grant ENV/GR/000285], 43 not-exposed subjects and 40 exposed workers were recruited to measure exposure to NMs (PCN and LDSA) in the proximity of the workstations and biological biomarkers (urinary metal concentrations—Aluminum (Al), Silica (Si), Titanium (Ti), and Chromium (Cr); urinary OS biomarkers—TAP, Isop, and MDA). The results showed that Si and Ti were directly associated with NM exposure (both PCN and LDSA), as well as with OS biomarkers, especially in exposed workers. Moreover, the mediation analyses showed that Si could account for about 2.8% in the relationship between LDSA and OS biomarkers, possibly by decreasing OS antioxidant defenses in exposed people. In conclusion, our study provides evidence that occupational exposure to mixtures containing NMs can represent an underestimated hazard for exposed people, increasing the body burden and the oxidative balance.
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(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)
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Senegenin Attenuates Pulmonary Fibrosis by Inhibiting Oxidative-Stress-Induced Epithelial Cell Senescence through Activation of the Sirt1/Pgc-1α Signaling Pathway
by
Qian Zeng, Yuyang Luo, Xiaoxue Sang, Minlin Liao, Binbin Wen, Zhengang Hu, Mei Sun, Ziqiang Luo, Xiaoting Huang, Wei Liu and Siyuan Tang
Antioxidants 2024, 13(6), 675; https://doi.org/10.3390/antiox13060675 - 31 May 2024
Abstract
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Idiopathic pulmonary fibrosis is a fatal interstitial lung disease for which effective drug therapies are lacking. Senegenin, an effective active compound from the traditional Chinese herb Polygala tenuifolia Willd, has been shown to have a wide range of pharmacological effects. In this
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Idiopathic pulmonary fibrosis is a fatal interstitial lung disease for which effective drug therapies are lacking. Senegenin, an effective active compound from the traditional Chinese herb Polygala tenuifolia Willd, has been shown to have a wide range of pharmacological effects. In this study, we investigated the therapeutic effects of senegenin on pulmonary fibrosis and their associated mechanisms of action. We found that senegenin inhibited the senescence of epithelial cells and thus exerted anti-pulmonary-fibrosis effects by inhibiting oxidative stress. In addition, we found that senegenin promoted the expression of Sirt1 and Pgc-1α and that the antioxidative and antisenescent effects of senegenin were suppressed by specific silencing of the Sirt1 and Pgc–1α genes, respectively. Moreover, the senegenin-induced effects of antioxidation, antisenescence of epithelial cells, and antifibrosis were inhibited by treatment with Sirt1 inhibitors in vivo. Thus, the Sirt1/Pgc-1α pathway exerts its antifibrotic effect on lung fibrosis by mediating the antioxidative and antisenescent effects of senegenin.
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