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 (Chemistry, Medicinal) / CiteScore - Q1 (Food Science)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 15.5 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the first half of 2024).
- 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:
6.0 (2023);
5-Year Impact Factor:
6.7 (2023)
Latest Articles
N-acetyl Cysteine Overdose Induced Acute Toxicity and Hepatic Microvesicular Steatosis by Disrupting GSH and Interfering Lipid Metabolisms in Normal Mice
Antioxidants 2024, 13(7), 832; https://doi.org/10.3390/antiox13070832 (registering DOI) - 11 Jul 2024
Abstract
N-acetyl cysteine (NAC) is a versatile drug used in various conditions, but the limitations and toxicities are not clear. The acute toxicity and toxicological mechanisms of an intraperitoneal injection of NAC in normal mice were deciphered. The LD50 for male and female BALB/cByJNarl
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N-acetyl cysteine (NAC) is a versatile drug used in various conditions, but the limitations and toxicities are not clear. The acute toxicity and toxicological mechanisms of an intraperitoneal injection of NAC in normal mice were deciphered. The LD50 for male and female BALB/cByJNarl mice were 800 mg/kg and 933 mg/kg. The toxicological mechanisms of 800 mg/kg NAC (N800) were investigated. The serum biomarkers of hepatic and renal indices dramatically increased, followed by hepatic microvesicular steatosis, renal tubular injury and necrosis, and splenic red pulp atrophy and loss. Thus, N800 resulted in mouse mortality mainly due to acute liver, kidney, and spleen damages. The safe dose (275 mg/kg) of NAC (N275) increased hepatic antioxidant capacity by increasing glutathione levels and catalase activity. N275 elevated the hepatic gene expressions of lipid transporter, lipid synthesis, β-oxidation, and ketogenesis, suggesting a balance between lipid production and consumption, and finally, increased ATP production. In contrast, N800 increased hepatic oxidative stress by decreasing glutathione levels through suppressing Gclc, and reducing catalase activity. N800 decreased the hepatic gene expressions of lipid transporter, lipid synthesis, and interferred β-oxidation, leading to lipid accumulation and increasing Cyp2E1 expression, and finally, decreased ATP production. Therefore, NAC doses are limited for normal individuals, especially via intraperitoneal injection or similar means.
Full article
(This article belongs to the Section Health Outcomes of Antioxidants and Oxidative Stress)
Open AccessArticle
Canagliflozin Inhibits Palmitic Acid-Induced Vascular Cell Aging In Vitro through ROS/ERK and Ferroptosis Pathways
by
Fang Wan, Xin He and Weidong Xie
Antioxidants 2024, 13(7), 831; https://doi.org/10.3390/antiox13070831 (registering DOI) - 11 Jul 2024
Abstract
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Vascular aging is one of the reasons for the high incidence of cardiovascular diseases nowadays, as vascular cells age due to various internal and external factors. Among them, high fat is an important inducer. Canagliflozin (CAN) is one of the SGLT2 inhibitors that
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Vascular aging is one of the reasons for the high incidence of cardiovascular diseases nowadays, as vascular cells age due to various internal and external factors. Among them, high fat is an important inducer. Canagliflozin (CAN) is one of the SGLT2 inhibitors that has been shown to have cardiovascular protective effects in addition to lowering blood sugar, but the specific mechanism is not clear. This study first established a vascular aging model using palmitic acid (PA), then tested the effect of CAN on PA-induced vascular aging, and finally examined the mechanism of CAN’s anti-vascular aging via ROS/ERK and ferroptosis pathways. We found that CAN alleviates PA-induced vascular cell aging by inhibiting the activation of ROS/ERK and ferroptosis signaling pathways. This study reveals new mechanisms of lipid-induced vascular aging and CAN inhibition of vascular aging from the perspectives of ROS/ERK and ferroptosis pathways, which is expected to provide new ideas for the development of related drugs in the future.
Full article
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Open AccessCorrection
Correction: Chen et al. Bromelain Ameliorates Atherosclerosis by Activating the TFEB-Mediated Autophagy and Antioxidant Pathways. Antioxidants 2023, 12, 72
by
Chia-Hui Chen, Chien-Chung Hsia, Po-An Hu, Chung-Hsin Yeh, Chun-Tang Chen, Cheng-Liang Peng, Chih-Hsien Wang and Tzong-Shyuan Lee
Antioxidants 2024, 13(7), 830; https://doi.org/10.3390/antiox13070830 (registering DOI) - 11 Jul 2024
Abstract
In the original publication [...]
Full article
Open AccessReview
Harnessing the Potential of Quinoa: Nutritional Profiling, Bioactive Components, and Implications for Health Promotion
by
Xiaomin Xi, Guanghe Fan, Huimin Xue, Shuai Peng, Weidong Huang and Jicheng Zhan
Antioxidants 2024, 13(7), 829; https://doi.org/10.3390/antiox13070829 (registering DOI) - 10 Jul 2024
Abstract
Quinoa, a globally cultivated “golden grain” belonging to Chenopodium in the Amaranthaceae family, is recognized for being gluten-free, with a balanced amino acid profile and multiple bioactive components, including peptides, polysaccharides, polyphenols, and saponins. The bioactive compounds extracted from quinoa offer multifaceted health
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Quinoa, a globally cultivated “golden grain” belonging to Chenopodium in the Amaranthaceae family, is recognized for being gluten-free, with a balanced amino acid profile and multiple bioactive components, including peptides, polysaccharides, polyphenols, and saponins. The bioactive compounds extracted from quinoa offer multifaceted health benefits, including antioxidative, anti-inflammatory, antimicrobial, cardiovascular disease (CVD) improvement, gut microbiota regulation, and anti-cancer effects. This review aims to intricately outline quinoa’s nutritional value, functional components, and physiological benefits. Importantly, we comprehensively provide conclusions on the effects and mechanisms of these quinoa-derived bioactive components on multiple cancer types, revealing the potential of quinoa seeds as promising and effective anti-cancer agents. Furthermore, the health-promoting role of quinoa in modulating gut microbiota, maintaining gut homeostasis, and protecting intestinal integrity was specifically emphasized. Finally, we provided a forward-looking description of the opportunities and challenges for the future exploration of quinoa. However, in-depth studies of molecular targets and clinical trials are warranted to fully understand the bioavailability and therapeutic application of quinoa-derived compounds, especially in cancer treatment and gut microbiota regulation. This review sheds light on the prospect of developing dietary quinoa into functional foods or drugs to prevent and manage human diseases.
Full article
(This article belongs to the Special Issue Natural Products: Biological, Antioxidant Properties and Health Effects—3rd Edition)
Open AccessReview
Targeting Metabolic–Redox Nexus to Regulate Drug Resistance: From Mechanism to Tumor Therapy
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Yuke Wang, Jingqiu He, Shan Lian, Yan Zeng, Sheng He, Jue Xu, Li Luo, Wenyong Yang and Jingwen Jiang
Antioxidants 2024, 13(7), 828; https://doi.org/10.3390/antiox13070828 (registering DOI) - 10 Jul 2024
Abstract
Drug resistance is currently one of the biggest challenges in cancer treatment. With the deepening understanding of drug resistance, various mechanisms have been revealed, including metabolic reprogramming and alterations of redox balance. Notably, metabolic reprogramming mediates the survival of tumor cells in harsh
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Drug resistance is currently one of the biggest challenges in cancer treatment. With the deepening understanding of drug resistance, various mechanisms have been revealed, including metabolic reprogramming and alterations of redox balance. Notably, metabolic reprogramming mediates the survival of tumor cells in harsh environments, thereby promoting the development of drug resistance. In addition, the changes during metabolic pattern shift trigger reactive oxygen species (ROS) production, which in turn regulates cellular metabolism, DNA repair, cell death, and drug metabolism in direct or indirect ways to influence the sensitivity of tumors to therapies. Therefore, the intersection of metabolism and ROS profoundly affects tumor drug resistance, and clarifying the entangled mechanisms may be beneficial for developing drugs and treatment methods to thwart drug resistance. In this review, we will summarize the regulatory mechanism of redox and metabolism on tumor drug resistance and highlight recent therapeutic strategies targeting metabolic–redox circuits, including dietary interventions, novel chemosynthetic drugs, drug combination regimens, and novel drug delivery systems.
Full article
(This article belongs to the Special Issue Recent Advances in Redox Biology Research in China)
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Open AccessArticle
Colistin Induces Oxidative Stress and Apoptotic Cell Death through the Activation of the AhR/CYP1A1 Pathway in PC12 Cells
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Baofu Xie, Yue Liu, Chunhong Chen, Tony Velkov, Shusheng Tang, Jianzhong Shen and Chongshan Dai
Antioxidants 2024, 13(7), 827; https://doi.org/10.3390/antiox13070827 (registering DOI) - 10 Jul 2024
Abstract
Colistin is commonly regarded as the “last-resort” antibiotic for combating life-threatening infections caused by multidrug-resistant (MDR) gram-negative bacteria. Neurotoxicity is a potential adverse event associated with colistin application in clinical settings, yet the exact molecular mechanisms remain unclear. This study examined the detrimental
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Colistin is commonly regarded as the “last-resort” antibiotic for combating life-threatening infections caused by multidrug-resistant (MDR) gram-negative bacteria. Neurotoxicity is a potential adverse event associated with colistin application in clinical settings, yet the exact molecular mechanisms remain unclear. This study examined the detrimental impact of colistin exposure on PC12 cells and the associated molecular mechanisms. Colistin treatment at concentrations of 0–400 μM decreased cell viability and induced apoptotic cell death in both time- and concentration-dependent manners. Exposure to colistin triggered the production of reactive oxygen species (ROS) and caused oxidative stress damage in PC12 cells. N-acetylcysteine (NAC) supplementation partially mitigated the cytotoxic and apoptotic outcomes of colistin. Evidence of mitochondrial dysfunction was observed through the dissipation of membrane potential. Additionally, colistin treatment upregulated the expression of AhR and CYP1A1 mRNAs in PC12 cells. Pharmacological inhibition of AhR (e.g., using α-naphthoflavone) or intervention with the CYP1A1 gene significantly decreased the production of ROS induced by colistin, subsequently lowering caspase activation and cell apoptosis. In conclusion, our findings demonstrate, for the first time, that the activation of the AhR/CYP1A1 pathway contributes partially to colistin-induced oxidative stress and apoptosis, offering insights into the cytotoxic effects of colistin.
Full article
(This article belongs to the Special Issue Oxidative Stress, Mitochondrial Dysfunction, and Neurotoxicity)
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Open AccessArticle
Characterization and Therapeutic Potential of Curcumin-Loaded Cerium Oxide Nanoparticles for Interstitial Cystitis Management
by
Yang-Chen Lin, Ya-Jyun Liang, Chun-Hong Zhang, Li-Jia Liu and Feng-Huei Lin
Antioxidants 2024, 13(7), 826; https://doi.org/10.3390/antiox13070826 - 10 Jul 2024
Abstract
Oxidative stress resulting from reactive oxygen species (ROS) is often considered to be the leading cause of interstitial cystitis (IC), which is a chronic inflammatory disease. Antioxidants have been proven to have promising therapeutic effects on IC. In this study, we present an
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Oxidative stress resulting from reactive oxygen species (ROS) is often considered to be the leading cause of interstitial cystitis (IC), which is a chronic inflammatory disease. Antioxidants have been proven to have promising therapeutic effects on IC. In this study, we present an antioxidant intervention for IC by introducing curcumin-loaded cerium oxide nanoparticles (Cur-CONPs). Recognizing oxidative stress as the primary contributor to IC, our research builds on previous work utilizing cerium oxide nanoparticles (CONPs) for their outstanding antioxidant and anti-inflammatory properties. However, given the need to effectively relieve acute inflammation, we engineered Cur-CONPs to harness the short-term radical-scavenging antioxidant prowess of curcumin. Through in vitro studies, we demonstrate that the Cur-CONPs exhibit not only robust antioxidant capabilities but also superior anti-inflammatory properties over CONPs alone. Furthermore, in vivo studies validate the therapeutic effects of Cur-CONPs on IC. Mice with IC subjected to the Cur-CONP treatment exhibited improved micturition behaviors, relief from pelvic pain sensitivity, and reduced expression of inflammatory proteins (IL-6, IL-1β, TNF-α, Cox2). These findings suggest that the synergistic antioxidant properties of the Cur-CONPs that combine the sustained antioxidant properties of CONPs and acute anti-inflammatory capabilities of curcumin hold promise as a novel treatment strategy for IC.
Full article
(This article belongs to the Special Issue Antioxidant Potential and Bioactivity of Sustainable Green Nanoparticles)
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Open AccessReview
Metallothionein: A Comprehensive Review of Its Classification, Structure, Biological Functions, and Applications
by
Ruoqiu Yang, Dumila Roshani, Boya Gao, Pinglan Li and Nan Shang
Antioxidants 2024, 13(7), 825; https://doi.org/10.3390/antiox13070825 - 9 Jul 2024
Abstract
Metallothionein is a cysteine-rich protein with a high metal content that is widely found in nature. In addition to heavy metal detoxification, metallothionein is well known as a potent antioxidant. The high sulfhydryl content of metallothionein confers excellent antioxidant activity, enabling it to
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Metallothionein is a cysteine-rich protein with a high metal content that is widely found in nature. In addition to heavy metal detoxification, metallothionein is well known as a potent antioxidant. The high sulfhydryl content of metallothionein confers excellent antioxidant activity, enabling it to effectively scavenge free radicals and mitigate oxidative stress damage. In addition, metallothionein can play a neuroprotective role by alleviating oxidative damage in nerve cells, have an anticancer effect by enhancing the ability of normal cells to resist unfavorable conditions through its antioxidant function, and reduce inflammation by scavenging reactive oxygen species. Due to its diverse biological functions, metallothionein has a broad potential for application in alleviating environmental heavy metal pollution, predicting and diagnosing diseases, and developing skin care products and health foods. This review summarizes the recent advances in the classification, structure, biological functions, and applications of metallothionein, focusing on its powerful antioxidant effects and related functions.
Full article
(This article belongs to the Section ROS, RNS and RSS)
Open AccessArticle
Phenolic Composition and Bioactivities of Invasive Ailanthus altissima (Mill.) Swingle Leaf Extracts Obtained by Two-Step Sequential Extraction
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Maria Denisa Cocîrlea, Amalia Soare, Anca Roxana Petrovici, Mihaela Silion, Teodora Călin and Simona Oancea
Antioxidants 2024, 13(7), 824; https://doi.org/10.3390/antiox13070824 - 9 Jul 2024
Abstract
Ailanthus altissima, a highly invasive species, contains valuable compounds in different plant parts, indicating great practical potential. This paper proposes the use of non-polar (n-hexane) and polar (ethanol) solvents for the extraction of antioxidant compounds from A. altissima (family Simaroubaceae)
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Ailanthus altissima, a highly invasive species, contains valuable compounds in different plant parts, indicating great practical potential. This paper proposes the use of non-polar (n-hexane) and polar (ethanol) solvents for the extraction of antioxidant compounds from A. altissima (family Simaroubaceae) leaves in a sequential two-step process. Fresh and dried leaves were examined for their microstructure by scanning electron microscopy, and for color changes in the CIELAB color space co-ordinates. An investigation of the harvesting season, processing (freezing and drying), and solvent indicates ethanol can be used for the highly efficient extraction of phenolics, flavonoids, tannins, and carotenoids. Statistically significant differences were found between the autumn and summer samples for phenolic content, and between dried and frozen samples for tannin content. The HPLC phenolic profile indicates more phenolics (nine polyphenols) in dried leaves harvested in both seasons compared to those in frozen ones (five to six polyphenols). Frozen leaves showed a higher antioxidant activity in a ferric-reducing antioxidant power assay than that of the dried samples, which exhibited a higher antioxidant activity using the 1, 1-diphenyl-2-picryl-hydrazyl assay, but it was not statistically significant. The phenolic, flavonoid, and carotenoid contents significantly influenced the antioxidant activities. Among the ethanolic extracts, those from dried leaves showed better antibacterial activity, in particular, on Staphylococcus aureus and Enterococcus faecalis. The high bioactive content and activity of A. altissima leaves make them suitable natural raw materials for various applications.
Full article
(This article belongs to the Special Issue Plant Phenolics: Extraction, Analysis and Their Antioxidant Properties)
Open AccessSystematic Review
OxInflammatory Responses in the Wound Healing Process: A Systematic Review
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Fernanda Barbosa Lopes, Mariáurea Matias Sarandy, Rômulo Dias Novaes, Giuseppe Valacchi and Reggiani Vilela Gonçalves
Antioxidants 2024, 13(7), 823; https://doi.org/10.3390/antiox13070823 - 9 Jul 2024
Abstract
Significant sums are spent every year to find effective treatments to control inflammation and speed up the repair of damaged skin. This study investigated the main mechanisms involved in the skin wound cure. Consequently, it offered guidance to develop new therapies to control
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Significant sums are spent every year to find effective treatments to control inflammation and speed up the repair of damaged skin. This study investigated the main mechanisms involved in the skin wound cure. Consequently, it offered guidance to develop new therapies to control OxInflammation and infection and decrease functional loss and cost issues. This systematic review was conducted using the PRISMA guidelines, with a structured search in the MEDLINE (PubMed), Scopus, and Web of Science databases, analyzing 23 original studies. Bias analysis and study quality were assessed using the SYRCLE tool (Prospero number is CRD262 936). Our results highlight the activation of membrane receptors (IFN-δ, TNF-α, toll-like) in phagocytes, especially macrophages, during early wound healing. The STAT1, IP3, and NF-kβ pathways are positively regulated, while Ca2+ mobilization correlates with ROS production and NLRP3 inflammasome activation. This pathway activation leads to the proteolytic cleavage of caspase-1, releasing IL-1β and IL-18, which are responsible for immune modulation and vasodilation. Mediators such as IL-1, iNOS, TNF-α, and TGF-β are released, influencing pro- and anti-inflammatory cascades, increasing ROS levels, and inducing the oxidation of lipids, proteins, and DNA. During healing, the respiratory burst depletes antioxidant defenses (SOD, CAT, GST), creating a pro-oxidative environment. The IFN-δ pathway, ROS production, and inflammatory markers establish a positive feedback loop, recruiting more polymorphonuclear cells and reinforcing the positive interaction between oxidative stress and inflammation. This process is crucial because, in the immune system, the vicious positive cycle between ROS, the oxidative environment, and, above all, the activation of the NLRP3 inflammasome inappropriately triggers hypoxia, increases ROS levels, activates pro-inflammatory cytokines and inhibits the antioxidant action and resolution of anti-inflammatory cytokines, contributing to the evolution of chronic inflammation and tissue damage.
Full article
(This article belongs to the Special Issue The OxInflammation Process and Tissue Repair)
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Open AccessArticle
Green Synthesis of Metallic Nanoparticles from Quercus Bark Extracts: Characterization and Functional Properties
by
Năstaca-Alina Coman, Alexandra Nicolae-Maranciuc, Lavinia Berța, Alexandru Nicolescu, Mihai Babotă, Adrian Man, Dan Chicea, Lenard Farczadi, László Jakab-Farkas, Barbara Silva, Jéssica Veiga-Matos and Corneliu Tanase
Antioxidants 2024, 13(7), 822; https://doi.org/10.3390/antiox13070822 - 9 Jul 2024
Abstract
Quercus species are utilized for their durable wood, providing sustenance for wildlife, conserving biodiversity, and contributing ecological, medicinal, and esthetic benefits to ecosystems and landscapes. In this study, we aimed to use the bark of three Quercus species (Q. dalechampi, Q.
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Quercus species are utilized for their durable wood, providing sustenance for wildlife, conserving biodiversity, and contributing ecological, medicinal, and esthetic benefits to ecosystems and landscapes. In this study, we aimed to use the bark of three Quercus species (Q. dalechampi, Q. fraineto, and Q. petraea) for the synthesis of silver and gold nanoparticles (AgNPs and AuNPs). The aqueous extracts from the bark of Quercus sp. acted both as reducing and stabilizing agent, facilitating the rapid synthesis of AuNPs (AuQD, AuQF, and AuQP) and AgNPs (AgQD, AgQF, and AgQP). The obtained nanoparticles were characterized using UV-vis spectroscopy, TEM, DLS, and FTIR. Characterizations revealed that the nanoparticles exhibited a variety of shapes, such as polygonal, triangular, and spherical forms, with sizes ranging between 14 and 24 nm for AuNPs and 45–70 nm for AgNPs. The total phenolic content was assessed through spectroscopic methods, while several individual phenolic compounds were identified and quantified using UPLC-PDA. Furthermore, we assessed the antioxidant, antibacterial, and antifungal capacities of AuNPs, AgNPs, and raw extracts. The highest antioxidant activity was observed for raw extracts, followed by AgNPs and AuNPs, while the most potent antibacterial and antifungal activity was observed in AgQP. Moreover, cytotoxicity was examined in a human keratinocyte cell line (HaCaT). The results indicated no cytotoxic effects for AuNPs, while AgNPs and the raw extracts exhibited cytotoxic effects after 48 h of incubation. This research underscores the multifaceted utility of Quercus bark extracts in the green synthesis of metallic nanoparticles and their subsequent bioactivity assessment, suggesting promising perspectives for their application in various fields while urging cautious consideration of their cytotoxic implications.
Full article
(This article belongs to the Section Natural and Synthetic Antioxidants)
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Open AccessArticle
Differential Effects of Three Medium-Chain Fatty Acids on Mitochondrial Quality Control and Skeletal Muscle Maturation
by
Ryoichi Nishida, Shota Nukaga, Isao Kawahara, Yoshihiro Miyagawa, Kei Goto, Chie Nakashima, Yi Luo, Takamitsu Sasaki, Kiyomu Fujii, Hitoshi Ohmori, Ruiko Ogata, Shiori Mori, Rina Fujiwara-Tani and Hiroki Kuniyasu
Antioxidants 2024, 13(7), 821; https://doi.org/10.3390/antiox13070821 - 9 Jul 2024
Abstract
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Nutritional interventions are one focus of sarcopenia treatment. As medium-chain fatty acids (MCFAs) are oxidized in the mitochondria and produce energy through oxidative phosphorylation (OXPHOS), they are key parts of nutritional interventions. We investigated the in vitro effects of three types of MCFA,
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Nutritional interventions are one focus of sarcopenia treatment. As medium-chain fatty acids (MCFAs) are oxidized in the mitochondria and produce energy through oxidative phosphorylation (OXPHOS), they are key parts of nutritional interventions. We investigated the in vitro effects of three types of MCFA, caprylic acid (C8), capric acid (C10), and lauric acid (C12), in skeletal muscle cells. Compared with C10 and C12, C8 promoted mitophagy through the phosphatase and tensin homolog (PTEN)-induced kinase 1-Parkin pathway and increased the expression of peroxisome proliferator-activated receptor gamma coactivator 1-α and dynamin-related protein 1 to reduce mitochondrial oxidative stress and promote OXPHOS. Furthermore, the expression of myogenic differentiation 1 and myosin heavy chain increased in myotubes, thus promoting muscle differentiation and maturation. These results suggest that C8 improves mitochondrial quality and promotes skeletal muscle maturation; in contrast, C10 and C12 poorly promoted mitochondrial quality control and oxidative stress and suppressed energy production. Future animal experiments are required to establish the usefulness of C8 for nutritional interventions for sarcopenia.
Full article
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Open AccessReview
The Roles of White Adipose Tissue and Liver NADPH in Dietary Restriction-Induced Longevity
by
Leah E. Jamerson and Patrick C. Bradshaw
Antioxidants 2024, 13(7), 820; https://doi.org/10.3390/antiox13070820 - 8 Jul 2024
Abstract
Dietary restriction (DR) protocols frequently employ intermittent fasting. Following a period of fasting, meal consumption increases lipogenic gene expression, including that of NADPH-generating enzymes that fuel lipogenesis in white adipose tissue (WAT) through the induction of transcriptional regulators SREBP-1c and CHREBP. SREBP-1c knockout
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Dietary restriction (DR) protocols frequently employ intermittent fasting. Following a period of fasting, meal consumption increases lipogenic gene expression, including that of NADPH-generating enzymes that fuel lipogenesis in white adipose tissue (WAT) through the induction of transcriptional regulators SREBP-1c and CHREBP. SREBP-1c knockout mice, unlike controls, did not show an extended lifespan on the DR diet. WAT cytoplasmic NADPH is generated by both malic enzyme 1 (ME1) and the pentose phosphate pathway (PPP), while liver cytoplasmic NADPH is primarily synthesized by folate cycle enzymes provided one-carbon units through serine catabolism. During the daily fasting period of the DR diet, fatty acids are released from WAT and are transported to peripheral tissues, where they are used for beta-oxidation and for phospholipid and lipid droplet synthesis, where monounsaturated fatty acids (MUFAs) may activate Nrf1 and inhibit ferroptosis to promote longevity. Decreased WAT NADPH from PPP gene knockout stimulated the browning of WAT and protected from a high-fat diet, while high levels of NADPH-generating enzymes in WAT and macrophages are linked to obesity. But oscillations in WAT [NADPH]/[NADP+] from feeding and fasting cycles may play an important role in maintaining metabolic plasticity to drive longevity. Studies measuring the WAT malate/pyruvate as a proxy for the cytoplasmic [NADPH]/[NADP+], as well as studies using fluorescent biosensors expressed in the WAT of animal models to monitor the changes in cytoplasmic [NADPH]/[NADP+], are needed during ad libitum and DR diets to determine the changes that are associated with longevity.
Full article
(This article belongs to the Special Issue Oxidative Stress in Adipose Tissue)
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Open AccessArticle
Kinetic Insights into the Antioxidant Effect of Isatin-Thiosemicarbazone in Biodiesel Blends
by
Nalan Türköz Karakullukçu, Halit Muğlu, Hasan Yakan, Volkan Murat Yılmaz, Sarmad Marah and İkbal Agah İnce
Antioxidants 2024, 13(7), 819; https://doi.org/10.3390/antiox13070819 - 8 Jul 2024
Abstract
Biodiesel has several drawbacks, such as being prone to oxidation, having reduced stability, and having limited storage time. Antioxidants compatible with biodiesel are being used to address its drawbacks. Utilizing antioxidants effectively improves the quality of biodiesel. Enhancing the quality of biodiesel for
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Biodiesel has several drawbacks, such as being prone to oxidation, having reduced stability, and having limited storage time. Antioxidants compatible with biodiesel are being used to address its drawbacks. Utilizing antioxidants effectively improves the quality of biodiesel. Enhancing the quality of biodiesel for use as a clean energy source benefits both the global economy and ecology. Therefore, we believe that our work will contribute to the advancement of the biodiesel industry worldwide. This study used blends consisting of 20% biodiesel and 80% diesel fuel. Isatin-thiosemicarbazones were tested as additives in blends at a concentration of 3000 parts per million (ppm) using an oxifast device and were compared with the chemical antioxidant Trolox. FT-IR, DSC, and TGA were used to characterize these samples. DSC measured sample crystallization temperatures (Tc). Samples with antioxidants showed decreased values compared to the non-antioxidant diesel sample D100. Several DSC tests were conducted to determine the antioxidant strengths of various samples. The results show that the FT-IR spectrum’s antioxidant effect regions grow clearer with antioxidants. The extra antioxidant is effective. Biodiesel’s oxidative stability improves with isatin-thiosemicarbazones at varying concentrations. The kinetics of thermal decomposition of isatin-thiosemicarbazones under non-isothermal conditions were determined using the Kissinger, Ozawa, and Boswell techniques. The activation energies of compounds 1 and 2 were calculated as 137–147 kJ mol−1 and 173–183 kJ mol−1, respectively.
Full article
Open AccessArticle
Nrf2 Deficiency Accelerates IL-17-Dependent Neutrophilic Airway Inflammation in Asthmatic Mice
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Kenya Kuramoto, Yuko Morishima, Kazufumi Yoshida, Satoshi Ano, Kai Kawashima, Yuki Yabuuchi, Chio Sakai, Sosuke Matsumura, Kengo Nishino, Kai Yazaki, Masashi Matsuyama, Takumi Kiwamoto, Yukio Ishii and Nobuyuki Hizawa
Antioxidants 2024, 13(7), 818; https://doi.org/10.3390/antiox13070818 - 8 Jul 2024
Abstract
Asthma is a heterogeneous disease that can be broadly classified into type 2, which is primarily steroid-sensitive and eosinophilic, and non-type 2, which is primarily steroid-resistant and neutrophilic. While the mechanisms leading to the development of molecular-targeted therapies for type 2 asthma are
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Asthma is a heterogeneous disease that can be broadly classified into type 2, which is primarily steroid-sensitive and eosinophilic, and non-type 2, which is primarily steroid-resistant and neutrophilic. While the mechanisms leading to the development of molecular-targeted therapies for type 2 asthma are being elucidated, much remains to be learned about non-type 2 asthma. To investigate the role of oxidative stress in refractory allergic airway inflammation, we compared asthma models generated by immunizing wild-type and nuclear factor erythroid-2-related factor 2 (Nrf2)-deficient mice with the house dust mite antigen. Both asthma models had similar levels of airway inflammation and hyperresponsiveness, but the Nrf2-deficient mice had increased oxidative stress and exacerbated neutrophilic airway inflammation compared with the wild-type mice. Type 2 cytokines and the expression of GATA3, a transcription factor that is important for Th2 cell differentiation, had decreased in Nrf2-deficient mice compared with the wild-type mice, whereas helper T (Th) 17 cytokines and the expression of RORγt, which is important for Th17 cell differentiation, had increased. Furthermore, the neutrophilic airway inflammation caused by Nrf2 deficiency was ameliorated by interleukin (IL)-17 neutralization. We have concluded that the disruption of the Nrf2-mediated antioxidant defense system contributed to the induction of Th17 differentiation and exacerbated allergic neutrophilic airway inflammation.
Full article
(This article belongs to the Special Issue Oxidative Stress in Respiratory Diseases)
Open AccessArticle
Ganoderma Microsporum Immunomodulatory Protein Alleviates Inflammaging and Oxidative Stress in Diabetes-Associated Periodontitis via Nrf2 Signaling Activation: An In Vitro Study
by
Ni-Yu Su, Min Yee Ng, Heng-Yi Liao, Yi-Wen Liao, Movina Wu, Shih-Chi Chao, Cheng-Chia Yu and Yu-Chao Chang
Antioxidants 2024, 13(7), 817; https://doi.org/10.3390/antiox13070817 - 8 Jul 2024
Abstract
Periodontitis, characterized by inflammation and loss of periodontal tissue, is a significant health complication for individuals with diabetes mellitus (DM). Buildup of advanced glycation end-products (AGEs) in DM poses an increased risk of periodontitis via inflammaging. Ganoderma immunomodulatory protein (GMI) shows promise in
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Periodontitis, characterized by inflammation and loss of periodontal tissue, is a significant health complication for individuals with diabetes mellitus (DM). Buildup of advanced glycation end-products (AGEs) in DM poses an increased risk of periodontitis via inflammaging. Ganoderma immunomodulatory protein (GMI) shows promise in suppressing inflammaging by mitigating oxidative stress and inflammation via Nrf2 modulation. However, its specific protective effects are not fully understood. Thus, this study aimed to investigate GMI’s anti-inflammaging properties and its underlying mechanism in diabetic-associated periodontitis (DP). We first simulated DP by culturing human gingival fibroblasts (HGFs) with AGEs and lipopolysaccharides from P. gingivalis (LPS). We then evaluated the impact of GMI on cell proliferation, migration and wound healing. Additionally, we assessed GMI’s effects on the components of inflammaging such as reactive oxygen species (ROS) formation, cellular senescence expression, IL-6 and IL-8 secretions, and NF-κB phosphorylation. Next, we explored whether GMI’s anti-inflammaging effects are mediated through the Nrf2 pathway by evaluating Nrf2 and HO-1, followed by the assessment of IL-6 and IL-8 post-Nrf2 knockdown. Our findings revealed that GMI treatment suppressed ROS production, cell senescence, IL-6 and IL-8 and NF-κB phosphorylation. Furthermore, GMI upregulated Nrf2/HO-1 expression and its protective effects were reversed when Nrf2 was knocked down. In conclusion, GMI exerts its anti-inflammaging effect via the modulation of the Nrf2/NF-κB signaling axis in DP in vitro, highlighting its potential as an effective adjunct treatment for diabetes-related periodontitis.
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(This article belongs to the Special Issue Free Radicals, Antioxidants and Oxidative Stress in Aging and Age-Related Diseases)
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Open AccessArticle
Dietary Protease Supplementation Improved Growth Performance and Nutrients Digestion via Modulating Intestine Barrier, Immunological Response, and Microbiota Composition in Weaned Piglets
by
Tao Liu, Wen Ma, Jun Wang, Yulong Wei, Yibo Wang, Zheng Luo, Ying Zhang, Xiangfang Zeng, Wutai Guan, Dan Shao and Fang Chen
Antioxidants 2024, 13(7), 816; https://doi.org/10.3390/antiox13070816 - 8 Jul 2024
Abstract
Despite mounting evidence for dietary protease benefits, the mechanisms beyond enhanced protein degradation are poorly understood. This study aims to thoroughly investigate the impact of protease addition on the growth performance, intestinal function, and microbial composition of weaned piglets. Ninety 28-day-old weaned pigs
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Despite mounting evidence for dietary protease benefits, the mechanisms beyond enhanced protein degradation are poorly understood. This study aims to thoroughly investigate the impact of protease addition on the growth performance, intestinal function, and microbial composition of weaned piglets. Ninety 28-day-old weaned pigs were randomly assigned to the following three experimental diets based on their initial body weight for a 28-day experiment: (1) control (CC), a basic diet with composite enzymes without protease; (2) negative control (NC), a diet with no enzymes; and (3) dietary protease (PR), a control diet with protease. The results show that dietary proteases significantly enhanced growth performance and boosted antioxidant capacity, increasing the total antioxidant capacity (T-AOC) levels (p < 0.05) while reducing malonaldehyde levels (p < 0.05). Additionally, protease addition reduced serum levels of inflammatory markers TNF-α, IL-1β, and IL-6 (p < 0.05), suppressed mRNA expression of pro-inflammatory factors in the jejunum (p < 0.01), and inhibited MAPK and NF-κB signaling pathways. Moreover, protease-supplemented diets improved intestinal morphology and barrier integrity, including zonula occludens protein 1(ZO-1), Occludin, and Claudin-1 (p < 0.05). Microbiota compositions were also significantly altered by protease addition with increased abundance of beneficial bacteria (Lachnospiraceae_AC2044_group and Prevotellaceae_UCG-001) (p < 0.05) and reduced harmful Terrisporobacter (p < 0.05). Further correlation analysis revealed a positive link between beneficial bacteria and growth performance and a negative association with inflammatory factors and intestinal permeability. In summary, dietary protease addition enhanced growth performance in weaned piglets, beneficial effects which were associated with improved intestinal barrier integrity, immunological response, and microbiota composition.
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(This article belongs to the Special Issue Role of Antioxidants Intake on Gut Microbiome)
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Open AccessReview
Synergistic Mechanisms of Selected Polyphenols in Overcoming Chemoresistance and Enhancing Chemosensitivity in Colorectal Cancer
by
Kha Wai Hon and Rakesh Naidu
Antioxidants 2024, 13(7), 815; https://doi.org/10.3390/antiox13070815 - 7 Jul 2024
Abstract
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Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide. Despite significant advances in medical treatment, chemotherapy as monotherapy can lead to substantial side effects and chemoresistance. This underscores the need for therapeutic approaches that are not only pharmacologically safe but also
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Colorectal cancer (CRC) is a leading cause of cancer deaths worldwide. Despite significant advances in medical treatment, chemotherapy as monotherapy can lead to substantial side effects and chemoresistance. This underscores the need for therapeutic approaches that are not only pharmacologically safe but also modulate multiple potent signaling pathways and sensitize cancer cells to overcome resistance to standard drugs. In recent years, scientists have been searching for natural compounds that can be used as chemosensitizers in addition to conventional medications for the synergistic treatment of CRC. Polyphenols represent a diverse group of natural compounds that can target multiple signaling pathways in cancer cells to induce anti-cancer effects. Additionally, polyphenols have been shown to work synergistically with chemotherapeutics and other natural compounds in cancer cells. This review aims to provide a comprehensive insight into the synergistic mechanisms of selected polyphenols as chemosensitizers in CRC cells. Further research and clinical trials are warranted to fully harness the synergistic mechanisms of selected polyphenols combined with chemotherapy or natural compounds in improving cancer treatment outcomes.
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Open AccessArticle
Mitochondria of Porcine Oocytes Synthesize Melatonin, Which Improves Their In Vitro Maturation and Embryonic Development
by
Tianqi Zhu, Laiqing Yan, Shoulong Deng, Wenkui Ma, Fan Xia, Likai Wang, Xiao Ma, Guangdong Li, Zixia Shen, Yiwei Wang, Yao Fu, Pengyun Ji, Bingyuan Wang, Lu Zhang and Guoshi Liu
Antioxidants 2024, 13(7), 814; https://doi.org/10.3390/antiox13070814 - 7 Jul 2024
Abstract
The in vitro maturation efficiency of porcine oocytes is relatively low, and this limits the production of in vitro porcine embryos. Since melatonin is involved in mammalian reproductive physiology, in this study, we have explored whether endogenously produced melatonin can help in porcine
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The in vitro maturation efficiency of porcine oocytes is relatively low, and this limits the production of in vitro porcine embryos. Since melatonin is involved in mammalian reproductive physiology, in this study, we have explored whether endogenously produced melatonin can help in porcine oocyte in vitro maturation. We have found, for the first time in the literature, that mitochondria are the major sites for melatonin biosynthesis in porcine oocytes. This mitochondrially originated melatonin reduces ROS production and increases the activity of the mitochondrial respiratory electron transport chain, mitochondrial biogenesis, mitochondrial membrane potential, and ATP production. Therefore, melatonin improves the quality of oocytes and their in vitro maturation. In contrast, the reduced melatonin level caused by siRNA to knockdown AANAT (siAANAT) is associated with the abnormal distribution of mitochondria, decreasing the ATP level of porcine oocytes and inhibiting their in vitro maturation. These abnormalities can be rescued by melatonin supplementation. In addition, we found that siAANAT switches the mitochondrial oxidative phosphorylation to glycolysis, a Warburg effect. This metabolic alteration can also be corrected by melatonin supplementation. All these activities of melatonin appear to be mediated by its membrane receptors since the non-selective melatonin receptor antagonist Luzindole can blunt the effects of melatonin. Taken together, the mitochondria of porcine oocytes can synthesize melatonin and improve the quality of oocyte maturation. These results provide an insight from a novel aspect to study oocyte maturation under in vitro conditions.
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(This article belongs to the Special Issue Free-Radical Scavenging and Antioxidant Properties of Melatonin, 2nd Edition)
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Open AccessArticle
α-Cyclodextrin/Moringin Induces an Antioxidant Transcriptional Response Activating Nrf2 in Differentiated NSC-34 Motor Neurons
by
Agnese Gugliandolo, Gabriella Calì, Claudia Muscarà, Osvaldo Artimagnella, Patrick Rollin, Daniele Perenzoni, Renato Iori, Emanuela Mazzon and Luigi Chiricosta
Antioxidants 2024, 13(7), 813; https://doi.org/10.3390/antiox13070813 - 6 Jul 2024
Abstract
Oxidative stress is a common feature of neurodegenerative diseases. Different natural compounds mediate neuroprotective effects by activating the Nrf2 antioxidant response. Some isothiocyanates are Nrf2 activators, including Moringin (MOR). In this study, the transcriptional profile of differentiated NSC-34 motor neurons was evaluated after
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Oxidative stress is a common feature of neurodegenerative diseases. Different natural compounds mediate neuroprotective effects by activating the Nrf2 antioxidant response. Some isothiocyanates are Nrf2 activators, including Moringin (MOR). In this study, the transcriptional profile of differentiated NSC-34 motor neurons was evaluated after treatment for 48 h and 96 h with concentrations of 0.5, 5, and 10 µM of a new MOR formulation obtained with α-cyclodextrin (α-CD). All the concentrations increased gene expression and cytoplasmic protein levels of Nrf2 at 96 h. However, the highest dose also increased nuclear Nrf2 levels at 96 h. Then, Nrf2 interactors were selected using STRING, and common biological process (BP) terms between the groups were evaluated. α-CD/MOR was able to modulate BP related to responses to oxidative stress, proteostasis, and autophagy. Specifically, the treatment with 10 µM of α-CD/MOR for 96 h induced genes involved in glutathione synthesis and proteasome subunits and reduced the expression of genes related to endoplasmic reticulum stress. Moreover, this group showed the lowest levels of the apoptotic markers Bax, cleaved caspase 9, and cleaved caspase 3. These results indicate the beneficial effects of prolonged α-CD/MOR supplementation that are mediated, at least in part, by Nrf2 activation. Then, α-CD/MOR could be a valuable treatment against neurodegenerative diseases, in particular motor neuron degeneration.
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(This article belongs to the Special Issue Role of Nrf2 in Neurodegenerative Diseases)
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