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Antioxidants
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Antioxidant Enzymes and Human Health
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Antioxidant Enzymes and Human Health

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 18069

Special Issue Editors

Dr. Janka Vašková

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Guest Editor
Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Tr. SNP 1, 040 11 Košice, Slovak Republic
Interests: antioxidant; antioxidant enzyme; antioxidant activity; glutathione; humic acids; chelators
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Mária Mareková

E-Mail Website
Guest Editor
Department of Medical and Clinical Biochemistry, Faculty of Medicine, Pavol Jozef Šafárik University in Košice, Tr. SNP 1, 040 11 Košice, Slovakia
Interests: antioxidant enzymes; Melanoma; cardivascular; MMP; obesity

Special Issue Information

Dear Colleagues,

The reactive forms of oxygen and nitrogen are formed in the organism under physiological and induced conditions. At low, physiological levels, they act as redox messengers in intracellular signaling pathways and regulations, but the increased intensity of production can induce oxidative stress conditions. Proteins with enzymatic activity that contain transition metals as cofactors are the most effective defense. Due to their importance, they are ubiquitous molecules in the body, and thus become suitable markers for monitoring the extent of the effect of various substances and the characterization of normal physiological conditions (leading to the maintenance of health or pathophysiological processes, as well as the development or deepening of a disease state). The antioxidant defense system, which includes enzymatic antioxidants as well as non-enzymatic low-molecular metabolites, is influenced by a number of other factors and circumstances, such as the intake of exogenous anti- or pro-oxidant substances and the subsequent possible compensatory induction of antioxidant enzymes or even prooxidant catalysis. It also includes the intake, transportation, and binding of metals to organic compounds in the body, since antioxidant enzymes are mostly metalloproteins and genetic polymorphisms affecting enzyme activities and different organ-specific isoform expressions.

Dr. Janka Vašková
Prof. Dr. Mária Mareková
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • oxygen
  • nitrogen
  • oxidative stress
  • enzymatic activity
  • antioxidant defense system
  • antioxidant enzymes
  • metalloproteins

Published Papers (7 papers)

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Research

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14 pages, 2678 KiB  
Article
Peroxiredoxin V Protects against UVB-Induced Damage of Keratinocytes
by Sin Ri Kim, Ji Won Park, Byung-Hoon Lee, Kyung Min Lim and Tong-Shin Chang
Antioxidants 2023, 12(7), 1435; https://doi.org/10.3390/antiox12071435 - 16 Jul 2023
Viewed by 1751
Abstract
Ultraviolet B (UVB) irradiation generates reactive oxygen species (ROS), which can damage exposed skin cells. Mitochondria and NADPH oxidase are the two principal producers of ROS in UVB-irradiated keratinocytes. Peroxiredoxin V (PrxV) is a mitochondrial and cytosolic cysteine-dependent peroxidase enzyme that robustly removes [...] Read more.
Ultraviolet B (UVB) irradiation generates reactive oxygen species (ROS), which can damage exposed skin cells. Mitochondria and NADPH oxidase are the two principal producers of ROS in UVB-irradiated keratinocytes. Peroxiredoxin V (PrxV) is a mitochondrial and cytosolic cysteine-dependent peroxidase enzyme that robustly removes H2O2. We investigated PrxV’s role in protecting epidermal keratinocytes against UVB-induced ROS damage. We separated mitochondrial and cytosolic H2O2 levels from other types of ROS using fluorescent H2O2 indicators. Upon UVB irradiation, PrxV-knockdown HaCaT human keratinocytes showed higher levels of mitochondrial and cytosolic H2O2 than PrxV-expressing controls. PrxV depletion enhanced hyperoxidation-mediated inactivation of mitochondrial PrxIII and cytosolic PrxI and PrxII in UVB-irradiated keratinocytes. PrxV-depleted keratinocytes exhibited mitochondrial dysfunction and were more susceptible to apoptosis through decreased oxygen consumption rate, loss of mitochondrial membrane potential, cardiolipin oxidation, cytochrome C release, and caspase activation. Our findings show that PrxV serves to protect epidermal keratinocytes from UVB-induced damage such as mitochondrial dysfunction and apoptosis, not only by directly removing mitochondrial and cytosolic H2O2 but also by indirectly improving the catalytic activity of mitochondrial PrxIII and cytosolic PrxI and PrxII. It is possible that strengthening PrxV defenses could aid in preventing UVB-induced skin damage. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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19 pages, 5859 KiB  
Article
Regulation of CD163 Receptor in Patients with Abdominal Aortic Aneurysm and Associations with Antioxidant Enzymes HO-1 and NQO1
by Bianca Hamann, Anna Klimova, Felicia Klotz, Frieda Frank, Christian Jänichen, Marvin Kapalla, Pamela Sabarstinski, Steffen Wolk, Henning Morawietz, David M. Poitz, Anja Hofmann and Christian Reeps
Antioxidants 2023, 12(4), 947; https://doi.org/10.3390/antiox12040947 - 18 Apr 2023
Cited by 1 | Viewed by 1095
Abstract
Red blood cells are found within the abdominal aortic aneurysm (AAA), in the intraluminal thrombus (ILT), and in neovessels. Hemolysis promotes aortic degeneration, e.g., by heme-induced reactive oxygen species formation. To reduce its toxicity, hemoglobin is endocytosed by the CD163 receptor and heme [...] Read more.
Red blood cells are found within the abdominal aortic aneurysm (AAA), in the intraluminal thrombus (ILT), and in neovessels. Hemolysis promotes aortic degeneration, e.g., by heme-induced reactive oxygen species formation. To reduce its toxicity, hemoglobin is endocytosed by the CD163 receptor and heme is degraded by heme oxygenase-1 (HO-1). A soluble form (sCD163) is discussed as an inflammatory biomarker representing the activation of monocytes and macrophages. HO-1 and NAD(P)H quinone dehydrogenase 1 (NQO1) are antioxidant genes that are induced by the Nrf2 transcription factor, but their regulation in AAA is only poorly understood. The aim of the present study was to analyze linkages between CD163, Nrf2, HO-1, and NQO1 and to clarify if plasma sCD163 has diagnostic and risk stratification potential. Soluble CD163 was 1.3-fold (p = 0.015) higher in AAA compared to patients without arterial disease. The difference remained significant after adjusting for age and sex. sCD163 correlated with the thickness of the ILT (rs = 0.26; p = 0.02) but not with the AAA diameter or volume. A high aneurysmal CD163 mRNA was connected to increases in NQO1, HMOX1, and Nrf2 mRNA. Further studies are needed to analyze the modulation of the CD163/HO-1/NQO1 pathway with the overall goal of minimizing the detrimental effects of hemolysis. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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16 pages, 2152 KiB  
Article
Binding to Iron Quercetin Complexes Increases the Antioxidant Capacity of the Major Birch Pollen Allergen Bet v 1 and Reduces Its Allergenicity
by Andreas Regner, Nathalie Szepannek, Markus Wiederstein, Aila Fakhimahmadi, Luis F. Paciosis, Bart R. Blokhuis, Frank A. Redegeld, Gerlinde Hofstetter, Zdenek Dvorak, Erika Jensen-Jarolim, Karin Hufnagl and Franziska Roth-Walter
Antioxidants 2023, 12(1), 42; https://doi.org/10.3390/antiox12010042 - 26 Dec 2022
Cited by 4 | Viewed by 2636
Abstract
Bet v 1 is the major allergen in birch pollen to which up to 95% of patients sensitized to birch respond. As a member of the pathogenesis-related PR 10 family, its natural function is implicated in plant defense, with a member of the [...] Read more.
Bet v 1 is the major allergen in birch pollen to which up to 95% of patients sensitized to birch respond. As a member of the pathogenesis-related PR 10 family, its natural function is implicated in plant defense, with a member of the PR10 family being reported to be upregulated under iron deficiency. As such, we assessed the function of Bet v 1 to sequester iron and its immunomodulatory properties on human immune cells. Binding of Bet v 1 to iron quercetin complexes FeQ2 was determined in docking calculations and by spectroscopy. Serum IgE-binding to Bet v 1 with (holoBet v1) and without ligands (apoBet v 1) were assessed by ELISA, blocking experiments and Western Blot. Crosslinking-capacity of apo/holoBet v 1 were assessed on human mast cells and Arylhydrocarbon receptor (AhR) activation with the human reporter cellline AZ-AHR. Human PBMCs were stimulated and assessed for labile iron and phenotypic changes by flow cytometry. Bet v 1 bound to FeQ2 strongly with calculated Kd values of 1 nm surpassing affinities to quercetin alone nearly by a factor of 1000. Binding to FeQ2 masked IgE epitopes and decreased IgE binding up to 80% and impaired degranulation of sensitized human mast cells. Bet v 1 facilitated the shuttling of quercetin, which activated the anti-inflammatory AhR pathway and increased the labile iron pool of human monocytic cells. The increase of labile iron was associated with an anti-inflammatory phenotype in CD14+monocytes and downregulation of HLADR. To summarize, we reveal for the first time that FeQ2 binding reduces the allergenicity of Bet v 1 due to ligand masking, but also actively contributes anti-inflammatory stimuli to human monocytes, thereby fostering tolerance. Nourishing immune cells with complex iron may thus represent a promising antigen-independent immunotherapeutic approach to improve efficacy in allergen immunotherapy. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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22 pages, 5967 KiB  
Article
UHPLC-MS Chemical Fingerprinting and Antioxidant, Enzyme Inhibition, Anti-Inflammatory In Silico and Cytoprotective Activities of Cladonia chlorophaea and C. gracilis (Cladoniaceae) from Antarctica
by Alfredo Torres-Benítez, José Erick Ortega-Valencia, Marta Sánchez, Mathias Hillmann-Eggers, María Pilar Gómez-Serranillos, Gabriel Vargas-Arana and Mario J. Simirgiotis
Antioxidants 2023, 12(1), 10; https://doi.org/10.3390/antiox12010010 - 21 Dec 2022
Cited by 4 | Viewed by 1606
Abstract
The lichen species Cladonia chlorophaea and C. gracilis (Cladoniaceae) are widely distributed in the island archipelago of maritime Antarctica and represent a natural resource of scientific interest. In this work, the metabolomic characterization of the ethanolic extracts of these species and the determination [...] Read more.
The lichen species Cladonia chlorophaea and C. gracilis (Cladoniaceae) are widely distributed in the island archipelago of maritime Antarctica and represent a natural resource of scientific interest. In this work, the metabolomic characterization of the ethanolic extracts of these species and the determination of the antioxidant activity, enzymatic inhibition and anti-inflammatory potential of selected compounds on the 5-lipoxygenase enzyme by molecular docking and cytoprotective activity in the SH-SY5Y cell line were carried out. Nineteen compounds were identified by liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry (UHPLC-ESI-QTOF-MS) in each of the species. The contents of phenolic compounds, antioxidant activity, the inhibition of cholinesterases (acetylcholinesterase and butyrylcholinesterase) and digestive enzymes (α-glucosidase and pancreatic lipase) were variable among species, with better results in C. chlorophaea. Molecular docking evidenced significant binding affinities of some compounds for the 5-lipoxygenase enzyme, together with outstanding pharmacokinetic properties. Both extracts were shown to promote cell viability and a reduction in reactive oxygen species production in an H2O2-induced oxidative stress model. This study contributes to the chemical knowledge of the Cladonia species and demonstrates the biological potential for the prevention and promising treatment of central nervous system pathologies, inflammatory disorders and metabolic alterations. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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19 pages, 6310 KiB  
Article
Recombinant Photolyase-Thymine Alleviated UVB-Induced Photodamage in Mice by Repairing CPD Photoproducts and Ameliorating Oxidative Stress
by Zhaoyang Wang, Ziyi Li, Yaling Lei, Yuan Liu, Yuqing Feng, Derong Chen, Siying Ma, Ziyan Xiao, Meirong Hu, Jingxian Deng, Yuxin Wang, Qihao Zhang, Yadong Huang and Yan Yang
Antioxidants 2022, 11(12), 2312; https://doi.org/10.3390/antiox11122312 - 22 Nov 2022
Cited by 2 | Viewed by 1663
Abstract
Cyclobutane pyrimidine dimers (CPDs) are the main mutagenic DNA photoproducts caused by ultraviolet B (UVB) radiation and represent the major cause of photoaging and skin carcinogenesis. CPD photolyase can efficiently and rapidly repair CPD products. Therefore, they are candidates for the prevention of [...] Read more.
Cyclobutane pyrimidine dimers (CPDs) are the main mutagenic DNA photoproducts caused by ultraviolet B (UVB) radiation and represent the major cause of photoaging and skin carcinogenesis. CPD photolyase can efficiently and rapidly repair CPD products. Therefore, they are candidates for the prevention of photodamage. However, these photolyases are not present in placental mammals. In this study, we produced a recombinant photolyase-thymine (rPHO) from Thermus thermophilus (T. thermophilus). The rPHO displayed CPD photorepair activity. It prevented UVB-induced DNA damage by repairing CPD photoproducts to pyrimidine monomers. Furthermore, it inhibited UVB-induced ROS production, lipid peroxidation, inflammatory responses, and apoptosis. UVB-induced wrinkle formation, epidermal hyperplasia, and collagen degradation in mice skin was significantly inhibited when the photolyase was applied topically to the skin. These results demonstrated that rPHO has promising protective effects against UVB-induced photodamage and may contribute to the development of anti-UVB skin photodamage drugs and cosmetic products. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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Review

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20 pages, 2380 KiB  
Review
The Applications and Mechanisms of Superoxide Dismutase in Medicine, Food, and Cosmetics
by Mengli Zheng, Yating Liu, Guanfeng Zhang, Zhikang Yang, Weiwei Xu and Qinghua Chen
Antioxidants 2023, 12(9), 1675; https://doi.org/10.3390/antiox12091675 - 27 Aug 2023
Cited by 11 | Viewed by 6153
Abstract
Superoxide dismutase (SOD) is a class of enzymes that restrict the biological oxidant cluster enzyme system in the body, which can effectively respond to cellular oxidative stress, lipid metabolism, inflammation, and oxidation. Published studies have shown that SOD enzymes (SODs) could maintain a [...] Read more.
Superoxide dismutase (SOD) is a class of enzymes that restrict the biological oxidant cluster enzyme system in the body, which can effectively respond to cellular oxidative stress, lipid metabolism, inflammation, and oxidation. Published studies have shown that SOD enzymes (SODs) could maintain a dynamic balance between the production and scavenging of biological oxidants in the body and prevent the toxic effects of free radicals, and have been shown to be effective in anti-tumor, anti-radiation, and anti-aging studies. This research summarizes the types, biological functions, and regulatory mechanisms of SODs, as well as their applications in medicine, food production, and cosmetic production. SODs have proven to be a useful tool in fighting disease, and mimetics and conjugates that report SODs have been developed successively to improve the effectiveness of SODs. There are still obstacles to solving the membrane permeability of SODs and the persistence of enzyme action, which is still a hot spot and difficulty in mining the effect of SODs and promoting their application in the future. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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25 pages, 1122 KiB  
Review
Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review
by Marina M. Tavleeva, Elena S. Belykh, Anna V. Rybak, Elena E. Rasova, Aleksey A. Chernykh, Zaur B. Ismailov and Ilya O. Velegzhaninov
Antioxidants 2022, 11(12), 2316; https://doi.org/10.3390/antiox11122316 - 23 Nov 2022
Cited by 5 | Viewed by 2214
Abstract
Reactive oxygen species (ROS) are normal products of a number of biochemical reactions and are important signaling molecules. However, at the same time, they are toxic to cells and have to be strictly regulated by their antioxidant systems. The etiology and pathogenesis of [...] Read more.
Reactive oxygen species (ROS) are normal products of a number of biochemical reactions and are important signaling molecules. However, at the same time, they are toxic to cells and have to be strictly regulated by their antioxidant systems. The etiology and pathogenesis of many diseases are associated with increased ROS levels, and many external stress factors directly or indirectly cause oxidative stress in cells. Within this context, the overexpression of genes encoding the proteins in antioxidant systems seems to have become a viable approach to decrease the oxidative stress caused by pathological conditions and to increase cellular stress resistance. However, such manipulations unavoidably lead to side effects, the most dangerous of which is an increased probability of healthy tissue malignization or increased tumor aggression. The aims of the present review were to collect and systematize the results of studies devoted to the effects resulting from the overexpression of antioxidant system genes on stress resistance and carcinogenesis in vitro and in vivo. In most cases, the overexpression of these genes was shown to increase cell and organism resistances to factors that induce oxidative and genotoxic stress but to also have different effects on cancer initiation and promotion. The last fact greatly limits perspectives of such manipulations in practice. The overexpression of GPX3 and SOD3 encoding secreted proteins seems to be the “safest” among the genes that can increase cell resistance to oxidative stress. High efficiency and safety potential can also be found for SOD2 overexpression in combinations with GPX1 or CAT and for similar combinations that lead to no significant changes in H2O2 levels. Accumulation, systematization, and the integral analysis of data on antioxidant gene overexpression effects can help to develop approaches for practical uses in biomedical and agricultural areas. Additionally, a number of factors such as genetic and functional context, cell and tissue type, differences in the function of transcripts of one and the same gene, regulatory interactions, and additional functions should be taken into account. Full article
(This article belongs to the Special Issue Antioxidant Enzymes and Human Health)
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