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Antioxidants
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Commemorative Issue of Antioxidants Dedicated to Peter Eckl
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Commemorative Issue of Antioxidants Dedicated to Peter Eckl

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Aberrant Oxidation of Biomolecules".

Deadline for manuscript submissions: closed (15 May 2021) | Viewed by 20091

Special Issue Editors

Dr. Nikolaus Bresgen

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Guest Editor
Department of Biosciences, Universitat Salzburg, Salzburg, Austria
Prof. Dr. Werner Siems

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Guest Editor
Institute of Physiotherapy and Gerontology of Kortexmed, 38667 Bad Harzburg, Germany

Special Issue Information

 Dear Colleagues,

Peter ECKL (born in 1954), who held a professorship at the Department of Biosciences at the University of Salzburg, Austria started his scientific career in the field of radiation research. During his stay as post-doc in the laboratory of Randy Jirtle at Duke University (Durham, North Carolina, USA), Peter Eckl successfully developed a protocol for the serum-free culture of proliferating primary rat hepatocytes to be used in geno- and cytotoxicity testing. Among the first applications of this in vitro system, Peter Eckl, in collaboration with the 4-hydoxynoenenal (HNE) pioneer Hermann Esterbauer, studied the genotoxic potential of lipid peroxidation-derived 4-hydroxyalkenals. This early study revealed a strong mutagenic potential of HNE in primary hepatocytes exceeding that seen in other, non-hepatic test systems; a finding which emphasized the metabolic aspect of HNE toxicity. From this time on, the subject oxidative stress, and in particular lipid peroxidation and “the cell biology of HNE”, became most influential to Peter Eckl’s scientific career. Research conducted in the “Eckl Lab” comprised studies on the effects of oxidative stress and HNE in cerebral endothelial cells and astrocytes, investigations on the genotoxicity of beta-carotene breakdown products, and studies on the antioxidant/anti-mutagenic properties of vitamins and compounds of ethno-pharmacological interest. The finding of ferritin cytotoxicity directed his research interests to iron-related effects, which, not unexpectedly, also turned out to be intimately linked with lipid-peroxidation. Most of the recent research was dealing with mechanisms by which oxidatively stressed cells manage to eliminate lipid-peroxidation products, especially highly-crosslinked aggregates of HNE-modified proteins. Peter Eckl’s long standing fascination for the oxidative stress mediator HNE became also manifest by his dedicated activity for the HNE-club, an international association of scientists affiliated to oxidative stress research. The next biannual meeting of the HNE-club will take place from 15th–17th of June, 2020 in Milan, Italy (https://sites.unimi.it/HNECLUB/hne2020/).

Professor Peter ECKL has been the Editorial Board member of Antioxidants since 2015. This commemorative issue of Antioxidants aims at compiling recent progress in the still expanding field of oxidative stress and lipid peroxidation covering its manifold biological and medical implications as well as aspects of antioxidant defence. Submissions of previously unpublished manuscripts (original research or reviews) are welcome. It is planned to receive submission until end of September 2020. Manuscripts will be published on an ongoing basis after being processed.

Dr. Nikolaus Bresgen
Prof. Dr. Werner Siems
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.

Published Papers (7 papers)

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Editorial

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7 pages, 750 KiB  
Editorial
Peter Eckl: Research on the Pro-/Antioxidant Balance
by Nikolaus Bresgen and Werner Siems
Antioxidants 2022, 11(6), 1079; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061079 - 28 May 2022
Cited by 1 | Viewed by 1300
Abstract
Peter Maria ECKL started his scientific career in the late 1970s at the Paris-Lodron University of Salzburg working in the field of radiation research [...] Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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Research

Jump to: Editorial

15 pages, 1569 KiB  
Article
Towards Aldehydomics: Untargeted Trapping and Analysis of Reactive Diet-Related Carbonyl Compounds Formed in the Intestinal Lumen
by Sylvie Chevolleau, Maria-Helena Noguer-Meireles, Loïc Mervant, Jean-François Martin, Isabelle Jouanin, Fabrice Pierre, Nathalie Naud, Françoise Guéraud and Laurent Debrauwer
Antioxidants 2021, 10(8), 1261; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10081261 - 06 Aug 2021
Cited by 4 | Viewed by 2098
Abstract
Lipid peroxidation and subsequent formation of toxic aldehydes, such as 4-hydroxynonenal, is known to be involved in numerous pathophysiological processes, possibly including the development of colorectal cancer. This work aimed at the development of an untargeted approach using high-performance liquid chromatography coupled with [...] Read more.
Lipid peroxidation and subsequent formation of toxic aldehydes, such as 4-hydroxynonenal, is known to be involved in numerous pathophysiological processes, possibly including the development of colorectal cancer. This work aimed at the development of an untargeted approach using high-performance liquid chromatography coupled with high-resolution mass spectrometry (HPLC–HRMS) for tracking aldehydes in both suspect screening and untargeted methods in fecal water, representing the aqueous environment of colon epithelial cells. This original approach is based on the introduction of a characteristic isotopic labeling by selective derivatization of the carbonyl function using a brominated reagent. Following a metabolomics workflow, the developed methodology was applied to the characterization of aldehyde compounds formed by lipid peroxidation in rats fed two different diets differentially prone to lipoperoxidation. Derivatized aldehydes were first selectively detected on the basis of their isotopic pattern, then annotated and finally identified by tandem mass spectrometry. This original approach allowed us to evidence the occurrence of expected aldehydes according to their fatty acid precursors in the diet, and to characterize other aldehydes differentiating the different diets. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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23 pages, 3738 KiB  
Article
Molecular Insight into the Regulation of Vimentin by Cysteine Modifications and Zinc Binding
by Andreia Mónico, Joan Guzmán-Caldentey, María A. Pajares, Sonsoles Martín-Santamaría and Dolores Pérez-Sala
Antioxidants 2021, 10(7), 1039; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071039 - 28 Jun 2021
Cited by 8 | Viewed by 2297
Abstract
The intermediate filament protein vimentin is involved in essential cellular processes, including cell division and stress responses, as well as in the pathophysiology of cancer, pathogen infection, and autoimmunity. The vimentin network undergoes marked reorganizations in response to oxidative stress, in which modifications [...] Read more.
The intermediate filament protein vimentin is involved in essential cellular processes, including cell division and stress responses, as well as in the pathophysiology of cancer, pathogen infection, and autoimmunity. The vimentin network undergoes marked reorganizations in response to oxidative stress, in which modifications of vimentin single cysteine residue, Cys328, play an important role, and is modulated by zinc availability. However, the molecular basis for this regulation is not fully understood. Here, we show that Cys328 displays a low pKa, supporting its reactivity, and is readily alkylated and oxidized in vitro. Moreover, combined oxidation and crosslinking assays and molecular dynamics simulations support that zinc ions interact with Cys328 in its thiolate form, whereas Glu329 and Asp331 stabilize zinc coordination. Vimentin oxidation can induce disulfide crosslinking, implying the close proximity of Cys328 from neighboring dimers in certain vimentin conformations, supported by our computational models. Notably, micromolar zinc concentrations prevent Cys328 alkylation, lipoxidation, and disulfide formation. Moreover, zinc selectively protects vimentin from crosslinking using short-spacer cysteine-reactive but not amine-reactive agents. These effects are not mimicked by magnesium, consistent with a lower number of magnesium ions hosted at the cysteine region, according to molecular dynamics simulations. Importantly, the region surrounding Cys328 is involved in interaction with several drugs targeting vimentin and is conserved in type III intermediate filaments, which include glial fibrillary acidic protein and desmin. Altogether, our results identify this region as a hot spot for zinc binding, which modulates Cys328 reactivity. Moreover, they provide a molecular standpoint for vimentin regulation through the interplay between cysteine modifications and zinc availability. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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10 pages, 1945 KiB  
Article
Reduced Liver Autophagy in High-Fat Diet Induced Liver Steatosis in New Zealand Obese Mice
by Ioanna Korovila, Annika Höhn, Tobias Jung, Tilman Grune and Christiane Ott
Antioxidants 2021, 10(4), 501; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10040501 - 24 Mar 2021
Cited by 14 | Viewed by 2961
Abstract
Non-alcoholic fatty liver disease (NAFLD), as a consequence of overnutrition caused by high-calorie diets, results in obesity and disturbed lipid homeostasis leading to hepatic lipid droplet formation. Lipid droplets can impair hepatocellular function; therefore, it is of utmost importance to degrade these cellular [...] Read more.
Non-alcoholic fatty liver disease (NAFLD), as a consequence of overnutrition caused by high-calorie diets, results in obesity and disturbed lipid homeostasis leading to hepatic lipid droplet formation. Lipid droplets can impair hepatocellular function; therefore, it is of utmost importance to degrade these cellular structures. This requires the normal function of the autophagic-lysosomal system and the ubiquitin-proteasomal system. We demonstrated in NZO mice, a polygenic model of obesity, which were compared to C57BL/6J (B6) mice, that a high-fat diet leads to obesity and accumulation of lipid droplets in the liver. This was accompanied by a loss of autophagy efficiency whereas the activity of lysosomal proteases and the 20S proteasome remained unaffected. The disturbance of cellular protein homeostasis was further demonstrated by the accumulation of 3-nitrotyrosine and 4-hydroxynonenal modified proteins, which are normally prone to degradation. Therefore, we conclude that fat accumulation in the liver due to a high-fat diet is associated with a failure of autophagy and leads to the disturbance of proteostasis. This might further contribute to lipid droplet stabilization and accumulation. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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15 pages, 761 KiB  
Article
CFTR Modulator Therapy with Lumacaftor/Ivacaftor Alters Plasma Concentrations of Lipid-Soluble Vitamins A and E in Patients with Cystic Fibrosis
by Olaf Sommerburg, Susanne Hämmerling, S. Philipp Schneider, Jürgen Okun, Claus-Dieter Langhans, Patricia Leutz-Schmidt, Mark O. Wielpütz, Werner Siems, Simon Y. Gräber, Marcus A. Mall and Mirjam Stahl
Antioxidants 2021, 10(3), 483; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030483 - 19 Mar 2021
Cited by 23 | Viewed by 3349
Abstract
Rationale: Cystic fibrosis (CF), caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, leads to impaired pancreatic function and therefore reduced intestinal absorption of lipids and fat-soluble vitamins especially in patients with CF developing pancreatic insufficiency (PI). Previous studies showed [...] Read more.
Rationale: Cystic fibrosis (CF), caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, leads to impaired pancreatic function and therefore reduced intestinal absorption of lipids and fat-soluble vitamins especially in patients with CF developing pancreatic insufficiency (PI). Previous studies showed that CFTR modulator therapy with lumacaftor-ivacaftor (LUM/IVA) in Phe508del-homozygous patients with CF results in improvement of pulmonary disease and thriving. However, the effects of LUM/IVA on plasma concentration of the lipid soluble vitamins A and E remain unknown. Objectives: To investigate the course of plasma vitamin A and E in patients with CF under LUM/IVA therapy. Methods: Data from annual follow-up examinations of patients with CF were obtained to assess clinical outcomes including pulmonary function status, body mass index (BMI), and clinical chemistry as well as fat-soluble vitamins in Phe508del-homozygous CF patients before initiation and during LUM/IVA therapy. Results: Patients with CF receiving LUM/IVA improved substantially, including improvement in pulmonary inflammation, associated with a decrease in blood immunoglobulin G (IgG) from 9.4 to 8.2 g/L after two years (p < 0.001). During the same time, plasma vitamin A increased significantly from 1.2 to 1.6 µmol/L (p < 0.05), however, levels above the upper limit of normal were not detected in any of the patients. In contrast, plasma vitamin E as vitamin E/cholesterol ratio decreased moderately over the same time from 6.2 to 5.5 µmol/L (p < 0.01). Conclusions: CFTR modulator therapy with LUM/IVA alters concentrations of vitamins A and vitamin E in plasma. The increase of vitamin A must be monitored critically to avoid hypervitaminosis A in patients with CF. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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16 pages, 3604 KiB  
Article
N-Acetyl-Cysteine Regenerates Albumin Cys34 by a Thiol-Disulfide Breaking Mechanism: An Explanation of Its Extracellular Antioxidant Activity
by Alessandra Altomare, Giovanna Baron, Maura Brioschi, Martina Longoni, Riccardo Butti, Edoardo Valvassori, Elena Tremoli, Marina Carini, Piergiuseppe Agostoni, Giulio Vistoli, Cristina Banfi and Giancarlo Aldini
Antioxidants 2020, 9(5), 367; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9050367 - 28 Apr 2020
Cited by 32 | Viewed by 4191
Abstract
In the present paper, the extracellular antioxidant activity of N-acetyl-cysteine (NAC) is explained by considering its ability to regenerate the free form of albumin Cys34 by breaking the disulfide bond of the cysteinylated form (HSA-Cys). NAC’s capability to regenerate albumin Cys34 (HSA-SH) [...] Read more.
In the present paper, the extracellular antioxidant activity of N-acetyl-cysteine (NAC) is explained by considering its ability to regenerate the free form of albumin Cys34 by breaking the disulfide bond of the cysteinylated form (HSA-Cys). NAC’s capability to regenerate albumin Cys34 (HSA-SH) was studied by MS intact protein analysis in human plasma and in a concentration range of NAC easily achievable after oral and i.v. administration (5–50 µg/mL). NAC dose-dependently broke the HSA-Cys bond to form the dimer NAC-Cys thus regenerating Cys34, whose reduced state was maintained for at least 120 min. Cys was faster in restoring Cys34, according to the reaction constant determined with the glutathione disulfide (GSSG) reaction, but after 60 min the mixed disulfide HSA-Cys turned back due to the reaction of the dimer Cys-Cys with Cys34. The explanation for the different rate exchanges between Cys-Cys and Cys-NAC with Cys34 was given by molecular modeling studies. Finally, the Cys34 regenerating effect of NAC was related to its ability to improve the total antioxidant capacity of plasma (TRAP assay). The results well indicate that NAC greatly increases the plasma antioxidant activity and this effect is not reached by a direct effect but through the regenerating effect of Cys34. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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15 pages, 2506 KiB  
Article
In Vitro Aging of Human Skin Fibroblasts: Age-Dependent Changes in 4-Hydroxynonenal Metabolism
by Igor Petkovic, Nikolaus Bresgen, Ettore Gilardoni, Luca Regazzoni, Koji Uchida, Giancarlo Aldini, Werner Siems and Peter Eckl
Antioxidants 2020, 9(2), 150; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9020150 - 11 Feb 2020
Cited by 4 | Viewed by 2931
Abstract
Evidence suggests that the increased production of free radicals and reactive oxygen species lead to cellular aging. One of the consequences is lipid peroxidation generating reactive aldehydic products, such as 4-hydroxynonenal (HNE) that modify proteins and form adducts with DNA bases. To prevent [...] Read more.
Evidence suggests that the increased production of free radicals and reactive oxygen species lead to cellular aging. One of the consequences is lipid peroxidation generating reactive aldehydic products, such as 4-hydroxynonenal (HNE) that modify proteins and form adducts with DNA bases. To prevent damage by HNE, it is metabolized. The primary metabolic products are the glutathione conjugate (GSH-HNE), the corresponding 4-hydroxynonenoic acid (HNA), and the alcohol 1,4-dihydroxynonene (DHN). Since HNE metabolism can potentially change during in vitro aging, cell cultures of primary human dermal fibroblasts from several donors were cultured until senescence. After different time points up to 30 min of incubation with 5 µM HNE, the extracellular medium was analyzed for metabolites via liquid chromatography coupled with electrospray ionization mass spectrometry (LC/ESI-MS). The metabolites appeared in the extracellular medium 5 min after incubation followed by a time-dependent increase. But, the formation of GSH-HNL and GSH-DHN decreased with increasing in vitro age. As a consequence, the HNE levels in the cells increase and there is more protein modification observed. Furthermore, after 3 h of incubation with 5 µM HNE, younger cells showed less proliferative capacity, while in older cells slight increase in the mitotic index was noticed. Full article
(This article belongs to the Special Issue Commemorative Issue of Antioxidants Dedicated to Peter Eckl)
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