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Antioxidants
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Oxidative Stress as a Crucial Factor in Liver Diseases: From...
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Oxidative Stress as a Crucial Factor in Liver Diseases: From Basic Research to Clinical Trials

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (20 March 2023) | Viewed by 6661

Special Issue Editor

Prof. Dr. Fábio Rodrigues Ferreira Seiva

E-Mail Website
Guest Editor
Biological Science Center, Department of Biology, Luiz Meneghel Campus, Universidade Estadual do Norte do Paraná-UENP, Bandeirantes 86360-000, PR, Brazil
Interests: liver metabolism; alternative therapy; metabolic disease; carcinogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Around the world, the incidence and prevalence of diseases affecting the liver have been increasing significantly. It should be noted that some of these diseases will gradually progress to cirrhosis and liver cancer, making it increasingly necessary to better understand the causes, pathophysiology, and prevention, as well as to study and propose new possible effective therapies. Some examples of liver diseases include non-alcoholic and alcoholic liver diseases, steatohepatitis, infectious hepatic diseases, metabolic and genetic diseases, drug or toxin liver failure, ischemia-reperfusion hepatic injury, autoimmune hepatitis, sepsis-related liver injury, liver fibrosis and cirrhosis, hepatocellular carcinoma, and others. The role of oxidative stress in liver dysfunction has been discussed for decades; a quick visit to the PubMed repository can offer an idea of the number of studies involving the combination of the terms “liver disease” and “oxidative stress”, just in the last 20 years. There is no doubt that laboratory, animal, and interventional studies with humans have been and continue to be indispensable and are therefore very welcome in this issue. Furthermore, the enormous amount of information already available in biological datasets makes it possible to integrate the different -omics sciences with relevant particularities of liver diseases and their outcomes; thus, in silico approaches employing bioinformatics tools will also be well received. I invite you to share, from bench to bed, your relevant results as well as your updated information in this Special Issue of the journal Antioxidants.

Prof. Dr. Fábio Rodrigues Ferreira Seiva
Guest Editor

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

  • reactive species metabolism
  • free radicals
  • oxidant and antioxidants
  • hepatic tissue
  • liver dysfunctions

Published Papers (3 papers)

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Research

16 pages, 5869 KiB  
Article
Unraveling Hepatic Metabolomic Profiles and Morphological Outcomes in a Hybrid Model of NASH in Different Mouse Strains
by Gabriel P. Bacil, Guilherme R. Romualdo, Priscila M. F. D. Piagge, Daniel R. Cardoso, Mathieu Vinken, Bruno Cogliati and Luís F. Barbisan
Antioxidants 2023, 12(2), 290; https://doi.org/10.3390/antiox12020290 - 27 Jan 2023
Cited by 3 | Viewed by 1524
Abstract
Nonalcoholic fatty liver disease (NAFLD) encompasses nonalcoholic steatohepatitis (NASH) and affects 25% of the global population. Although a plethora of experimental models for studying NASH have been proposed, still scarce findings regarding the hepatic metabolomic/molecular profile. In the present study, we sought to [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) encompasses nonalcoholic steatohepatitis (NASH) and affects 25% of the global population. Although a plethora of experimental models for studying NASH have been proposed, still scarce findings regarding the hepatic metabolomic/molecular profile. In the present study, we sought to unravel the hepatic metabolomic profile of mice subjected to a hybrid model of NASH, by combining a Western diet and carbon tetrachloride administration, for 8 weeks, in male C57BL/6J and BALB/c mice. In both mouse strains, the main traits of NASH—metabolic (glucose intolerance profile), morphologic (extensive microvesicular steatosis and fibrosis, lobular inflammation, and adipose tissue-related inflammation/hypertrophy), and molecular (impaired Nrf2/NF-κB pathway dynamics and altered metabolomic profile)—were observed. The hepatic metabolomic profile revealed that the hybrid protocol impaired, in both strains, the abundance of branched chain-aromatic amino acids, carboxylic acids, and glycosyl compounds, that might be linked to the Nrf2 pathway activation. Moreover, we observed a strain-dependent hepatic metabolomic signature, in which the tricarboxylic acid metabolites and pyruvate metabolism were dissimilarly modulated in C57BL/6J and BALB/c mice. Thus, we provide evidence that the strain-dependent hepatic metabolomic profile might be linked to the distinct underlying mechanisms of NASH, also prospecting potential mechanistic insights into the corresponding disease. Full article
(This article belongs to the Special Issue Oxidative Stress as a Crucial Factor in Liver Diseases: From Basic Research to Clinical Trials)
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13 pages, 3533 KiB  
Article
Nootkatone Supplementation Ameliorates Carbon Tetrachloride-Induced Acute Liver Injury via the Inhibition of Oxidative Stress, NF-κB Pathways, and the Activation of Nrf2/HO-1 Pathway
by Chongshan Dai, Xueyong Zhang, Jiahao Lin and Jianzhong Shen
Antioxidants 2023, 12(1), 194; https://doi.org/10.3390/antiox12010194 - 13 Jan 2023
Cited by 6 | Viewed by 2015
Abstract
Acute liver injury is a type of liver diseases, and it has raised concerns worldwide due to the lack of effective therapies. The aim of this study is to investigate the protective effects of nootkatone (NOOT) on carbon tetrachloride (CCl4)-caused acute [...] Read more.
Acute liver injury is a type of liver diseases, and it has raised concerns worldwide due to the lack of effective therapies. The aim of this study is to investigate the protective effects of nootkatone (NOOT) on carbon tetrachloride (CCl4)-caused acute liver injury in mice. Mice were randomly divided into control, CCl4 model, NOOT, and NOOT (5, 10, and 20 mg/kg/day) plus CCl4 groups, respectively. Mice in the CCl4 plus NOOT groups were orally administrated with NOOT at 5, 10, and 20 mg/kg/days for seven days prior to 0.3% CCl4 injection at 10 mL/kg body weight, respectively. Our results showed that NOOT supplementation significantly ameliorated CCl4-induced increases of serum AST and ALT levels, hepatocyte necrosis, inflammatory response, oxidative stress, and caspases-9 and -3 activities in the livers of mice. Moreover, NOOT supplementation significantly upregulated the expression of Nrf2 and HO-1 mRNAs but downregulated the expression of NF-κB mRNAs and the levels of IL-1β, IL-6, and TNF-α proteins in the liver tissues, compared to those in the CCl4 model group. In conclusion, for the first time, our results reveal that NOOT could offer protective effects against CCl4-caused oxidative stress and inflammatory response via the opposite regulation of Nrf2/HO-1 pathway and NF-κB pathway. Full article
(This article belongs to the Special Issue Oxidative Stress as a Crucial Factor in Liver Diseases: From Basic Research to Clinical Trials)
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22 pages, 16921 KiB  
Article
Experimental Conditions That Influence the Utility of 2′7′-Dichlorodihydrofluorescein Diacetate (DCFH2-DA) as a Fluorogenic Biosensor for Mitochondrial Redox Status
by Lianne R. de Haan, Megan J. Reiniers, Laurens F. Reeskamp, Ali Belkouz, Lei Ao, Shuqun Cheng, Baoyue Ding, Rowan F. van Golen and Michal Heger
Antioxidants 2022, 11(8), 1424; https://doi.org/10.3390/antiox11081424 - 22 Jul 2022
Cited by 10 | Viewed by 2433
Abstract
Oxidative stress has been causally linked to various diseases. Electron transport chain (ETC) inhibitors such as rotenone and antimycin A are frequently used in model systems to study oxidative stress. Oxidative stress that is provoked by ETC inhibitors can be visualized using the [...] Read more.
Oxidative stress has been causally linked to various diseases. Electron transport chain (ETC) inhibitors such as rotenone and antimycin A are frequently used in model systems to study oxidative stress. Oxidative stress that is provoked by ETC inhibitors can be visualized using the fluorogenic probe 2′,7′-dichlorodihydrofluorescein-diacetate (DCFH2-DA). Non-fluorescent DCFH2-DA crosses the plasma membrane, is deacetylated to 2′,7′-dichlorodihydrofluorescein (DCFH2) by esterases, and is oxidized to its fluorescent form 2′,7′-dichlorofluorescein (DCF) by intracellular ROS. DCF fluorescence can, therefore, be used as a semi-quantitative measure of general oxidative stress. However, the use of DCFH2-DA is complicated by various protocol-related factors that mediate DCFH2-to-DCF conversion independently of the degree of oxidative stress. This study therefore analyzed the influence of ancillary factors on DCF formation in the context of ETC inhibitors. It was found that ETC inhibitors trigger DCF formation in cell-free experiments when they are co-dissolved with DCFH2-DA. Moreover, the extent of DCF formation depended on the type of culture medium that was used, the pH of the assay system, the presence of fetal calf serum, and the final DCFH2-DA solvent concentration. Conclusively, experiments with DCFH2-DA should not discount the influence of protocol-related factors such as medium and mitochondrial inhibitors (and possibly other compounds) on the DCFH2-DA-DCF reaction and proper controls should always be built into the assay protocol. Full article
(This article belongs to the Special Issue Oxidative Stress as a Crucial Factor in Liver Diseases: From Basic Research to Clinical Trials)
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