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Oxidative Stress and Genotoxicity: New Insights
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Oxidative Stress and Genotoxicity: New Insights

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 13016

Special Issue Editor

Dr. Maria Giulia Lionetto

E-Mail Website
Guest Editor
Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Itay
Interests: carbonic anhydrase; antioxidant; biomarkers; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We invite you to submit your valuable research outcomes for publication in the Special Issue entitled “Oxidative Stress and Genotoxicity: New Insights" in the International Journal of Molecular Science (MDPI).

In recent years, a growing body of evidence has highlighted the relationship between genotoxicity, due to the induction of DNA damage by an endogenous or exogenous event, and oxidative stress, which arises from the imbalance between the production and accumulation of reactive species in the cells and the antioxidant defenses. The relationship between oxidative stress and genotoxicity has been recognized to be relevant for the genesis of several pathological conditions, first of all, cancer diseases.

This Special Issue aims to provide new insights into the molecular and cellular mechanisms underlying oxidative-stress-mediated genotoxicity and to indicate development perspectives.

The paper presented in this issue will be of valuable interest to the scientific community in several research areas, including cell biology, physiopathology, toxicology, etc.

Prof. Dr. Maria Giulia Lionetto
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • oxidative stress
  • genotoxicity
  • DNA damage
  • DNA repair
  • reactive species
  • cell signaling
  • cancer
  • assay development

Published Papers (4 papers)

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Research

22 pages, 3609 KiB  
Article
Oxidative Stress, Mutations and Chromosomal Aberrations Induced by In Vitro and In Vivo Exposure to Furan
by Maria Teresa Russo, Gabriele De Luca, Nieves Palma, Paola Leopardi, Paolo Degan, Serena Cinelli, Gaetano Pepe, Pasquale Mosesso, Emma Di Carlo, Carlo Sorrentino, Piero Musiani, Riccardo Crebelli, Margherita Bignami and Eugenia Dogliotti
Int. J. Mol. Sci. 2021, 22(18), 9687; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22189687 - 07 Sep 2021
Cited by 7 | Viewed by 1919
Abstract
Furan is a volatile compound that is formed in foods during thermal processing. It is classified as a possible human carcinogen by international authorities based on sufficient evidence of carcinogenicity from studies in experimental animals. Although a vast number of studies both in [...] Read more.
Furan is a volatile compound that is formed in foods during thermal processing. It is classified as a possible human carcinogen by international authorities based on sufficient evidence of carcinogenicity from studies in experimental animals. Although a vast number of studies both in vitro and in vivo have been performed to investigate furan genotoxicity, the results are inconsistent, and its carcinogenic mode of action remains to be clarified. Here, we address the mutagenic and clastogenic activity of furan and its prime reactive metabolite cis-2 butene-1,4-dial (BDA) in mammalian cells in culture and in mouse animal models in a search for DNA lesions responsible of these effects. To this aim, Fanconi anemia-derived human cell lines defective in the repair of DNA inter-strand crosslinks (ICLs) and Ogg1−/− mice defective in the removal of 8-hydroxyguanine from DNA, were used. We show that both furan and BDA present a weak (if any) mutagenic activity but are clear inducers of clastogenic damage. ICLs are strongly indicated as key lesions for chromosomal damage whereas oxidized base lesions are unlikely to play a critical role. Full article
(This article belongs to the Special Issue Oxidative Stress and Genotoxicity: New Insights)
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18 pages, 3582 KiB  
Article
A Shortage of FTH Induces ROS and Sensitizes RAS-Proficient Neuroblastoma N2A Cells to Ferroptosis
by Ruiqing Lu, Yinan Jiang, Xianxin Lai, Shujie Liu, Litao Sun and Zhong-Wei Zhou
Int. J. Mol. Sci. 2021, 22(16), 8898; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168898 - 18 Aug 2021
Cited by 26 | Viewed by 5017
Abstract
Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, a common child malignant tumor with minimal treatment, is unclear. [...] Read more.
Ferroptosis, an iron-dependent form of programmed cell death, has excellent potential as an anti-cancer therapeutic strategy in different types of tumors, especially in RAS-mutated ones. However, the function of ferroptosis for inhibiting neuroblastoma, a common child malignant tumor with minimal treatment, is unclear. This study investigated the anti-cancer function of ferroptosis inducer Erastin or RSL3 in neuroblastoma N2A cells. Our results show that Erastin or RSL3 induces ROS level and cell death and, therefore, reduces the viability of RAS-proficient N2A cells. Importantly, inhibitors to ferroptosis, but not apoptosis, ameliorate the high ROS level and viability defect in Erastin- or RSL3-treated cells. In addition, our data also show that N2A cells are much more sensitive to ferroptosis inducers than primary mouse cortical neural stem cells (NSCs) or neurons. Moreover, a higher level of ROS and PARylation is evidenced in N2A, but not NSCs. Mechanically, ferritin heavy chain 1 (Fth), the ferroxidase function to oxidate redox-active Fe2+ to redox-inactive Fe3+, is likely responsible for the hypersensitivity of N2A to ferroptosis induction since its expression is lower in N2A compared to NSCs; ectopic expression of Fth reduces ROS levels and cell death, and induces expression of GPX4 and cell viability in N2A cells. Most importantly, neuroblastoma cell lines express a significantly low level of Fth than almost all other types of cancer cell lines. All these data suggest that Erastin or RSL3 induce ferroptosis cell death in neuroblastoma N2A cells, but not normal neural cells, regardless of RAS mutations, due to inadequate FTH. This study, therefore, provides new evidence that ferroptosis could be a promising therapeutic target for neuroblastoma. Full article
(This article belongs to the Special Issue Oxidative Stress and Genotoxicity: New Insights)
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20 pages, 10053 KiB  
Article
Effects of Aqueous Dispersions of C60, C70 and Gd@C82 Fullerenes on Genes Involved in Oxidative Stress and Anti-Inflammatory Pathways
by Elena V. Proskurnina, Ivan V. Mikheev, Ekaterina A. Savinova, Elizaveta S. Ershova, Natalia N. Veiko, Larisa V. Kameneva, Olga A. Dolgikh, Ivan V. Rodionov, Mikhail A. Proskurnin and Svetlana V. Kostyuk
Int. J. Mol. Sci. 2021, 22(11), 6130; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22116130 - 07 Jun 2021
Cited by 6 | Viewed by 2300
Abstract
Background: Fullerenes and metallofullerenes can be considered promising nanopharmaceuticals themselves and as a basis for chemical modification. As reactive oxygen species homeostasis plays a vital role in cells, the study of their effect on genes involved in oxidative stress and anti-inflammatory responses are [...] Read more.
Background: Fullerenes and metallofullerenes can be considered promising nanopharmaceuticals themselves and as a basis for chemical modification. As reactive oxygen species homeostasis plays a vital role in cells, the study of their effect on genes involved in oxidative stress and anti-inflammatory responses are of particular importance. Methods: Human fetal lung fibroblasts were incubated with aqueous dispersions of C60, C70, and Gd@C82 in concentrations of 5 nM and 1.5 µM for 1, 3, 24, and 72 h. Cell viability, intracellular ROS, NOX4, NFκB, PRAR-γ, NRF2, heme oxygenase 1, and NAD(P)H quinone dehydrogenase 1 expression have been studied. Results & conclusion: The aqueous dispersions of C60, C70, and Gd@C82 fullerenes are active participants in reactive oxygen species (ROS) homeostasis. Low and high concentrations of aqueous fullerene dispersions (AFD) have similar effects. C70 was the most inert substance, C60 was the most active substance. All AFDs have both “prooxidant” and “antioxidant” effects but with a different balance. Gd@C82 was a substance with more pronounced antioxidant and anti-inflammatory properties, while C70 had more pronounced “prooxidant” properties. Full article
(This article belongs to the Special Issue Oxidative Stress and Genotoxicity: New Insights)
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20 pages, 3746 KiB  
Article
Ablation of Selenbp1 Alters Lipid Metabolism via the Pparα Pathway in Mouse Kidney
by Yingxia Song, Atsushi Kurose, Renshi Li, Tomoki Takeda, Yuko Onomura, Takayuki Koga, Junpei Mutoh, Takumi Ishida, Yoshitaka Tanaka and Yuji Ishii
Int. J. Mol. Sci. 2021, 22(10), 5334; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22105334 - 19 May 2021
Cited by 6 | Viewed by 2656
Abstract
Selenium-binding protein 1 (Selenbp1) is a 2,3,7,8-tetrechlorodibenzo-p-dioxin inducible protein whose function is yet to be comprehensively elucidated. As the highly homologous isoform, Selenbp2, is expressed at low levels in the kidney, it is worthwhile comparing wild-type C57BL mice and Selenbp1-deficient mice [...] Read more.
Selenium-binding protein 1 (Selenbp1) is a 2,3,7,8-tetrechlorodibenzo-p-dioxin inducible protein whose function is yet to be comprehensively elucidated. As the highly homologous isoform, Selenbp2, is expressed at low levels in the kidney, it is worthwhile comparing wild-type C57BL mice and Selenbp1-deficient mice under dioxin-free conditions. Accordingly, we conducted a mouse metabolomics analysis under non-dioxin-treated conditions. DNA microarray analysis was performed based on observed changes in lipid metabolism-related factors. The results showed fluctuations in the expression of numerous genes. Real-time RT-PCR confirmed the decreased expression levels of the cytochrome P450 4a (Cyp4a) subfamily, known to be involved in fatty acid ω- and ω-1 hydroxylation. Furthermore, peroxisome proliferator-activated receptor-α (Pparα) and retinoid-X-receptor-α (Rxrα), which form a heterodimer with Pparα to promote gene expression, were simultaneously reduced. This indicated that reduced Cyp4a expression was mediated via decreased Pparα and Rxrα. In line with this finding, increased levels of leukotrienes and prostaglandins were detected. Conversely, decreased hydrogen peroxide levels and reduced superoxide dismutase (SOD) activity supported the suppression of the renal expression of Sod1 and Sod2 in Selenbp1-deficient mice. Therefore, we infer that ablation of Selenbp1 elicits oxidative stress caused by increased levels of superoxide anions, which alters lipid metabolism via the Pparα pathway. Full article
(This article belongs to the Special Issue Oxidative Stress and Genotoxicity: New Insights)
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