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Special Issue "DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: 31 March 2020.

Special Issue Editors

Prof. Dr. Marco E. M. Peluso
E-Mail Website
Guest Editor
Cancer Risk Factor Branch, Regional Cancer Prevention Laboratory, Study, Prevention and Oncology Network Institute (ISPRO), 50139, Florence, Italy
Tel. (39)05532697867; Fax: (39)05532697879
Interests: genetic damage; oxidative stress; DNA adducts; epigenetics; mutations; carcinogenesis; molecular epidemiology.
Prof. Dr. Andrea Galli
E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139, Florence, Italy
Tel. +390554271419
Interests: basic research; HCC; pancreatic cancer; clinical trials; cancer therapy; gastroenterology
Dr. Tommaso Mello
E-Mail Website
Guest Editor
Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139, Florence, Italy
Interests: molecular and cellular biology; NASH/NAFLD; HCC; liver regeneration; liver metabolism

Special Issue Information

Dear Colleagues,

Oxidative stress and associated reactive products have been shown to play a central role in carcinogenesis. Metabolic reactive species are associated with the generation of high levels of reactive species capable to attack lipids, proteins, and DNA. Interconnected modifications of the physiological processes designed to maintain metabolic homeostasis can reduce individual xenobiotic tolerance to oxidative stress and related by-products in susceptible subjects. Subsequently, this can cause over-sensitive reactions to various exogenous and endogenous challenges, resulting in phenotypes characterized by high levels of genomic and other cellular alterations. It is conceivable that such cellular alterations could contribute to a general decline of the physiological mechanisms designed to maintain cellular homeostasis, including DNA damage, mutations, genomic instability, and the disturbance of critical pathways, such as transcription and replication.

Molecular epidemiology can play a major role in elucidating the multi-step transformation of normal cells to a malignant state, potentially leading to predictive biomarkers of cancer risk and carcinogen exposure. In this Special Issue, I would like to invite review and original articles that focus on the link between DNA damage, oxidative stress, and related metabolic by-products in cancer and environmental studies.

Prof. Dr. Marco E. M. Peluso
Prof. Dr. Andrea Galli
Dr. Tommaso Mello
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 papers will be 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.

Published Papers (2 papers)

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Research

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Open AccessArticle
A Cross-Sectional Study on 3-(2-Deoxy-β-D-Erythro-Pentafuranosyl)Pyrimido[1,2-α]Purin-10(3H)-One Deoxyguanosine Adducts among Woodworkers in Tuscany, Italy
Int. J. Mol. Sci. 2019, 20(11), 2763; https://doi.org/10.3390/ijms20112763 - 05 Jun 2019
Abstract
Occupational exposure to wood dust has been estimated to affect 3.6 million workers within the European Union (EU). The most serious health effect caused by wood dust is the nasal and sinonasal cancer (SNC), which has been observed predominantly among woodworkers. Free radicals [...] Read more.
Occupational exposure to wood dust has been estimated to affect 3.6 million workers within the European Union (EU). The most serious health effect caused by wood dust is the nasal and sinonasal cancer (SNC), which has been observed predominantly among woodworkers. Free radicals produced by inflammatory reactions as a consequence of wood dust could play a major role in SNC development. Therefore, we investigated the association between wood dust and oxidative DNA damage in the cells of nasal epithelia, the target site of SNC. We have analyzed oxidative DNA damage by determining the levels of 3-(2-deoxy-β-D-erythro-pentafuranosyl)pyrimido[1,2-α]purin-10(3H)-one deoxyguanosine (M1dG), a major-peroxidation-derived DNA adduct and a biomarker of cancer risk in 136 woodworkers compared to 87 controls in Tuscany, Italy. We then examined the association of M1dG with co-exposure to volatile organic compounds (VOCs), exposure length, and urinary 15-F2t isoprostane (15-F2t-IsoP), a biomarker of oxidant status. Wood dust at the workplace was estimated by the Information System for Recording Occupational Exposures to Carcinogens. M1dG was measured using 32P-postlabeling and mass spectrometry. 15-F2t-IsoP was analyzed using ELISA. Results show a significant excess of M1dG in the woodworkers exposed to average levels of 1.48 mg/m3 relative to the controls. The overall mean ratio (MR) between the woodworkers and the controls was 1.28 (95% C.I. 1.03–1.58). After stratification for smoking habits and occupational status (exposure to wood dust alone and co-exposure to VOCs), the association of M1dG with wood dust (alone) was even greater in non-smokers workers, MR of 1.43 (95% C.I. 1.09–1.87). Conversely, not consistent results were found in ex-smokers and current smokers. M1dG was significantly associated with co-exposure to VOCs, MR of 1.95 (95% C.I. 1.46–2.61), and occupational history, MR of 2.47 (95% C.I. 1.67–3.62). Next, the frequency of M1dG was significantly correlated to the urinary excretion of 15-F2t-IsoP, regression coefficient (β) = 0.442 ± 0.172 (SE). Consistent with the hypothesis of a genotoxic mechanism, we observed an enhanced frequency of M1dG adducts in woodworkers, even at the external levels below the regulatory limit. Our data implement the understanding of SNC and could be useful for the management of the adverse effects caused by this carcinogen. Full article

Review

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Open AccessReview
DNA Oxidation and Excision Repair Pathways
Int. J. Mol. Sci. 2019, 20(23), 6092; https://doi.org/10.3390/ijms20236092 - 03 Dec 2019
Abstract
The physiological impact of the aberrant oxidation products on genomic DNA were demonstrated by embryonic lethality or the cancer susceptibility and/or neurological symptoms of animal impaired in the base excision repair (BER); the major pathway to maintain genomic integrity against non-bulky DNA oxidation. [...] Read more.
The physiological impact of the aberrant oxidation products on genomic DNA were demonstrated by embryonic lethality or the cancer susceptibility and/or neurological symptoms of animal impaired in the base excision repair (BER); the major pathway to maintain genomic integrity against non-bulky DNA oxidation. However, growing evidence suggests that other DNA repair pathways or factors that are not primarily associated with the classical BER pathway are also actively involved in the mitigation of oxidative assaults on the genomic DNA, according to the corresponding types of DNA oxidation. Among others, factors dedicated to lesion recognition in the nucleotide excision repair (NER) pathway have been shown to play eminent roles in the process of lesion recognition and stimulation of the enzyme activity of some sets of BER factors. Besides, substantial bulky DNA oxidation can be preferentially removed by a canonical NER mechanism; therefore, loss of function in the NER pathway shares common features arising from BER defects, including cancer predisposition and neurological disorders, although NER defects generally are nonlethal. Here we discuss recent achievements for delineating newly arising roles of NER lesion recognition factors to facilitate the BER process, and cooperative works of BER and NER pathways in response to the genotoxic oxidative stress. Full article
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Dr. Henning Pop-DNA damage and the DNA damage response in cells of chronic myeloid leukemia patients

Dr. Vladimir Divoky-DNA damage response (DDR) as a critical mechanism rate-limiting for malignant transformation by the hematopoietic oncogene

Dr. Roberto Bono

Dr. Roger Giese

Dr. Pavel Vodička-colorectal cancer

Dr. Miloslav Hronek-Does Neuraxial Anaesthesia Damage DNA as General Anaesthesia

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