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

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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: closed (31 March 2020) | Viewed by 56209

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Prof. Dr. Marco E. M. Peluso

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Cancer Risk Factor Branch, Regional Cancer Prevention Laboratory, Study, Prevention and Oncology Network Institute (ISPRO), 50139 Florence, Italy
Interests: genetic damage; oxidative stress; DNA adducts; epigenetics; mutations; carcinogenesis; molecular epidemiology
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Andrea Galli

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Guest Editor

Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy
Interests: basic research; HCC; pancreatic cancer; clinical trials; cancer therapy; gastroenterology

Dr. Tommaso Mello

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Guest Editor

Department of Experimental and Clinical Biomedical Sciences, University of Florence, 50139 Florence, Italy
Interests: liver cancer; liver regeneration; liver fibrosis; hepatocellular carcinoma; NAFLD; NASH; cell metabolism; cell biology; molecular biology

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.

You are welcome to submit your contributions to the second volume.

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 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.

Related Special Issue

DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 3.0 in International Journal of Molecular Sciences (1 article)

Published Papers (11 papers)

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Editorial

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5 pages, 202 KiB

Open AccessEditorial

Oxidative Stress and DNA Damage in Chronic Disease and Environmental Studies

by Marco Peluso, Valentina Russo, Tommaso Mello and Andrea Galli

Int. J. Mol. Sci. 2020, 21(18), 6936; https://doi.org/10.3390/ijms21186936 - 21 Sep 2020

Cited by 17 | Viewed by 1729

Abstract

Humans are continually exposed to a large number of environmental carcinogens [...] Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

Research

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22 pages, 4155 KiB

Open AccessArticle

Oxidative DNA Damage, Inflammatory Signature, and Altered Erythrocytes Properties in Diamond-Blackfan Anemia

by Katarina Kapralova, Ondrej Jahoda, Pavla Koralkova, Jan Gursky, Lucie Lanikova, Dagmar Pospisilova, Vladimir Divoky and Monika Horvathova

Int. J. Mol. Sci. 2020, 21(24), 9652; https://doi.org/10.3390/ijms21249652 - 17 Dec 2020

Cited by 14 | Viewed by 2896

Abstract

Molecular pathophysiology of Diamond-Blackfan anemia (DBA) involves disrupted erythroid-lineage proliferation, differentiation and apoptosis; with the activation of p53 considered as a key component. Recently, oxidative stress was proposed to play an important role in DBA pathophysiology as well. CRISPR/Cas9-created Rpl5- and Rps19-deficient murine erythroleukemia (MEL) cells and DBA patients’ samples were used to evaluate proinflammatory cytokines, oxidative stress, DNA damage and DNA damage response. We demonstrated that the antioxidant defense capacity of Rp-mutant cells is insufficient to meet the greater reactive oxygen species (ROS) production which leads to oxidative DNA damage, cellular senescence and activation of DNA damage response signaling in the developing erythroblasts and altered characteristics of mature erythrocytes. We also showed that the disturbed balance between ROS formation and antioxidant defense is accompanied by the upregulation of proinflammatory cytokines. Finally, the alterations detected in the membrane of DBA erythrocytes may cause their enhanced recognition and destruction by reticuloendothelial macrophages, especially during infections. We propose that the extent of oxidative stress and the ability to activate antioxidant defense systems may contribute to high heterogeneity of clinical symptoms and response to therapy observed in DBA patients. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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16 pages, 2514 KiB

Open AccessArticle

Modulatory Effects of Silymarin on Benzo[a]pyrene-Induced Hepatotoxicity

by Seung-Cheol Jee, Min Kim and Jung-Suk Sung

Int. J. Mol. Sci. 2020, 21(7), 2369; https://doi.org/10.3390/ijms21072369 - 30 Mar 2020

Cited by 16 | Viewed by 3599

Abstract

Benzo[a]pyrene (B[a]P), a polycyclic aromatic hydrocarbon, is a group 1 carcinogen that introduces mutagenic DNA adducts into the genome. In this study, we investigated the molecular mechanisms underlying the involvement of silymarin in the reduction of DNA adduct formation by B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE), induced by B[a]P. B[a]P exhibited toxicity in HepG2 cells, whereas co-treatment of the cells with B[a]P and silymarin reduced the formation of BPDE-DNA adducts, thereby increasing cell viability. Determination of the level of major B[a]P metabolites in the treated cells showed that BPDE levels were reduced by silymarin. Nuclear factor erythroid 2-related factor 2 (Nrf2) and pregnane X receptor (PXR) were found to be involved in the activation of detoxifying genes against B[a]P-mediated toxicity. Silymarin did not increase the expression of these major transcription factors, but greatly facilitated their nuclear translocation. In this manner, treatment of HepG2 cells with silymarin modulated detoxification enzymes through NRF2 and PXR to eliminate B[a]P metabolites. Knockdown of Nrf2 abolished the preventive effect of silymarin on BPDE-DNA adduct formation, indicating that activation of the Nrf2 pathway plays a key role in preventing B[a]P-induced genotoxicity. Our results suggest that silymarin has anti-genotoxic effects, as it prevents BPDE-DNA adduct formation by modulating the Nrf2 and PXR signaling pathways. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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12 pages, 6805 KiB

Open AccessArticle

DNA Damage and DNA Damage Response in Chronic Myeloid Leukemia

by Henning D. Popp, Vanessa Kohl, Nicole Naumann, Johanna Flach, Susanne Brendel, Helga Kleiner, Christel Weiss, Wolfgang Seifarth, Susanne Saussele, Wolf-Karsten Hofmann and Alice Fabarius

Int. J. Mol. Sci. 2020, 21(4), 1177; https://doi.org/10.3390/ijms21041177 - 11 Feb 2020

Cited by 21 | Viewed by 3248

Abstract

DNA damage and alterations in the DNA damage response (DDR) are critical sources of genetic instability that might be involved in BCR-ABL1 kinase-mediated blastic transformation of chronic myeloid leukemia (CML). Here, increased DNA damage is detected by γH2AX foci analysis in peripheral blood mononuclear cells (PBMCs) of de novo untreated chronic phase (CP)-CML patients (n = 5; 2.5 γH2AX foci per PBMC ± 0.5) and blast phase (BP)-CML patients (n = 3; 4.4 γH2AX foci per PBMC ± 0.7) as well as CP-CML patients with loss of major molecular response (MMR) (n = 5; 1.8 γH2AX foci per PBMC ± 0.4) when compared to DNA damage in PBMC of healthy donors (n = 8; 1.0 γH2AX foci per PBMC ± 0.1) and CP-CML patients in deep molecular response or MMR (n = 26; 1.0 γH2AX foci per PBMC ± 0.1). Progressive activation of erroneous non-homologous end joining (NHEJ) repair mechanisms during blastic transformation in CML is indicated by abundant co-localization of γH2AX/53BP1 foci, while a decline of the DDR is suggested by defective expression of (p-)ATM and (p-)CHK2. In summary, our data provide evidence for the accumulation of DNA damage in the course of CML and suggest ongoing DNA damage, erroneous NHEJ repair mechanisms, and alterations in the DDR as critical mediators of blastic transformation in CML. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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14 pages, 1578 KiB

Open AccessArticle

Does Neuraxial Anesthesia as General Anesthesia Damage DNA? A Pilot Study in Patients Undergoing Orthopedic Traumatological Surgery

by Monika Kucharova, David Astapenko, Veronika Zubanova, Maria Koscakova, Rudolf Stetina, Zdenek Zadak and Miloslav Hronek

Int. J. Mol. Sci. 2020, 21(1), 84; https://doi.org/10.3390/ijms21010084 - 20 Dec 2019

Cited by 4 | Viewed by 2362

Abstract

The human organism is exposed daily to many endogenous and exogenous substances that are the source of oxidative damage. Oxidative damage is one of the most frequent types of cell component damage, leading to oxidation of lipids, proteins, and the DNA molecule. The predominance of these damaging processes may later be responsible for human diseases such as cancer, neurodegenerative disease, or heart failure. Anesthetics undoubtedly belong to the group of substances harming DNA integrity. The goal of this pilot study is to evaluate the range of DNA damage by general and neuraxial spinal anesthesia in two groups of patients undergoing orthopedic traumatological surgery. Each group contained 20 patients, and blood samples were collected before and after anesthesia; the degree of DNA damage was evaluated by the comet assay method. Our results suggest that general anesthesia can cause statistically significant damage to the DNA of patients, whereas neuraxial anesthesia has no negative influence. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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10 pages, 250 KiB

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

by Filippo Cellai, Fabio Capacci, Carla Sgarrella, Carla Poli, Luciano Arena, Lorenzo Tofani, Roger W. Giese and Marco Peluso

Int. J. Mol. Sci. 2019, 20(11), 2763; https://doi.org/10.3390/ijms20112763 - 05 Jun 2019

Cited by 7 | Viewed by 2300

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 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-F_2t isoprostane (15-F_2t-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-F_2t-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-F_2t-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

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

Review

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19 pages, 1676 KiB

Open AccessReview

Increased Thyroid Cancer Incidence in Volcanic Areas: A Role of Increased Heavy Metals in the Environment?

by Pasqualino Malandrino, Marco Russo, Fiorenza Gianì, Gabriella Pellegriti, Paolo Vigneri, Antonino Belfiore, Enrico Rizzarelli and Riccardo Vigneri

Int. J. Mol. Sci. 2020, 21(10), 3425; https://doi.org/10.3390/ijms21103425 - 12 May 2020

Cited by 19 | Viewed by 3229

Abstract

Thyroid cancer incidence is significantly increased in volcanic areas, where relevant non-anthropogenic pollution with heavy metals is present in the environment. This review will discuss whether chronic lifelong exposure to slightly increased levels of metals can contribute to the increase in thyroid cancer in the residents of a volcanic area. The influence of metals on living cells depends on the physicochemical properties of the metals and their interaction with the target cell metallostasis network, which includes transporters, intracellular binding proteins, and metal-responsive elements. Very little is known about the carcinogenic potential of slightly increased metal levels on the thyroid, which might be more sensitive to mutagenic damage because of its unique biology related to iodine, which is a very reactive and strongly oxidizing agent. Different mechanisms could explain the specific carcinogenic effect of borderline/high environmental levels of metals on the thyroid, including (a) hormesis, the nonlinear response to chemicals causing important biological effects at low concentrations; (b) metal accumulation in the thyroid relative to other tissues; and (c) the specific effects of a mixture of different metals. Recent evidence related to all of these mechanisms is now available, and the data are compatible with a cause–effect relationship between increased metal levels in the environment and an increase in thyroid cancer incidence. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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20 pages, 1067 KiB

Open AccessReview

Reactive Oxygen Species, Metabolic Plasticity, and Drug Resistance in Cancer

by Vikas Bhardwaj and Jun He

Int. J. Mol. Sci. 2020, 21(10), 3412; https://doi.org/10.3390/ijms21103412 - 12 May 2020

Cited by 49 | Viewed by 9583

Abstract

The metabolic abnormality observed in tumors is characterized by the dependence of cancer cells on glycolysis for their energy requirements. Cancer cells also exhibit a high level of reactive oxygen species (ROS), largely due to the alteration of cellular bioenergetics. A highly coordinated interplay between tumor energetics and ROS generates a powerful phenotype that provides the tumor cells with proliferative, antiapoptotic, and overall aggressive characteristics. In this review article, we summarize the literature on how ROS impacts energy metabolism by regulating key metabolic enzymes and how metabolic pathways e.g., glycolysis, PPP, and the TCA cycle reciprocally affect the generation and maintenance of ROS homeostasis. Lastly, we discuss how metabolic adaptation in cancer influences the tumor’s response to chemotherapeutic drugs. Though attempts of targeting tumor energetics have shown promising preclinical outcomes, the clinical benefits are yet to be fully achieved. A better understanding of the interaction between metabolic abnormalities and involvement of ROS under the chemo-induced stress will help develop new strategies and personalized approaches to improve the therapeutic efficiency in cancer patients. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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20 pages, 745 KiB

Open AccessReview

Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases in Colorectal Cancer Patients

by Pavel Vodicka, Marketa Urbanova, Pavol Makovicky, Kristyna Tomasova, Michal Kroupa, Rudolf Stetina, Alena Opattova, Klara Kostovcikova, Anna Siskova, Michaela Schneiderova, Veronika Vymetalkova and Ludmila Vodickova

Int. J. Mol. Sci. 2020, 21(7), 2473; https://doi.org/10.3390/ijms21072473 - 02 Apr 2020

Cited by 29 | Viewed by 4133

Abstract

Oxidative stress with subsequent premutagenic oxidative DNA damage has been implicated in colorectal carcinogenesis. The repair of oxidative DNA damage is initiated by lesion-specific DNA glycosylases (hOGG1, NTH1, MUTYH). The direct evidence of the role of oxidative DNA damage and its repair is proven by hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome), where germline mutations cause loss-of-function in glycosylases of base excision repair, thus enabling the accumulation of oxidative DNA damage and leading to the adenoma-colorectal cancer transition. Unrepaired oxidative DNA damage often results in G:C>T:A mutations in tumor suppressor genes and proto-oncogenes and widespread occurrence of chromosomal copy-neutral loss of heterozygosity. However, the situation is more complicated in complex and heterogeneous disease, such as sporadic colorectal cancer. Here we summarized our current knowledge of the role of oxidative DNA damage and its repair on the onset, prognosis and treatment of sporadic colorectal cancer. Molecular and histological tumor heterogeneity was considered. Our study has also suggested an additional important source of oxidative DNA damage due to intestinal dysbiosis. The roles of base excision repair glycosylases (hOGG1, MUTYH) in tumor and adjacent mucosa tissues of colorectal cancer patients, particularly in the interplay with other factors (especially microenvironment), deserve further attention. Base excision repair characteristics determined in colorectal cancer tissues reflect, rather, a disease prognosis. Finally, we discuss the role of DNA repair in the treatment of colon cancer, since acquired or inherited defects in DNA repair pathways can be effectively used in therapy. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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24 pages, 1194 KiB

Open AccessReview

DNA Damage Response and Oxidative Stress in Systemic Autoimmunity

by Vassilis L. Souliotis, Nikolaos I. Vlachogiannis, Maria Pappa, Alexandra Argyriou, Panagiotis A. Ntouros and Petros P. Sfikakis

Int. J. Mol. Sci. 2020, 21(1), 55; https://doi.org/10.3390/ijms21010055 - 20 Dec 2019

Cited by 67 | Viewed by 6031

Abstract

The DNA damage response and repair (DDR/R) network, a sum of hierarchically structured signaling pathways that recognize and repair DNA damage, and the immune response to endogenous and/or exogenous threats, act synergistically to enhance cellular defense. On the other hand, a deregulated interplay between these systems underlines inflammatory diseases including malignancies and chronic systemic autoimmune diseases, such as systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Patients with these diseases are characterized by aberrant immune response to self-antigens with widespread production of autoantibodies and multiple-tissue injury, as well as by the presence of increased oxidative stress. Recent data demonstrate accumulation of endogenous DNA damage in peripheral blood mononuclear cells from these patients, which is related to (a) augmented DNA damage formation, at least partly due to the induction of oxidative stress, and (b) epigenetically regulated functional abnormalities of fundamental DNA repair mechanisms. Because endogenous DNA damage accumulation has serious consequences for cellular health, including genomic instability and enhancement of an aberrant immune response, these results can be exploited for understanding pathogenesis and progression of systemic autoimmune diseases, as well as for the development of new treatments. Full article

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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13 pages, 636 KiB

Open AccessReview

DNA Oxidation and Excision Repair Pathways

by Tae-Hee Lee and Tae-Hong Kang

Int. J. Mol. Sci. 2019, 20(23), 6092; https://doi.org/10.3390/ijms20236092 - 03 Dec 2019

Cited by 57 | Viewed by 16335

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. 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

(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies)

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