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DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0

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 (15 January 2023) | Viewed by 14170

Special Issue Editor

Prof. Dr. Marco E. M. Peluso

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Guest Editor
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

Special Issue Information

Dear Colleagues,

Oxidative stress and associated reactive products have been shown to play a central role in carcinogenesis through the generation of high levels of reactive species capable of attacking 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 in 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 the definition of predictive biomarkers of cancer risk and carcinogen exposure. In this Special Issue, I invite you to submit reviews 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 read papers in the first volume.

Prof. Dr. Marco E. M. Peluso
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.

Related Special Issue

Published Papers (7 papers)

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Research

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14 pages, 2786 KiB  
Article
The Effect of the Stress Induced by Hydrogen Peroxide and Corticosterone on Tryptophan Metabolism, Using Human Neuroblastoma Cell Line (SH-SY5Y)
by Ana Salomé Correia, Isabel Silva, Henrique Reguengo, José Carlos Oliveira, Francisco Vasques-Nóvoa, Armando Cardoso and Nuno Vale
Int. J. Mol. Sci. 2023, 24(5), 4389; https://doi.org/10.3390/ijms24054389 - 23 Feb 2023
Cited by 2 | Viewed by 1629
Abstract
L-tryptophan (L-Trp) is an important amino acid in several physiological mechanisms, being metabolized into two important pathways: the kynurenine and the serotonin (5-HT) pathways. It is important in processes such as mood and stress response, the 5-HT pathway begins with the conversion of [...] Read more.
L-tryptophan (L-Trp) is an important amino acid in several physiological mechanisms, being metabolized into two important pathways: the kynurenine and the serotonin (5-HT) pathways. It is important in processes such as mood and stress response, the 5-HT pathway begins with the conversion of L-Trp to 5-hydroxytryptophan (5-HTP), that is metabolized into 5-HT, converted to melatonin or to 5-hydroxyindoleacetic acid (5-HIAA). Disturbances in this pathway are reported to be connected with oxidative stress and glucocorticoid-induced stress, are important to explore. Thus, our study aimed to understand the role of hydrogen peroxide (H2O2) and corticosterone (CORT)-induced stress on the serotonergic pathway of L-Trp metabolism, and on SH-SY5Y cells, focusing on the study of L-Trp, 5-HTP, 5-HT, and 5-HIAA in combination with H2O2 or CORT. We evaluated the effect of these combinations on cellular viability, morphology, and on the extracellular levels of the metabolites. The data obtained highlighted the different ways that stress induction led to different extracellular medium concentration of the studied metabolites. These distinct chemical transformations did not lead to differences in cell morphology/viability. Additionally, serotonin may be the most sensitive metabolite to the exposure to the different stress inducers, being more promissory to study conditions associated with cellular stress. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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13 pages, 314 KiB  
Article
Traffic-Related Air Pollution and Ground-Level Ozone Associated Global DNA Hypomethylation and Bulky DNA Adduct Formation
by Armelle Munnia, Valentina Bollati, Valentina Russo, Luca Ferrari, Marcello Ceppi, Marco Bruzzone, Stefano Dugheri, Giulio Arcangeli, Franco Merlo and Marco Peluso
Int. J. Mol. Sci. 2023, 24(3), 2041; https://doi.org/10.3390/ijms24032041 - 20 Jan 2023
Viewed by 1693
Abstract
Studies have indicated that air pollution, including surface-level ozone (O3), can significantly influence the risk of chronic diseases. To better understand the carcinogenic mechanisms of air pollutants and identify predictive disease biomarkers, we examined the association between traffic-related pollutants with DNA [...] Read more.
Studies have indicated that air pollution, including surface-level ozone (O3), can significantly influence the risk of chronic diseases. To better understand the carcinogenic mechanisms of air pollutants and identify predictive disease biomarkers, we examined the association between traffic-related pollutants with DNA methylation alterations and bulky DNA adducts, two biomarkers of carcinogen exposure and cancer risk, in the peripheral blood of 140 volunteers—95 traffic police officers, and 45 unexposed subjects. The DNA methylation and adduct measurements were performed by bisulfite-PCR and pyrosequencing and 32P-postlabeling assay. Airborne levels of benzo(a)pyrene [B(a)P], carbon monoxide, and tropospheric O3 were determined by personal exposure biomonitoring or by fixed monitoring stations. Overall, air pollution exposure was associated with a significant reduction (1.41 units) in global DNA methylation (95% C.I. −2.65–0.04, p = 0.026). The decrement in ALU repetitive elements was greatest in the policemen working downtown (95% C.I. −3.23–−0.49, p = 0.008). The DNA adducts were found to be significantly increased (0.45 units) in the municipal officers with respect to unexposed subjects (95% C.I. 0.02–0.88, p = 0.039), mainly in those who were controlling traffic in downtown areas (95% C.I. 0.39–1.29, p < 0.001). Regression models indicated an increment of ALU methylation at higher B(a)P concentrations (95% C.I. 0.03–0.60, p = 0.032). Moreover, statistical models showed a decrement in ALU methylation and an increment of DNA damage only above the cut-off value of 30 µg/m3 O3. A significant increment of 0.73 units of IL-6 gene methylation was also found in smokers with respect to non-smokers. Our results highlighted the role of air pollution on epigenetic alterations and genotoxic effects, especially above the target value of 30 µg/m3 surface-level O3, supporting the necessity for developing public health strategies aimed to reduce traffic-related air pollution molecular alterations. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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11 pages, 295 KiB  
Article
miRNAs Participate in the Regulation of Oxidative Stress-Related Gene Expression in Endometrioid Endometrial Cancer
by Paweł Mieszczański, Szmon Januszyk, Nikola Zmarzły, Piotr Ossowski, Konrad Dziobek, Dorota Sagan, Dariusz Boroń, Marcin Opławski and Beniamin Oskar Grabarek
Int. J. Mol. Sci. 2022, 23(24), 15817; https://doi.org/10.3390/ijms232415817 - 13 Dec 2022
Cited by 1 | Viewed by 1362
Abstract
Reactive oxygen species are formed as by-products of normal cell metabolism. They are needed to maintain cell homeostasis and signaling, which is possible due to defense systems. Disruption of this balance leads to oxidative stress that can induce cancer. Redox regulation by miRNAs [...] Read more.
Reactive oxygen species are formed as by-products of normal cell metabolism. They are needed to maintain cell homeostasis and signaling, which is possible due to defense systems. Disruption of this balance leads to oxidative stress that can induce cancer. Redox regulation by miRNAs may be a potential therapeutic target. The aim of the study was to assess the activity of genes associated with oxidative stress in endometrial cancer and to determine their relationship with miRNAs. The study included 45 patients with endometrioid endometrial cancer and 45 without neoplastic changes. The expression profile of genes associated with oxidative stress was determined with mRNA microarrays, RT-qPCR and ELISA. The miRNA prediction was performed based on the miRNA microarray experiment and the mirDB tool. PRDX2 and AQP1 showed overexpression that was probably not related to miRNA activity. A high level of PKD2 may be the result of a decrease in the activity of miR-195-3p, miR-20a, miR-134. A SOD3 level reduction can be caused by miR-328, miR-363. In addition, miR-363 can also regulate KLF2 expression. In the course of endometrial cancer, the phenomenon of oxidative stress is observed, the regulation of which may be influenced by miRNAs. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
10 pages, 1368 KiB  
Article
Cysteine Regulates Oxidative Stress and Glutathione-Related Antioxidative Capacity before and after Colorectal Tumor Resection
by Feng-Fan Chiang, Te-Hsin Chao, Shih-Chien Huang, Chien-Hsiang Cheng, Yu-Yao Tseng and Yi-Chia Huang
Int. J. Mol. Sci. 2022, 23(17), 9581; https://doi.org/10.3390/ijms23179581 - 24 Aug 2022
Cited by 7 | Viewed by 1708
Abstract
Cysteine might scavenge free radicals and is a limiting substrate for the cellular synthesis of glutathione (GSH). We investigated the association of cysteine with oxidative stress and GSH-related antioxidant capacity in colorectal cancer (CRC) patients. Plasma samples were drawn from 66 patients 1 [...] Read more.
Cysteine might scavenge free radicals and is a limiting substrate for the cellular synthesis of glutathione (GSH). We investigated the association of cysteine with oxidative stress and GSH-related antioxidant capacity in colorectal cancer (CRC) patients. Plasma samples were drawn from 66 patients 1 day before (pre-resection) and 4 weeks after resection (post-resection). Tumor and adjacent normal tissues were collected. We measured levels of plasma and tissue cysteine, homocysteine, oxidative stress indicators (malondialdehyde, MDA; advanced oxidation protein products, AOPP), GSH, and antioxidant enzyme activities. After tumor resection, patients had significantly higher levels of plasma cysteine, homocysteine, MDA, AOPP, and GSH-related antioxidant enzyme activities when compared with pre-resection. Levels of cysteine, homocysteine, AOPP and all antioxidant capacity indicators in tumor tissue were significantly higher than those levels in the adjacent normal tissue. Plasma cysteine levels measured at pre-resection were positively associated with MDA levels in the tumor and in the adjacent normal tissues. Cysteine levels in tumor and adjacent normal tissues were significantly associated with tissue levels of homocysteine, almost as indicators of oxidative stress and antioxidant capacities. Cysteine in the circulation was likely utilized to mediate GSH-related antioxidant capacity and further cope with increased oxidative stress in tumor and adjacent normal tissues. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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13 pages, 1576 KiB  
Article
Oxidative Stress and DNA Damage in Peripheral Blood Mononuclear Cells from Normal, Obese, Prediabetic and Diabetic Persons Exposed to Thyroid Hormone In Vitro
by Ninoslav Djelić, Sunčica Borozan, Vesna Dimitrijević-Srećković, Nevena Pajović, Milorad Mirilović, Helga Stopper and Zoran Stanimirović
Int. J. Mol. Sci. 2022, 23(16), 9072; https://doi.org/10.3390/ijms23169072 - 13 Aug 2022
Cited by 2 | Viewed by 1298
Abstract
Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders [...] Read more.
Diabetes, a chronic group of medical disorders characterized byhyperglycemia, has become a global pandemic. Some hormones may influence the course and outcome of diabetes, especially if they potentiate the formation of reactive oxygen species (ROS). There is a close relationship between thyroid disorders and diabetes. The main objective of this investigation was to find out whether peripheral blood mononuclear cells (PBMCs) are more prone to DNA damage by triiodothyronine (T3) (0.1, 1 and 10 μM) at various stages of progression through diabetes (obese, prediabetics, and type 2 diabetes mellitus—T2DM persons). In addition, some biochemical parameters of oxidative stress (catalase-CAT, thiobarbituric acid reactive substances—TBARS) and lactate dehydrogenase (LDH) were evaluated. PBMCs from prediabetic and diabetic patients exhibited increased sensitivity for T3 regarding elevated level of DNA damage, inhibition of catalase, and increase of TBARS and LDH. PBMCs from obese patients reacted in the same manner, except for DNA damage. The results of this study should contribute to a better understanding of the role of thyroid hormones in the progression of T2DM. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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11 pages, 2417 KiB  
Article
Oxidative Damage in Sporadic Colorectal Cancer: Molecular Mapping of Base Excision Repair Glycosylases MUTYH and hOGG1 in Colorectal Cancer Patients
by Miriam J. Kavec, Marketa Urbanova, Pavol Makovicky, Alena Opattová, Kristyna Tomasova, Michal Kroupa, Klara Kostovcikova, Anna Siskova, Nazila Navvabi, Michaela Schneiderova, Veronika Vymetalkova, Ludmila Vodickova and Pavel Vodicka
Int. J. Mol. Sci. 2022, 23(10), 5704; https://doi.org/10.3390/ijms23105704 - 20 May 2022
Cited by 3 | Viewed by 1918
Abstract
Oxidative stress, oxidative DNA damage and resulting mutations play a role in colorectal carcinogenesis. Impaired equilibrium between DNA damage formation, antioxidant status, and DNA repair capacity is responsible for the accumulation of genetic mutations and genomic instability. The lesion-specific DNA glycosylases, e.g., hOGG1 [...] Read more.
Oxidative stress, oxidative DNA damage and resulting mutations play a role in colorectal carcinogenesis. Impaired equilibrium between DNA damage formation, antioxidant status, and DNA repair capacity is responsible for the accumulation of genetic mutations and genomic instability. The lesion-specific DNA glycosylases, e.g., hOGG1 and MUTYH, initiate the repair of oxidative DNA damage. Hereditary syndromes (MUTYH-associated polyposis, NTHL1-associated tumor syndrome) with germline mutations causing a loss-of-function in base excision repair glycosylases, serve as straight forward evidence on the role of oxidative DNA damage and its repair. Altered or inhibited function of above glycosylases result in an accumulation of oxidative DNA damage and contribute to the adenoma-adenocarcinoma transition. Oxidative DNA damage, unless repaired, often gives rise G:C > T:A mutations in tumor suppressor genes and proto-oncogenes with subsequent occurrence of chromosomal copy-neutral loss of heterozygosity. For instance, G>T transversions in position c.34 of a KRAS gene serves as a pre-screening tool for MUTYH-associated polyposis diagnosis. Since sporadic colorectal cancer represents more complex and heterogenous disease, the situation is more complicated. In the present study we focused on the roles of base excision repair glycosylases (hOGG1, MUTYH) in colorectal cancer patients by investigating tumor and adjacent mucosa tissues. Although we found downregulation of both glycosylases and significantly lower expression of hOGG1 in tumor tissues, accompanied with G>T mutations in KRAS gene, oxidative DNA damage and its repair cannot solely explain the onset of sporadic colorectal cancer. In this respect, other factors (especially microenvironment) per se or in combination with oxidative DNA damage warrant further attention. Base excision repair characteristics determined in colorectal cancer tissues and their association with disease prognosis have been discussed as well. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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Review

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19 pages, 1405 KiB  
Review
Role of Antioxidant Vitamins and Other Micronutrients on Regulations of Specific Genes and Signaling Pathways in the Prevention and Treatment of Cancer
by Oladapo F. Fagbohun, Caroline R. Gillies, Kieran P. J. Murphy and H. P. Vasantha Rupasinghe
Int. J. Mol. Sci. 2023, 24(7), 6092; https://doi.org/10.3390/ijms24076092 - 23 Mar 2023
Cited by 2 | Viewed by 3613
Abstract
Cancer is an escalating global issue, with 19.3 million new cases and 9.9 million deaths in 2020. Therefore, effective approaches to prevent cancer are urgently required. Diet plays a significant role in determining cancer risk. Nutrients and food bioactives influence specific signaling pathways [...] Read more.
Cancer is an escalating global issue, with 19.3 million new cases and 9.9 million deaths in 2020. Therefore, effective approaches to prevent cancer are urgently required. Diet plays a significant role in determining cancer risk. Nutrients and food bioactives influence specific signaling pathways in the body. Recently, there have been significant advances in cancer prevention research through nutrigenomics or with the effects of dietary components on the genome. Google Scholar, PubMed, and Scopus databases were used to search for peer-reviewed articles between 2017 and 2023. Criteria used were vitamins, minerals, tumors, cancer, genes, inflammation, signaling pathways, and nutrigenomics. Among the total of 1857 articles available, the highest relevant 90 articles that specifically discussed signaling pathways and genes on cancer cell lines and human cancer patients were selected and reviewed. Food sources are rich in antioxidant micronutrients, which are effective in activating or regulating signaling pathways involved in pathogenesis and cancer therapy by activating enzymes such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and phosphatidylinositol 3-kinase (PI3K). The micronutrients are involved in the regulation of β-catenin (WNT/β-catenin) including mutations in Kras and epidermal growth factor receptor (EGFR) alongside inhibition of the NF-kB pathway. The most common mechanism of cancer prevention by these micronutrients is their antioxidative, anti-inflammation, and anti-apoptosis effects. This review discusses how nutrigenomics is essential and beneficial for developing cancer prevention and treatment approaches. Full article
(This article belongs to the Special Issue DNA Damage, Oxidative Stress and Related Metabolic By-Products in Cancer and Environmental Studies 2.0)
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