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Toxics
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DNA Damage Response to Harmful Anthropogenic Substances
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DNA Damage Response to Harmful Anthropogenic Substances

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Exposome Analysis and Risk Assessment".

Deadline for manuscript submissions: closed (15 September 2020) | Viewed by 10325

Special Issue Editor

Dr. Carina Ladeira

E-Mail Website
Guest Editor
Escola Superior de Tecnologia da Saúde de Lisboa—Instituto Politécnico de Lisboa, Departamento das Ciências do Diagnóstico, Terapêutica e Saúde Pública, Av. D. João II, Lote 4.69.01 | 1990-096 Lisboa, Portugal
Interests: human biomonitoring; genetic toxicology; chemical mixtures; risk assessment; occupational health; in vitro
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

DNA is the repository of genetic information and its integrity and stability are crucial to life, thus there exist robust and efficient DNA repair systems. In addition to the intrinsic genetic insults from DNA replication during cell division, DNA oxidative damage from byproducts of metabolism—such as free radicals, and others—environmental agents can also interact with and damage DNA. The problematic issue of unrepaired DNA damage is the possibility of mutation and possibly disease, namely cancer, which is a genetic disease. There is a wide range of anthropogenic sources of harmful substances produces by the metallurgical industry, energy production by combustion, cooking, road traffic, waste treatment, industrial organics, and pesticides, among others, which can be found in the environment and/or in occupational contexts.

This Special Issue on “DNA damage responses to harmful anthropogenic substances” aims to highlight the research into DNA damage as an effect biomarker in the study of the effects, processes, objects, or materials derived from human activities, including all forms of chemical, physical and biological substances.

Authors are invited and welcome to submit original research papers, reviews, and short communications.

Prof. Carina Ladeira
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. Toxics 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 2600 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

  • DNA damage
  • biomarker
  • environment occupational
  • exposure
  • anthropogenic
  • toxicants
  • risk assessment

Published Papers (3 papers)

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Research

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15 pages, 2466 KiB  
Article
Potential of Inactivated Bifidobacterium Strain in Attenuating Benzo(A)Pyrene Exposure-Induced Damage in Colon Epithelial Cells In Vitro
by Mengfan Xu, Lili Fu, Junwen Zhang, Tao Wang, Junfeng Fan, Baoqing Zhu, Piotr Dziugan, Bolin Zhang and Hongfei Zhao
Toxics 2020, 8(1), 12; https://doi.org/10.3390/toxics8010012 - 11 Feb 2020
Cited by 8 | Viewed by 2927
Abstract
Long-term exposure to benzo(a)pyrene (BaP) poses a serious genotoxic threat to human beings. This in vitro study investigated the potential of inactivated Bifidobacterium animalis subsp. lactis BI-04 in alleviating the damage caused by BaP in colon epithelial cells. A concentration of BaP higher [...] Read more.
Long-term exposure to benzo(a)pyrene (BaP) poses a serious genotoxic threat to human beings. This in vitro study investigated the potential of inactivated Bifidobacterium animalis subsp. lactis BI-04 in alleviating the damage caused by BaP in colon epithelial cells. A concentration of BaP higher than 50 μM strongly inhibited the growth of colon epithelial cells. The colon epithelial cells were treated with 50 μM BaP in the presence or absence of inactivated strain BI-04 (~5 × 108 CFU/mL). The BaP-induced apoptosis of the colon epithelial cells was retarded in the presence of B. lactis BI-04 through activation of the PI3K/ AKT signaling pathway, and p53 gene expression was decreased. The presence of the BI-04 strain reduced the intracellular oxidative stress and DNA damage incurred in the colon epithelial cells by BaP treatment due to the enhanced expression of antioxidant enzymes and metabolism-related enzymes (CYP1A1). The data from comet assay, qRT-PCR, and western blot analysis showed that the cytotoxic effects of BaP on colon epithelial cells were largely alleviated because the bifidobacterial strain could bind to this carcinogenic compound. The in vitro study highlights that the consumption of commercial probiotic strain BI-04 might be a promising strategy to mitigate BaP cytotoxicity. Full article
(This article belongs to the Special Issue DNA Damage Response to Harmful Anthropogenic Substances)
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8 pages, 932 KiB  
Article
Environmentally Relevant Concentrations of Bisphenol A Interact with Doxorubicin Transcriptional Effects in Human Cell Lines
by Edna Ribeiro, Mariana Delgadinho and Miguel Brito
Toxics 2019, 7(3), 43; https://doi.org/10.3390/toxics7030043 - 29 Aug 2019
Cited by 9 | Viewed by 3818
Abstract
The worldwide production of synthetic chemicals, including endocrine disruptor chemicals (EDCs), such as Bisphenol A (BPA) has increased significantly in the last two decades. Human exposure to BPA, particularly through ingestion, is continuous and ubiquitous. Although, considered a weak environmental estrogen, BPA can [...] Read more.
The worldwide production of synthetic chemicals, including endocrine disruptor chemicals (EDCs), such as Bisphenol A (BPA) has increased significantly in the last two decades. Human exposure to BPA, particularly through ingestion, is continuous and ubiquitous. Although, considered a weak environmental estrogen, BPA can induce divergent biological responses through several signaling pathways, including carcinogenesis in hormone-responsive organs. However, and despite the continuous increase of tumor cell-resistance to therapeutic drugs, such as doxorubicin (DOX), information regarding BPA drug interactions is still scarce, although its potential role in chemo-resistance has been suggested. This study aims to assess the potential interactions between environmentally relevant levels of BPA and DOX at a therapeutic dosage on Hep-2 and MRC-5 cell lines transciptome. Transcriptional effects in key-player genes for cancer biology, namely c-fos, p21, and bcl-xl, were evaluated through qRT-PCR. The cellular response was analyzed after exposure to BPA, DOX, or co-exposure to both chemicals. Transcriptional analysis showed that BPA exposure induces upregulation of bcl-xl and endorses an antagonistic non-monotonic response on DOX transcriptional effects. Moreover, the BPA interaction with DOX on c-fos and p21 expression emphasize its cellular specificity and divergent effects. Overall, Hep-2 was more susceptible to BPA effects in a dose-dependent manner while MRC-5 transcriptional levels endorsed a non-monotonic response. Our data indicate that BPA environmental exposure may influence chemotherapy outcomes, which emphasize the urgency for a better understanding of BPA interactions with chemotherapeutic agents, in the context of risk assessment. Full article
(This article belongs to the Special Issue DNA Damage Response to Harmful Anthropogenic Substances)
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Review

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10 pages, 232 KiB  
Review
Methylmercury Epigenetics
by Megan Culbreth and Michael Aschner
Toxics 2019, 7(4), 56; https://doi.org/10.3390/toxics7040056 - 09 Nov 2019
Cited by 27 | Viewed by 3130
Abstract
Methylmercury (MeHg) has conventionally been investigated for effects on nervous system development. As such, epigenetic modifications have become an attractive mechanistic target, and research on MeHg and epigenetics has rapidly expanded in the past decade. Although, these inquiries are a recent advance in [...] Read more.
Methylmercury (MeHg) has conventionally been investigated for effects on nervous system development. As such, epigenetic modifications have become an attractive mechanistic target, and research on MeHg and epigenetics has rapidly expanded in the past decade. Although, these inquiries are a recent advance in the field, much has been learned in regards to MeHg-induced epigenetic modifications, particularly in the brain. In vitro and in vivo controlled exposure studies illustrate that MeHg effects microRNA (miRNA) expression, histone modifications, and DNA methylation both globally and at individual genes. Moreover, some effects are transgenerationally inherited, as organisms not directly exposed to MeHg exhibited biological and behavioral alterations. miRNA expression generally appears to be downregulated consequent to exposure. Further, global histone acetylation also seems to be reduced, persist at distinct gene promoters, and is contemporaneous with enhanced histone methylation. Moreover, global DNA methylation appears to decrease in brain-derived tissues, but not in the liver; however, selected individual genes in the brain are hypermethylated. Human epidemiological studies have also identified hypo- or hypermethylated individual genes, which correlated with MeHg exposure in distinct populations. Intriguingly, several observed epigenetic modifications can be correlated with known mechanisms of MeHg toxicity. Despite this knowledge, however, the functional consequences of these modifications are not entirely evident. Additional research will be necessary to fully comprehend MeHg-induced epigenetic modifications and the impact on the toxic response. Full article
(This article belongs to the Special Issue DNA Damage Response to Harmful Anthropogenic Substances)
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