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Toxics
Special Issues
Mechanisms of Cytotoxicity and Genotoxicity of Xenobiotics and Their Metabolites
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Mechanisms of Cytotoxicity and Genotoxicity of Xenobiotics and Their Metabolites

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Toxicology".

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 6344

Special Issue Editor

Dr. Beáta Holečková

E-Mail Website
Guest Editor
Department of Biology and Physiology, University of Veterinary Medicine and Pharmacy in Košice, Komenského 73, 041 84 Košice, Slovakia
Interests: genetic toxicology; mechanisms of pesticides genotoxicity; animal cell models; cytogenetics; molecular biology; animal hereditary diseases

Special Issue Information

Dear Colleagues,

Intensive human activities such as industrialisation, modern technologies and pesticide agriculture have created a situation where xenobiotics are omnipresent. These chemicals can affect living organisms in different and often unpredictable ways. One of the first xenobiotic properties that should be investigated is the cytotoxic potential, that is, the ability of a compound to cause cellular damage. In addition, some agents have the capacity to be genotoxic: to interact with genetic material resulting in alterations and possible DNA damage. Additionally, indirect genotoxicity is a feature of some xenobiotics, and is caused by alterations in spindle fibres or kinetochore proteins and the incorporation of DNA analogues, leading to incorrect chromosomal segregation and DNA strand breaks, respectively.

We are pleased to invite you to contribute to our Special Issue of Toxics focusing on the above topics. We welcome original research articles, reviews and short communications related to developing a better understanding of cytotoxicity and genotoxicity mechanisms of different types of xenobiotics and their metabolites to broaden and deepen the existing information and knowledge in the field. We look forward to receiving your contributions.

Dr. Beáta Holečková
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

  • xenobiotics
  • pesticides
  • mechanisms of action
  • cytotoxicity
  • genotoxicity
  • apoptosis
  • oxidative stress
  • DNA breaks
  • chromosomal segregation
  • test strategy

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Published Papers (2 papers)

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Research

15 pages, 2219 KiB  
Article
Anthraquinones: Genotoxic until Proven Otherwise? A Study on a Substance-Based Medical Device to Implement Available Data for a Correct Risk Assessment
by Veronica Cocchi, Sofia Gasperini and Monia Lenzi
Toxics 2022, 10(3), 142; https://doi.org/10.3390/toxics10030142 - 16 Mar 2022
Cited by 3 | Viewed by 2190
Abstract
A genotoxicological study was carried out on a substance-based medical device (SMD) containing anthraquinones in order to evaluate its potential mutagenic effect. The “In Vitro Mammalian Cell Micronucleus Test” was performed on human TK6 cells by flow cytometry. Cultures were treated with concentrations [...] Read more.
A genotoxicological study was carried out on a substance-based medical device (SMD) containing anthraquinones in order to evaluate its potential mutagenic effect. The “In Vitro Mammalian Cell Micronucleus Test” was performed on human TK6 cells by flow cytometry. Cultures were treated with concentrations of SMD tested in the range of 0–2 mg/mL for short treatment time (3 h) both in the absence and presence of an exogenous metabolic activation system, followed by a recovery period in fresh medium (23 h) and for extended treatment time (26 h) without an exogenous metabolic activation system. At the end of both treatment times, cytotoxicity, cytostasis, apoptosis and micronuclei (MNi) frequency were analysed in treated cultures and then compared with those measured in concurrent negative control cultures. The SMD did not induce a statistically significant increase MNi frequency under any of experimental conditions tested. The negative outcome shows that the SMD is non-mutagenic in terms of its ability to induce chromosomal aberrations both in the absence and presence of an exogenous metabolic activation system. The study ended by analyzing intracellular ROS levels to exclude the pro-oxidant ability, typically linked to DNA damage. On the contrary, our results demonstrated the ability the SMD to counteract oxidative stress. Full article
(This article belongs to the Special Issue Mechanisms of Cytotoxicity and Genotoxicity of Xenobiotics and Their Metabolites)
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15 pages, 3060 KiB  
Article
In Vitro Neurotoxicity of Flumethrin Pyrethroid on SH-SY5Y Neuroblastoma Cells: Apoptosis Associated with Oxidative Stress
by Luis Barrios-Arpi, Yurie Arias, Bernardo Lopez-Torres, Mariella Ramos-Gonzalez, Giulio Ticli, Ennio Prosperi and José-Luis Rodríguez
Toxics 2022, 10(3), 131; https://doi.org/10.3390/toxics10030131 - 7 Mar 2022
Cited by 8 | Viewed by 3488
Abstract
Pyrethroids are neurotoxicants for animals, showing a pattern of toxic action on the nervous system. Flumethrin, a synthetic pyrethroid, is used against ectoparasites in domestic animals, plants, and for public health. This compound has been shown to be highly toxic to bees, while [...] Read more.
Pyrethroids are neurotoxicants for animals, showing a pattern of toxic action on the nervous system. Flumethrin, a synthetic pyrethroid, is used against ectoparasites in domestic animals, plants, and for public health. This compound has been shown to be highly toxic to bees, while its effects on other animals have been less investigated. However, in vitro studies to evaluate cytotoxicity are scarce, and the mechanisms associated with this effect at the molecular level are still unknown. This study aimed to investigate the oxidative stress and cell death induction in SH-SY5Y neuroblastoma cells in response to flumethrin exposure (1–1000 µM). Flumethrin induced a significant cytotoxic effect, as evaluated by MTT and LDH leakage assays, and produced an increase in the biomarkers of oxidative stress as reactive oxygen species and nitric oxide (ROS and NO) generation, malondialdehyde (MDA) concentration, and caspase-3 activity. In addition, flumethrin significantly increased apoptosis-related gene expressions (Bax, Casp-3, BNIP3, APAF1, and AKT1) and oxidative stress and antioxidative (NFκB and SOD2) mediators. The results demonstrated, by biochemical and gene expression assays, that flumethrin induces oxidative stress and apoptosis, which could cause DNA damage. Detailed knowledge obtained about these molecular changes could provide the basis for elucidating the molecular mechanisms of flumethrin-induced neurotoxicity. Full article
(This article belongs to the Special Issue Mechanisms of Cytotoxicity and Genotoxicity of Xenobiotics and Their Metabolites)
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