Oxidative Stress and Neurotoxicity Induced by Chemicals

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

Deadline for manuscript submissions: 31 July 2024 | Viewed by 1399

Special Issue Editors


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Guest Editor
Neuroimmunology Laboratories, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Interests: oxidative stress; inflammation; mitochondrial dysfunction; depression; cognitive impairment; pain

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Guest Editor
Department of Biochemistry, University of Allahabad, Prayagraj, Uttar Pradesh, India
Interests: gerontology; natural products; chronobiology; clinical biochemistry

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Guest Editor
FEST & ASSIST Divisions, CSIR-Indian Institute of Toxicology Research, Lucknow, Uttar Pradesh, India
Interests: neurotoxicology; neurodegeneration; neurobiology of Parkinson's disease; oxidative stress

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Guest Editor
Neuroimmunology Laboratories, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
Interests: oxidative stress; Nrf2; neuropathic pain; neurodegeneration

Special Issue Information

Dear Colleagues,

Oxidative stress is a term used to describe the cytotoxic effects caused due to an imbalance between the generation of reactive oxygen/nitrogen species (ROS/RNS) or other free radicals and the capacity of cells to combat them. Compared to other physiological systems, the neurological system is particularly more susceptible to oxidative damage because of its high energy requirements, high oxygen consumption, the abundance of polyunsaturated fatty acids that are sensitive to free radicals, and low level of antioxidant scavengers. Numerous studies have compellingly indicated that oxidative stress is a key pathological factor in the emergence of a variety of neurological disorders. However, more research is required to clarify the mechanisms underlying oxidative stress-induced neurotoxicity.

Certain chemicals and/or their metabolites can directly mediate the formation of free radicals that may induce damage to biomolecules and result in the development of irreversible neurodegeneration and even death both in humans and animals. Thus, it is crucial to comprehend the precise molecular pathways underlying chemical-induced oxidative damage and neurotoxicity to create efficient treatments and cutting-edge therapeutic approaches for major neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis.

To better understand and ameliorate chemical-induced neurotoxicity, this Special Issue aims to compile cutting-edge original research and review articles that reveal new mechanistic pathways, potential therapeutic approaches, and neuroprotective agents, particularly focusing on oxidative stress and neurotoxicity caused by chemicals, as well as their metabolites.

It is intended that this Special Issue, entitled “Oxidative Stress and Neurotoxicity Induced by Chemicals”, will advance the discipline by increasing the scientific knowledge of the possible contribution of oxidative stress and chemical exposure to the etiology of neurological disorders both in the public and scientific domains.

Dr. Angela Maria Casaril
Prof. Dr. Syed Ibrahim Rizvi
Dr. Mahendra Pratap Singh
Dr. Mohd Sami Ur Rasheed
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. 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

  • neurotoxin
  • reactive oxygen species
  • free radicals
  • antioxidants
  • neuronal damage
  • neurodegeneration
  • neuroprotection

Published Papers (1 paper)

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Review

16 pages, 3066 KiB  
Review
Single-Nucleotide Polymorphisms Associated with Mercury Levels and Neurological Symptoms: An Overview
by Jamila Alessandra Perini, Jessica Vilarinho Cardoso, Alana de Oliveira Knesse, Felipe Oliveira Pessoa-Silva, Ana Claudia Santiago de Vasconcellos, Daniel Escorsim Machado and Paulo Cesar Basta
Toxics 2024, 12(3), 226; https://doi.org/10.3390/toxics12030226 - 20 Mar 2024
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Abstract
Mercury (Hg) pollution is a global public health concern because of its adverse effects on the environment and health. Single-nucleotide polymorphisms (SNPs) have been associated with Hg levels and outcomes. The aim of this review was to describe the research and discuss the [...] Read more.
Mercury (Hg) pollution is a global public health concern because of its adverse effects on the environment and health. Single-nucleotide polymorphisms (SNPs) have been associated with Hg levels and outcomes. The aim of this review was to describe the research and discuss the evidence on the genetic susceptibility of Hg-exposed individuals to the development of neurocognitive disorders. A systematic review was performed to identify the genes/SNPs associated with Hg toxicokinetics and that, therefore, affect neurological function in exposed populations. Observational and experimental studies were identified by screening three databases. Thirteen articles were included (quality score 82–100%) and 8124 individuals were evaluated. Hg exposure was mainly fish consumption (77%) and, in 31% of the studies, the Hg levels exceeded the reference limits. Genetic susceptibility to higher Hg levels and neurotoxicity risk in Hg poisoning were associated with eight (ALAD rs1800435, CYP3A4 rs2740574, CYP3A5 rs776746, CYP3A7 rs2257401, GSTP1 rs1695, MT1A rs8052394, MT1M rs2270836, and MT4 rs11643815) and three (MT1A rs8052394, MT1M rs2270837, and MT2A rs10636) SNPs, respectively, and rs8052394 was associated with both outcomes. The MT1A rs8052394 SNP may be used as a susceptibility biomarker to identify individuals at greater risk for higher Hg levels and the development of neurocognitive disorders in metal-exposed populations. Full article
(This article belongs to the Special Issue Oxidative Stress and Neurotoxicity Induced by Chemicals)
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