Neurotoxicity of Heavy Metals

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

Deadline for manuscript submissions: closed (20 March 2026) | Viewed by 1713

Special Issue Editors


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Guest Editor
Nantong Key Laboratory of Environmental Toxicology, Department of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China
Interests: heavy metal; neurotoxicity; epidemiology; air pollution; neurodegenerative diseases

E-Mail Website
Guest Editor
Department of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China
Interests: heavy metal; environmental pollution; neurotoxicity; neurodegenerative diseases; molecular mechanisms

Special Issue Information

Dear Colleagues,

There have been some human studies showing a significant correlation between serum or urine metals and cognitive function. At the same time, some animal studies have confirmed that a variety of heavy metals are neurotoxic, but the relevant mechanisms are still unclear. This Special Issue focuses on (1) the neurotoxic mechanism of heavy metals and (2) the results of human studies related to heavy metals and nervous system function. Authors are invited to submit original research papers, reviews, or short communications.

Dr. Xinyuan Zhao
Dr. Shali Yu
Guest Editors

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Keywords

  • molecular studies
  • epidemiology
  • oxidative stress
  • heavy metal
  • environmental pollution
  • cellular apoptosis
  • protein or rna regulation

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Published Papers (1 paper)

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Research

22 pages, 18852 KB  
Article
Mitochondrial Ultrastructure, Fission Proteins, Activity, and Motor Dysfunctions in the Innovative Parkinson’s Disease Model Induced by Manganese Inhalation
by Cesar Alfonso Garcia-Caballero, Jose Luis Ordoñez-Librado, Avril De Alba-Ríos, Enrique Montiel-Flores, Omar Emiliano Aparicio-Trejo, Fernando García-Arroyo, Belén Cuevas-Lopez, José Pedraza-Chaverri, Vianey Rodríguez-Lara, Rocío Tron-Alvarez, Ana Luisa Gutierréz-Valdez, Javier Sánchez-Betancourt, Leonardo Reynoso-Erazo and Maria Rosa Avila-Costa
Toxics 2026, 14(3), 208; https://doi.org/10.3390/toxics14030208 - 28 Feb 2026
Viewed by 1145
Abstract
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, yet its pathogenic mechanisms remain incompletely understood, highlighting the need for reliable experimental models. We previously developed a murine model based on inhalation of a manganese mixture (MnCl2 and Mn(OAc)3), [...] Read more.
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, yet its pathogenic mechanisms remain incompletely understood, highlighting the need for reliable experimental models. We previously developed a murine model based on inhalation of a manganese mixture (MnCl2 and Mn(OAc)3), which reproduces dopaminergic neuron loss in the substantia nigra pars compacta (SNc) and motor impairment. However, its capacity to mimic mitochondrial dysfunction, a key mechanism in PD, had not been explored. This study evaluated mitochondrial ultrastructure, fission and fusion proteins, and the activity of electron transport chain complexes I and IV, alongside fine motor performance. Forty male CD1 mice were divided into control (deionized water) and manganese-exposed groups (0.04 M MnCl2 + 0.02 M Mn(OAc)3), inhaled for 1 h twice weekly over five months. Manganese inhalation induced significant fine motor deficits, increased mitochondrial number with reduced area and circularity, and disorganized cristae. Drp1 and Fis1 levels were elevated, accompanied by decreased activity of complexes I and IV, predominantly in the SNc. These findings demonstrate that this progressive, bilateral model reproduces mitochondrial and motor alterations resembling those observed in PD, supporting its utility for testing mitochondria-targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Neurotoxicity of Heavy Metals)
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