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Toxics
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Heavy Metal Induced Neurotoxicity
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Heavy Metal Induced Neurotoxicity

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

Deadline for manuscript submissions: 7 February 2025 | Viewed by 2776

Special Issue Editor

Dr. Samuel Caito

E-Mail Website
Guest Editor
Department of Pharmaceutical Sciences, Husson University School of Pharmacy, Bangor, ME 04401, USA
Interests: heavy metal toxicology; C. elegans; metabolism; biochemistry

Special Issue Information

Dear Colleagues

The neurotoxicity of metals is an important topic, as metals can cause neurodevelopmental toxicities, cognative and behavorial alterations, and neurodegeneration. The risk due to exposure of metals such as lead, cadmium, mercury and manganese, has been appreciated for some time; nevertheless, insights into their roles in disease processes and their mechanisms of action continue to be described. Furthermore, exposures to metals once thought to be safe or negligable, such as tungsten and the lanthanide series, are gaining more attention due to their increased industrial use. This Special Issue aims to investigate both novel roles for traditional neurotoxic metals, as well as describe neurotoxicities for previously understudied metals.

Dr. Samuel Caito
Guest Editor

Manuscript Submission Information

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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

  • neurotoxicology
  • metal
  • brain
  • development
  • neurodegeneration

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Published Papers (3 papers)

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Research

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17 pages, 1606 KiB  
Article
Dopaminergic- and Serotonergic-Dependent Behaviors Are Altered by Lanthanide Series Metals in Caenorhabditis elegans
by Anthony Radzimirski, Michael Croft, Nicholas Ireland, Lydia Miller, Jennifer Newell-Caito and Samuel Caito
Toxics 2024, 12(10), 754; https://doi.org/10.3390/toxics12100754 - 17 Oct 2024
Viewed by 514
Abstract
The lanthanide series elements are transition metals used as critical components of electronics, as well as rechargeable batteries, fertilizers, antimicrobials, contrast agents for medical imaging, and diesel fuel additives. With the surge in their utilization, lanthanide metals are being found more in our [...] Read more.
The lanthanide series elements are transition metals used as critical components of electronics, as well as rechargeable batteries, fertilizers, antimicrobials, contrast agents for medical imaging, and diesel fuel additives. With the surge in their utilization, lanthanide metals are being found more in our environment. However, little is known about the health effects associated with lanthanide exposure. Epidemiological studies as well as studies performed in rodents exposed to lanthanum (La) suggest neurological damage, learning and memory impairment, and disruption of neurotransmitter signaling, particularly in serotonin and dopamine pathways. Unfortunately, little is known about the neurological effects of heavier lanthanides. As dysfunctions of serotonergic and dopaminergic signaling are implicated in multiple neurological conditions, including Parkinson’s disease, depression, generalized anxiety disorder, and post-traumatic stress disorder, it is of utmost importance to determine the effects of La and other lanthanides on these neurotransmitter systems. We therefore hypothesized that early-life exposure of light [La (III) or cerium (Ce (III))] or heavy [erbium (Er (III)) or ytterbium (Yb (III))] lanthanides in Caenorhabditis elegans could cause dysregulation of serotonergic and dopaminergic signaling upon adulthood. Serotonergic signaling was assessed by measuring pharyngeal pump rate, crawl-to-swim transition, as well as egg-laying behaviors. Dopaminergic signaling was assessed by measuring locomotor rate and egg-laying and swim-to-crawl transition behaviors. Treatment with La (III), Ce (III), Er (III), or Yb (III) caused deficits in serotonergic or dopaminergic signaling in all assays, suggesting both the heavy and light lanthanides disrupt these neurotransmitter systems. Concomitant with dysregulation of neurotransmission, all four lanthanides increased reactive oxygen species (ROS) generation and decreased glutathione and ATP levels. This suggests increased oxidative stress, which is a known modifier of neurotransmission. Altogether, our data suggest that both heavy and light lanthanide series elements disrupt serotonergic and dopaminergic signaling and may affect the development or pharmacological management of related neurological conditions. Full article
(This article belongs to the Special Issue Heavy Metal Induced Neurotoxicity)
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22 pages, 2143 KiB  
Article
Cerebral Vascular Toxicity after Developmental Exposure to Arsenic (As) and Lead (Pb) Mixtures
by Keturah Kiper, Breeann Mild, Jenny Chen, Chongli Yuan, Ellen M. Wells, Wei Zheng and Jennifer L. Freeman
Toxics 2024, 12(9), 624; https://doi.org/10.3390/toxics12090624 - 24 Aug 2024
Viewed by 841
Abstract
Arsenic (As) and lead (Pb) are environmental pollutants found in common sites linked to similar adverse health effects. This study determined driving factors of neurotoxicity on the developing cerebral vasculature with As and Pb mixture exposures. Cerebral vascular toxicity was evaluated at mixture [...] Read more.
Arsenic (As) and lead (Pb) are environmental pollutants found in common sites linked to similar adverse health effects. This study determined driving factors of neurotoxicity on the developing cerebral vasculature with As and Pb mixture exposures. Cerebral vascular toxicity was evaluated at mixture concentrations of As and Pb representing human exposures levels (10 or 100 parts per billion; ppb; µg/L) in developing zebrafish by assessing behavior, morphology, and gene expression. In the visual motor response assay, hyperactivity was observed in all three outcomes in dark phases in larvae with exposure (1–120 h post fertilization, hpf) to 10 ppb As, 10 ppb Pb, or 10 ppb mix treatment. Time spent moving exhibited hyperactivity in dark phases for 100 ppb As and 100 ppb mix treatment groups only. A decreased brain length and ratio of brain length to total length in the 10 ppb mix group was measured with no alterations in other treatment groups or other endpoints (i.e., total larval length, head length, or head width). Alternatively, measurements of cerebral vasculature in the midbrain and cerebellum uncovered decreased total vascularization at 72 hpf in all treatment groups in the mesencephalon and in all treatment groups, except the 100 ppb Pb and 10 ppb As groups, in the cerebellum. In addition, decreased sprouting and branching occurred in the mesencephalon, while only decreased branching was measured in the cerebellum. The 10 ppb Pb group showed several cerebral vasculature modifications that were aligned with a specific gene expression alteration pattern different from other treatment groups. Additionally, the 100 ppb As group drove gene alterations, along with several other endpoints, for changes observed in the 100 ppb mix treatment group. Perturbations assessed in this study displayed non-linear concentration-responses, which are important to consider in environmental health outcomes for As and Pb neurotoxicity. Full article
(This article belongs to the Special Issue Heavy Metal Induced Neurotoxicity)
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Review

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11 pages, 657 KiB  
Review
The Role of Copper in Alzheimer’s Disease Etiopathogenesis: An Updated Systematic Review
by Angela Sabalic, Veronica Mei, Giuliana Solinas and Roberto Madeddu
Toxics 2024, 12(10), 755; https://doi.org/10.3390/toxics12100755 - 17 Oct 2024
Viewed by 1030
Abstract
Background: Alzheimer’s disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, an increase in amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors, such as [...] Read more.
Background: Alzheimer’s disease (AD) is the most common cause of dementia and cognitive decline in the elderly. Although the etiology of AD is unknow, an increase in amyloid precursor protein (APP) leads to the toxic aggregation of Aβ plaques. Several factors, such as hypertension, diabetes, dyslipidemia, smoking, hormonal changes, and metal exposure, could increase the risk of developing AD. In this review, we will examine the role of copper (Cu) in the pathophysiology of AD, as well as the mechanisms involved in neurotoxicity and cognitive decline. Methods: This review was conducted in accordance with PRISMA guidelines. We performed a comprehensive literature analysis over the last ten years on AD and Cu. Only late-onset Alzheimer’s disease was considered; only studies on elderly people of both sexes were included. Results: A total of seven articles were picked for this review, three studies focused on non-ceruloplasmin-bound Copper (non-Cp-Cu) and four on ceruloplasmin-bound Copper (Cp-Cu). The results showed higher Cu concentrations in patients compared to healthy controls. Conclusions: Elevated concentrations of Cu may contribute to the progression of AD, potentially interacting with ATP7B mutations, oxidative stress (OS), and amyloid-β plaques. Future research is needed to provide more robust evidence and better characterize the relationship between AD and Cu. Full article
(This article belongs to the Special Issue Heavy Metal Induced Neurotoxicity)
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