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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (20 May 2024) | Viewed by 22586

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Prof. Dr. Toshiyuki Kaji

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Department of Environmental Health, Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda 278-8510, Japan
Interests: signaling and cell response; transporter; vascular toxicity; extracellular matrix; atherosclerosis; blood coagulation-fibrinolytic system; growth factors; cytokines
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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Mechanisms of Heavy Metal Toxicity”.

The toxicity of heavy metals has been a popular research topic for a long time. In the past, it was important to elucidate the actual health hazards caused by environmental pollution, accidents, and crimes involving metals, metalloids, and metal compounds, but now the main issues are related to the elucidation of the mechanisms of their toxicity and defense mechanisms against said toxicity.

This Special Issue is under production with the aim of addressing this contemporary issue. In this Special Issue, we welcome the submission of full reviews, original research papers, short communications, and perspectives that cover the following topics:

Cellular and molecular mechanisms underlying heavy metals, metalloids, and metal(loid)-containing compounds;
Mechanisms underlying the induction of metallothionein;
Cellular defense systems against the toxicity of heavy metals, metalloids, and metal(loid)-containing compounds;
The regulation and mechanisms of the expression of metal transporters such as SLC39A8.
Research that does not fit into the above topics but may contribute to them is also welcome.

By sharing these studies, we aim to make significant progress in metal toxicology.

Prof. Dr. Toshiyuki Kaji
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

heavy metal
metal compound
metallothionein
cellular defense mechanism
metal transporter

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Related Special Issue

Mechanisms of Heavy Metal Toxicity: 3rd Edition in International Journal of Molecular Sciences (4 articles)

Published Papers (10 papers)

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Research

Jump to: Review

12 pages, 1654 KiB

Open AccessArticle

Determining the Feasibility of a Cadmium Exposure Model to Activate the Inflammatory Arm of PANoptosis in Murine Monocytes

by Samuel Camilli, Tanush Madavarapu, Ritaj El Ghissassi, Apoorva Bhargavi Desaraju, Carli Busler, Ramani Soundararajan, Brenda Flam, Richard Lockey and Narasaiah Kolliputi

Int. J. Mol. Sci. 2024, 25(19), 10339; https://doi.org/10.3390/ijms251910339 - 26 Sep 2024

Viewed by 633

Abstract

A prevalence of cigarette smoking can cause the accumulation of cadmium (Cd²⁺) in the lungs, kidneys, and blood. The effects of exposure can cause multiple chronic disease types to emerge in the affected organ systems. The only moderately effective therapeutic option is chelation therapy; the health risks associated with this therapy have caused much criticism. The disease types associated with Cd²⁺ toxicity have inflammatory components and greatly impact innate immunity. These factors are affected at the cellular level and cause pathways like apoptosis, pyroptosis, and necroptosis. A development in understanding these pathways stipulates that these three pathways act as one complex of pathways, known together as PANoptosis. The inflammatory mechanisms of PANoptosis are particularly interesting in Cd²⁺ toxicity due to its inflammatory effects. Proteins in the gasdermin family act to release inflammatory cytokines, like interleukin-1β, into the extracellular environment. Cytokines cause inflammatory disease pathologies like fibrosis and cancer. RAW 264.7 monocytes are key in the murine immune system and provide an excellent model to investigate Cd²⁺ toxicity. Exposure of 0–15 µM CdCl₂ was sufficient to increase expression of cleaved gasdermin D (GSDMD) and gasdermin E (GSDME) in this cell type. Cd²⁺ also exhibits a dose–dependent cytotoxicity in this cell type. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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16 pages, 8286 KiB

Open AccessArticle

Manganese Overexposure Alters Neurogranin Expression and Causes Behavioral Deficits in Larval Zebrafish

by Anabel Alba-González, Elena I. Dragomir, Golsana Haghdousti, Julián Yáñez, Chris Dadswell, Ramón González-Méndez, Stephen W. Wilson, Karin Tuschl and Mónica Folgueira

Int. J. Mol. Sci. 2024, 25(9), 4933; https://doi.org/10.3390/ijms25094933 - 30 Apr 2024

Cited by 2 | Viewed by 1549

Abstract

Manganese (Mn), a cofactor for various enzyme classes, is an essential trace metal for all organisms. However, overexposure to Mn causes neurotoxicity. Here, we evaluated the effects of exposure to Mn chloride (MnCl₂) on viability, morphology, synapse function (based on neurogranin expression) and behavior of zebrafish larvae. MnCl₂ exposure from 2.5 h post fertilization led to reduced survival (60%) at 5 days post fertilization. Phenotypical changes affected body length, eye and olfactory organ size, and visual background adaptation. This was accompanied by a decrease in both the fluorescence intensity of neurogranin immunostaining and expression levels of the neurogranin-encoding genes nrgna and nrgnb, suggesting the presence of synaptic alterations. Furthermore, overexposure to MnCl₂ resulted in larvae exhibiting postural defects, reduction in motor activity and impaired preference for light environments. Following the removal of MnCl₂ from the fish water, zebrafish larvae recovered their pigmentation pattern and normalized their locomotor behavior, indicating that some aspects of Mn neurotoxicity are reversible. In summary, our results demonstrate that Mn overexposure leads to pronounced morphological alterations, changes in neurogranin expression and behavioral impairments in zebrafish larvae. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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19 pages, 1746 KiB

Open AccessArticle

Toxicogenomics of the Freshwater Oligochaete, Tubifex tubifex (Annelida, Clitellata), in Acute Water-Only Exposure to Arsenic

by Iñigo Moreno-Ocio, Mónica Aquilino, Lola Llorente, Maite Martínez-Madrid, Pilar Rodríguez, Leire Méndez-Fernández and Rosario Planelló

Int. J. Mol. Sci. 2024, 25(6), 3382; https://doi.org/10.3390/ijms25063382 - 16 Mar 2024

Cited by 1 | Viewed by 1215

Abstract

A toxicogenomic approach was used for toxicity evaluation of arsenic in the aquatic environment, and differential gene expression was investigated from 24 h and 96 h water-only acute toxicity tests with the aquatic oligochaete, Tubifex tubifex (Annelida, Clitellata). Several toxicological endpoints (survival and autotomy) of the oligochaete and tissue residues were measured, and dose-response modelling of gene expression data was studied. A reference transcriptome of the aquatic oligochaete, T. tubifex, was reconstructed for the first time, and genes related to cell stress response (Hsc70, Hsp10, Hsp60, and Hsp83), energy metabolism (COX1), oxidative stress (Cat, GSR, and MnSOD), and the genes involved in the homeostasis of organisms (CaM, RpS13, and UBE2) were identified and characterised. The potential use of the genes identified for risk assessment in freshwater ecosystems as early biomarkers of arsenic toxicity is discussed. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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15 pages, 3382 KiB

Open AccessArticle

Hexavalent-Chromium-Induced Disruption of Mitochondrial Dynamics and Apoptosis in the Liver via the AMPK-PGC-1α Pathway in Ducks

by Chang Wang, Xueyan Dai, Chenghong Xing, Caiying Zhang, Huabin Cao, Xiaoquan Guo, Ping Liu, Fan Yang, Yu Zhuang and Guoliang Hu

Int. J. Mol. Sci. 2023, 24(24), 17241; https://doi.org/10.3390/ijms242417241 - 8 Dec 2023

Cited by 5 | Viewed by 4538

Abstract

Hexavalent chromium (Cr(VI)) is a hazardous substance that poses significant risks to environmental ecosystems and animal organisms. However, the specific consequences of Cr(VI) exposure in terms of liver damage remain incompletely understood. This study aims to elucidate the mechanism by which Cr(VI) disrupts mitochondrial dynamics, leading to hepatic injury in ducks. Forty-eight healthy 8-day-old ducks were divided into four groups and subjected to diets containing varying doses of Cr(VI) (0, 9.28, 46.4, and 232 mg/kg) for 49 days. Our results demonstrated that Cr(VI) exposure resulted in disarranged liver lobular vacuolation, along with increasing the serum levels of ALT, AST, and AKP in a dose-dependent manner, which indicated liver damage. Furthermore, Cr(VI) exposure induced oxidative stress by reducing the activities of T-SOD, SOD, GSH-Px, GSH, and CAT, while increasing the contents of MDA and H₂O₂. Moreover, Cr(VI) exposure downregulated the activities of CS and MDH, resulting in energy disturbance, as evidenced by the reduced AMPK/p-AMPK ratio and PGC-1α protein expression. Additionally, Cr(VI) exposure disrupted mitochondrial dynamics through decreased expression of OPA1, Mfn1, and Mfn2 and increased expression of Drp-1, Fis1, and MFF proteins. This disruption ultimately triggered mitochondria-mediated apoptosis, as evidenced by elevated levels of caspase-3, Cyt C, and Bax, along with decreased expression of Bcl-2 and the Bcl-2/Bax ratio, at both the protein and mRNA levels. In summary, this study highlights that Cr(VI) exposure induces oxidative stress, inhibits the AMPK-PGC-1α pathway, disrupts mitochondrial dynamics, and triggers liver cell apoptosis in ducks. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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18 pages, 3588 KiB

Open AccessArticle

AsHC 360 Exposure Influence on Epileptiform Discharges in Hippocampus of Infantile Male Rats In Vitro

by Lei Dong, Ling Zhao, Lei Tian, Wenjun Zhao, Chan Xiong and Yu Zheng

Int. J. Mol. Sci. 2023, 24(23), 16806; https://doi.org/10.3390/ijms242316806 - 27 Nov 2023

Cited by 1 | Viewed by 1131

Abstract

Arsenic-containing hydrocarbons (AsHCs) are typical arsenolipids found in various marine organisms. They can penetrate the blood–brain barrier, specifically affecting synaptic plasticity and the learning and memory ability of hippocampal neurons. Temporal lobe epilepsy often occurs in the hippocampus. Thus, the possible influence of AsHCs exposure to temporal lobe epilepsy garnered attention. The present study investigated the effects of epileptiform discharges (EDs) signals introduced by low-magnesium ACSF in the hippocampus of infantile male rats in vitro, using electrophysiological techniques with multi-electrode arrays under AsHC 360 exposure. In our study of the effects of AsHC 360 on EDs signals, we found that inter-ictal discharges (IIDs) were not significantly impacted. When AsHC 360 was removed, any minor effects observed were reversed. However, when we examined the impact of AsHC 360 on ictal discharges (IDs), distinct patterns emerged based on the concentration levels. For low-concentration groups (5, 20, 60 μg As L⁻¹), both the frequency and duration effects on IDs returned to normal post-elimination of AsHC 360. However, this recovery was not evident for concentrations of 100 μg As L⁻¹ or higher. IDs were only observed in EDs signals during exposures to AsHC 360 concentrations up to 60 μg As L⁻¹. In these conditions, ID frequencies significantly enhanced with the increased of AsHC 360 concentration. At high concentrations of AsHC 360 (≥100 μg As L⁻¹), the transition from IIDs or pre-ictal discharges (PIDs) to IDs was notably inhibited. Additional study on co-exposure of AsHC 360 (100 μg As L⁻¹) and agonist (10 nM (S)-(-)-Bay-K-8644) indicated that the regulation of EDs signals under AsHC 360 exposure could be due to directly interference with the α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR) expression which influences the binding of excitatory glutamate neurotransmitter to AMPAR. The results suggest that EDs activities in the hippocampus of infantile Sprague Dawley rats are concentration-dependent on AsHC 360 exposure. Thus, it provides a basis for the seafood intake with AsHCs for epileptic patients and those with potential seizures. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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17 pages, 2603 KiB

Open AccessArticle

The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR T⁺ Itpr^3tf/J Mice through the Regulation of Signaling Pathways Relevant to T Cells

by Mohammed A. Assiri, Thamer H. Albekairi, Mushtaq A. Ansari, Ahmed Nadeem, Sabry M. Attia, Saleh A. Bakheet, Mudassar Shahid, Abdullah A. Aldossari, Mohammed M. Almutairi, Taghreed N. Almanaa, Mohammad Y. Alwetaid and Sheikh F. Ahmad

Int. J. Mol. Sci. 2023, 24(22), 16218; https://doi.org/10.3390/ijms242216218 - 11 Nov 2023

Cited by 3 | Viewed by 1671

Abstract

Autism spectrum disorder (ASD) is a common neurodevelopmental illness characterized by abnormal social interactions, communication difficulties, and repetitive and limited behaviors or interests. The BTBR T⁺ Itpr3^tf/J (BTBR) mice have been used extensively to research the ASD-like phenotype. Lead (Pb) is a hazardous chemical linked to organ damage in the human body. It is regarded as one of the most common metal exposure sources and has been connected to the development of neurological abnormalities. We used flow cytometry to investigate the molecular mechanism behind the effect of Pb exposure on subsets of CD4⁺ T cells in the spleen expressing IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, AhR, IL-10, and Foxp3. Furthermore, using RT-PCR, we studied the effect of Pb on the expression of numerous genes in brain tissue, including IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, AhR, IL-10, and Foxp3. Pb exposure increased the population of CD4⁺IFN-γ⁺, CD4⁺T-bet⁺, CD4⁺STAT1⁺, CD4⁺STAT4⁺, CD4⁺IL-9⁺, CD4⁺IRF4⁺, CD4⁺IL-22⁺, and CD4⁺AhR⁺ cells in BTBR mice. In contrast, CD4⁺IL-10⁺ and CD4⁺Foxp3⁺ cells were downregulated in the spleen cells of Pb-exposed BTBR mice compared to those treated with vehicle. Furthermore, Pb exposure led to a significant increase in IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, and AhR mRNA expression in BTBR mice. In contrast, IL-10 and Foxp3 mRNA expression was significantly lower in those treated with the vehicle. Our data suggest that Pb exposure exacerbates immunological dysfunctions associated with ASD. These data imply that Pb exposure may increase the risk of ASD. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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15 pages, 2212 KiB

Open AccessArticle

Chronic Kidney Disease Induced by Cadmium and Diabetes: A Quantitative Case-Control Study

by Supabhorn Yimthiang, David A. Vesey, Phisit Pouyfung, Tanaporn Khamphaya, Glenda C. Gobe and Soisungwan Satarug

Int. J. Mol. Sci. 2023, 24(10), 9050; https://doi.org/10.3390/ijms24109050 - 20 May 2023

Cited by 11 | Viewed by 2824

Abstract

Kidney disease associated with chronic cadmium (Cd) exposure is primarily due to proximal tubule cell damage. This results in a sustained decline in glomerular filtration rate (GFR) and tubular proteinuria. Similarly, diabetic kidney disease (DKD) is marked by albuminuria and a declining GFR and both may eventually lead to kidney failure. The progression to kidney disease in diabetics exposed to Cd has rarely been reported. Herein, we assessed Cd exposure and the severity of tubular proteinuria and albuminuria in 88 diabetics and 88 controls, matched by age, gender and locality. The overall mean blood and Cd excretion normalized to creatinine clearance (C_cr) as E_Cd/C_cr were 0.59 µg/L and 0.0084 µg/L filtrate (0.96 µg/g creatinine), respectively. Tubular dysfunction, assessed by β₂-microglobulin excretion rate normalized to C_cr(E_β2M/C_cr) was associated with both diabetes and Cd exposure. Doubling of Cd body burden, hypertension and a reduced estimated GFR (eGFR) increased the risks for a severe tubular dysfunction by 1.3-fold, 2.6-fold, and 84-fold, respectively. Albuminuria did not show a significant association with E_Cd/C_cr, but hypertension and eGFR did. Hypertension and a reduced eGFR were associated with a 3-fold and 4-fold increases in risk of albuminuria. These findings suggest that even low levels of Cd exposure exacerbate progression of kidney disease in diabetics. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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13 pages, 797 KiB

Open AccessReview

Metal Toxicity: Effects on Energy Metabolism in Fish

by Natalia A. Gashkina

Int. J. Mol. Sci. 2024, 25(9), 5015; https://doi.org/10.3390/ijms25095015 - 3 May 2024

Cited by 1 | Viewed by 1788

Abstract

Metals are dispersed in natural environments, particularly in the aquatic environment, and accumulate, causing adverse effects on aquatic life. Moreover, chronic polymetallic water pollution is a common problem, and the biological effects of exposure to complex mixtures of metals are the most difficult to interpret. In this review, metal toxicity is examined with a focus on its impact on energy metabolism. Mechanisms regulating adenosine triphosphate (ATP) production and reactive oxygen species (ROS) emission are considered in their dual roles in the development of cytotoxicity and cytoprotection, and mitochondria may become target organelles of metal toxicity when the transmembrane potential is reduced below its phosphorylation level. One of the main consequences of metal toxicity is additional energy costs, and the metabolic load can lead to the disruption of oxidative metabolism and enhanced anaerobiosis. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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21 pages, 3291 KiB

Open AccessReview

Toward a Mechanism-Driven Integrated Framework to Link Human Exposure to Multiple Toxic Metal(loid) Species with Environmental Diseases

by Jürgen Gailer

Int. J. Mol. Sci. 2024, 25(6), 3393; https://doi.org/10.3390/ijms25063393 - 16 Mar 2024

Cited by 1 | Viewed by 1437

Abstract

The ongoing anthropogenic pollution of the biosphere with As, Cd, Hg and Pb will inevitably result in an increased influx of their corresponding toxic metal(loid) species into the bloodstream of human populations, including children and pregnant women. To delineate whether the measurable concentrations of these inorganic pollutants in the bloodstream are tolerable or implicated in the onset of environmental diseases urgently requires new insight into their dynamic bioinorganic chemistry in the bloodstream–organ system. Owing to the human exposure to multiple toxic metal(loid) species, the mechanism of chronic toxicity of each of these needs to be integrated into a framework to better define the underlying exposure–disease relationship. Accordingly, this review highlights some recent advances into the bioinorganic chemistry of the Cd²⁺, Hg²⁺ and CH₃Hg⁺ in blood plasma, red blood cells and target organs and provides a first glimpse of their emerging mechanisms of chronic toxicity. Although many important knowledge gaps remain, it is essential to design experiments with the intent of refining these mechanisms to eventually establish a framework that may allow us to causally link the cumulative exposure of human populations to multiple toxic metal(loid) species with environmental diseases of unknown etiology that do not appear to have a genetic origin. Thus, researchers from a variety of scientific disciplines need to contribute to this interdisciplinary effort to rationally address this public health threat which may require the implementation of stronger regulatory requirements to improve planetary and human health, which are fundamentally intertwined. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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35 pages, 1087 KiB

Open AccessReview

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

by Sergey M. Korotkov

Int. J. Mol. Sci. 2023, 24(19), 14459; https://doi.org/10.3390/ijms241914459 - 22 Sep 2023

Cited by 17 | Viewed by 3980

Abstract

This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag⁺, Tl⁺, Hg²⁺, Cd²⁺, Pb²⁺, Al³⁺, Ga³⁺, In³⁺, As³⁺, Sb³⁺, Cr⁶⁺, and U⁶⁺). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H₂O₂, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨ_mito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca²⁺ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe²⁺ metabolism disturbance. Similarities and differences in the toxic effects of Tl⁺ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl⁺ and these metals. One difference discussed is the failure to decrease Tl⁺ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl⁺ to Tl³⁺ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc. Full article

(This article belongs to the Special Issue Mechanisms of Heavy Metal Toxicity 2.0)

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