Cadmium and Trace Elements Toxicity

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Metals and Radioactive Substances".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 9138

Special Issue Editors


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Guest Editor
Department of Biomedical Sciences, University of Sassari, Sassari, Italy
Interests: trace elements; cadmium; toxicity; neurodegenerative disorders; cancer stem cells; oncology; miRNA
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Guest Editor
Centre for Kidney Disease Research, Translational Research Institute, Woolloongabba, Brisbane, Australia
Interests: epidemiology of cadmium toxicity; genetic and nutritional influence of cadmium toxicity outcomes; cadmium toxicity in at-risk subpopulations; novel methods of measuring cadmium in tissues; reverse dosimetry
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Guest Editor
Institute of Applied Biology, Slovak University of Agriculture in Nitra, Nitra, Slovakia
Interests: animal; physiology; toxicology; cell; factors
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Special Issue Information

Dear Colleagues,

Cadmium is considered a highly toxic pollutant, and has spread globally following the rapid development of industries and modern technologies, as a component of television screens, lasers, batteries, paint pigments, cosmetics, etc. Cd is such a toxic redox-inactive metal, even at low doses, that the Agency for Toxic Substances and Disease Registry (ATSDR) has classified it among the seven most dangerous substances for health.

Human exposure to Cd occurs mainly through the respiratory tract, to a lesser extent from the gastrointestinal tract, and rarely through the skin. In humans, Cd exposure causes a broad spectrum of adverse effects, including renal and hepatic dysfunction, pulmonary edema, male and female infertility, osteomalacia, and damage to the adrenal glands and hematopoietic and cardiovascular systems. After exposure, Cd exerts cell toxicity inducing oxidative stress via an indirect mechanism, including the production of reactive oxygen species such as superoxide radicals, hydrogen peroxide, hydroxyl radicals, and nitric oxide.

Current evidence suggests that Cd exposure induces genomic instability through complex and multifactorial mechanisms, the main one of which seems to be the direct interaction of Cd with the DNA repair mechanism, leading to inhibition of DNA repair mechanisms, cell proliferation, and apoptotic inhibition.  Furthermore, Cd is implicated in the development of cancer. It has been classified as a type I carcinogen by the International Agency for Research on Cancer, being associated with cancers of the lung, prostate, breast, pancreas and kidney. More recently, it was proposed also a relationship between Cd and neurological disorders.

Interestingly, Cd may interfere with other essential elements and vice versa micronutrient deficiency may exacerbate Cd toxicity. However, whether the differences in the Cd accumulation and Cd-induced health effects are due to different storage of the metal in the human body or they reflect a different sensitivity to its toxic effects remains unclear.

This Special Issue will focus on recent studies on Cadmium and trace elements, and in particular, on elements such as zinc, selenium, and those related to cadmium toxicity. We expect that the topics, both research papers and reviews, will include, but will not be limited to, the most recent approaches to the study of Cadmium and trace elements in humans and in pathologies such as neurodegenerative diseases or diabetes, both in tumors as factors promoting or aggravating the pathology itself, both in agonist and antagonist relationships in drugs, as well as the possible biochemical and biomolecular correlations in the onset of tumors or cardiovascular, renal, and hepatic pathologies.

We also expect topics on the impact of cadmium on animal models, on the correlations with the territory linked to the diet, soil and geology of the same.

Authors are invited and welcome to submit original research papers, reviews, and short communications.

Prof. Dr. Roberto Madeddu
Prof. Dr. Soisungwan Satarug
Prof. Dr. Peter Massányi
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

  • cadmium
  • trace elements
  • toxicity
  • cancer
  • environment
  • zinc
  • selenium
  • diet intake
  • cadmium biomarkers
  • antioxidants
  • neurodegenerative disorders
  • gemcitabine
  • microRna and trace elements
  • epidemiology
  • diabetes

Published Papers (5 papers)

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Research

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13 pages, 1312 KiB  
Article
Accumulation and Release of Cadmium Ions in the Lichen Evernia prunastri (L.) Ach. and Wood-Derived Biochar: Implication for the Use of Biochar for Environmental Biomonitoring
by Andrea Vannini, Luca Pagano, Marco Bartoli, Riccardo Fedeli, Alessio Malcevschi, Michele Sidoli, Giacomo Magnani, Daniele Pontiroli, Mauro Riccò, Marta Marmiroli, Alessandro Petraglia and Stefano Loppi
Toxics 2024, 12(1), 66; https://doi.org/10.3390/toxics12010066 - 13 Jan 2024
Cited by 1 | Viewed by 1805
Abstract
Biochar (BC) boasts diverse environmental applications. However, its potential for environmental biomonitoring has, surprisingly, remained largely unexplored. This study presents a preliminary analysis of BC’s potential as a biomonitor for the environmental availability of ionic Cd, utilizing the lichen Evernia prunastri (L.) Ach. [...] Read more.
Biochar (BC) boasts diverse environmental applications. However, its potential for environmental biomonitoring has, surprisingly, remained largely unexplored. This study presents a preliminary analysis of BC’s potential as a biomonitor for the environmental availability of ionic Cd, utilizing the lichen Evernia prunastri (L.) Ach. as a reference organism. For this purpose, the lichen E. prunastri and two types of wood-derived biochar, biochar 1 (BC1) and biochar 2 (BC2), obtained from two anonymous producers, were investigated for their ability to accumulate, or sequester and subsequently release, Cd when exposed to Cd-depleted conditions. Samples of lichen and biochar (fractions between 2 and 4 mm) were soaked for 1 h in a solution containing deionized water (control), 10 µM, and 100 µM Cd2+ (accumulation phase). Then, 50% of the treated samples were soaked for 24 h in deionized water (depuration phase). The lichen showed a very good ability to adsorb ionic Cd, higher than the two biochar samples (more than 46.5%), and a weak ability to release the metal (ca. 6%). As compared to the lichen, BC2 showed a lower capacity for Cd accumulation (−48%) and release (ca. 3%). BC1, on the other hand, showed a slightly higher Cd accumulation capacity than BC2 (+3.6%), but a release capacity similar to that of the lichen (ca. 5%). The surface area and the cation exchange capacity of the organism and the tested materials seem to play a key role in their ability to accumulate and sequester Cd, respectively. This study suggests the potential use of BC as a (bio)monitor for the presence of PTEs in atmospheric depositions and, perhaps, water bodies. Full article
(This article belongs to the Special Issue Cadmium and Trace Elements Toxicity)
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12 pages, 267 KiB  
Article
Toxic Metal and Essential Element Concentrations in the Blood and Tissues of Pancreatic Ductal Adenocarcinoma Patients
by Giovanni Forte, Andrea Pisano, Beatrice Bocca, Grazia Fenu, Cristiano Farace, Federica Etzi, Teresa Perra, Angela Sabalic, Alberto Porcu and Roberto Madeddu
Toxics 2024, 12(1), 32; https://doi.org/10.3390/toxics12010032 - 1 Jan 2024
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Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive lethal neoplasm, and it has an average 5-year survival rate of less than 10%. Although the factors that influence PDAC development remain unclear, exposure to toxic metals or the imbalance in essential elements may [...] Read more.
Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive lethal neoplasm, and it has an average 5-year survival rate of less than 10%. Although the factors that influence PDAC development remain unclear, exposure to toxic metals or the imbalance in essential elements may have a role in PDAC-associated metabolic pathways. Methods: This study determined the concentrations of Cd, Cr, Cu, Fe, Mn, Ni, Pb, Se and Zn in whole blood, cancer and non-cancer tissues of patients affected by PDAC, and compared them with levels in healthy controls using inductively coupled plasma mass spectrometry. Results: Results of the whole blood showed significantly higher levels of Cr, Cu and Cu/Zn ratio in PDAC patients compared to the controls. In addition, the concentrations of Cu, Se, Fe and Zn significantly increased in cancer tissue compared to the healthy counterparts. Conclusions: This study revealed evidence of altered metal levels in the blood and pancreatic tissues of PDAC patients with respect to healthy controls. These changes may contribute to multiple mechanisms involved in metal-induced carcinogenesis, including oxidative stress, DNA damage, genetic alteration, decreased antioxidant barriers and inflammatory responses. Thus, the analysis of metals can be used in the diagnosis and monitoring of PDAC neoplasms. Full article
(This article belongs to the Special Issue Cadmium and Trace Elements Toxicity)
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12 pages, 3297 KiB  
Article
Long-Term Exposure to Cadmium Causes Hepatic Iron Deficiency through the Suppression of Iron-Transport-Related Gene Expression in the Proximal Duodenum
by Maki Tokumoto, Jin-Yong Lee, Yasuyuki Fujiwara and Masahiko Satoh
Toxics 2023, 11(7), 641; https://doi.org/10.3390/toxics11070641 - 24 Jul 2023
Cited by 5 | Viewed by 1396
Abstract
Cadmium (Cd) is an environmental pollutant that damages various tissues. Cd may cause a depletion of iron stores and subsequently an iron deficiency state in the liver. However, the molecular mechanism of decreased iron accumulation in the liver induced by long-term exposure to [...] Read more.
Cadmium (Cd) is an environmental pollutant that damages various tissues. Cd may cause a depletion of iron stores and subsequently an iron deficiency state in the liver. However, the molecular mechanism of decreased iron accumulation in the liver induced by long-term exposure to Cd is unknown. In this study, we investigated the hepatic accumulation of iron and the proximal duodenal expression of the genes involved in iron transport using mice chronically exposed to Cd. Five-week-old female C57BL/6J mice were fed a diet containing 300 ppm Cd for 12, 15, 19 and 21 months. The iron concentration in the liver was markedly decreased by Cd. Among iron-transport-related genes in the proximal duodenum, the gene expression of HCP1 and Cybrd1 was significantly decreased by Cd. HCP1 is an influx transporter of heme iron. Cybrd1 is a reductase that allows non-heme iron to enter cells. The expression of iron-transport-related genes on the duodenal basolateral membrane side was hardly altered by Cd. These results suggest that long-term exposure to Cd suppresses the expression of HCP1 and Cybrd1 in the proximal duodenum, resulting in reduced iron absorption and iron accumulation in the liver. Full article
(This article belongs to the Special Issue Cadmium and Trace Elements Toxicity)
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15 pages, 1515 KiB  
Article
Gender Differences in the Severity of Cadmium Nephropathy
by Supabhorn Yimthiang, David A. Vesey, Glenda C. Gobe, Phisit Pouyfung, Tanaporn Khamphaya and Soisungwan Satarug
Toxics 2023, 11(7), 616; https://doi.org/10.3390/toxics11070616 - 15 Jul 2023
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Abstract
The excretion of β2-microglobulin (β2M) above 300 µg/g creatinine, termed tubulopathy, was regarded as the critical effect of chronic exposure to the metal pollutant cadmium (Cd). However, current evidence suggests that Cd may induce nephron atrophy, resulting in a [...] Read more.
The excretion of β2-microglobulin (β2M) above 300 µg/g creatinine, termed tubulopathy, was regarded as the critical effect of chronic exposure to the metal pollutant cadmium (Cd). However, current evidence suggests that Cd may induce nephron atrophy, resulting in a reduction in the estimated glomerular filtration rate (eGFR) below 60 mL/min/1.73 m2. Herein, these pathologies were investigated in relation to Cd exposure, smoking, diabetes, and hypertension. The data were collected from 448 residents of Cd-polluted and non-polluted regions of Thailand. The body burden of Cd, indicated by the mean Cd excretion (ECd), normalized to creatinine clearance (Ccr) as (ECd/Ccr) × 100 in women and men did not differ (3.21 vs. 3.12 µg/L filtrate). After adjustment of the confounding factors, the prevalence odds ratio (POR) for tubulopathy and a reduced eGFR were increased by 1.9-fold and 3.2-fold for every 10-fold rise in the Cd body burden. In women only, a dose–effect relationship was seen between β2M excretion (Eβ2M/Ccr) and ECd/Ccr (F = 3.431, η2 0.021). In men, Eβ2M/Ccr was associated with diabetes (β = 0.279). In both genders, the eGFR was inversely associated with Eβ2M/Ccr. The respective covariate-adjusted mean eGFR values were 16.5 and 12.3 mL/min/1.73 m2 lower in women and men who had severe tubulopathy ((Eβ2M/Ccr) × 100 ≥ 1000 µg/L filtrate). These findings indicate that women were particularly susceptible to the nephrotoxicity of Cd, and that the increment of Eβ2M/Ccr could be attributable mostly to Cd-induced impairment in the tubular reabsorption of the protein together with Cd-induced nephron loss, which is evident from an inverse relationship between Eβ2M/Ccr and the eGFR. Full article
(This article belongs to the Special Issue Cadmium and Trace Elements Toxicity)
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Review

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18 pages, 385 KiB  
Review
The Role of Trace Elements in Cardiovascular Diseases
by Christian Wechselberger, Barbara Messner and David Bernhard
Toxics 2023, 11(12), 956; https://doi.org/10.3390/toxics11120956 - 23 Nov 2023
Cited by 2 | Viewed by 1609
Abstract
Essential trace elements play an important role in human physiology and are associated with various functions regulating cellular metabolism. Non-essential trace elements, on the other hand, often have well-documented toxicities that are dangerous for the initiation and development of diseases due to their [...] Read more.
Essential trace elements play an important role in human physiology and are associated with various functions regulating cellular metabolism. Non-essential trace elements, on the other hand, often have well-documented toxicities that are dangerous for the initiation and development of diseases due to their widespread occurrence in the environment and their accumulation in living organisms. Non-essential trace elements are therefore regarded as serious environmental hazards that are harmful to health even in low concentrations. Many representatives of these elements are present as pollutants in our environment, and many people may be exposed to significant amounts of these substances over the course of their lives. Among the most common non-essential trace elements are heavy metals, which are also associated with acute poisoning in humans. When these elements accumulate in the body over years of chronic exposure, they often cause severe health damage in a variety of tissues and organs. In this review article, the role of selected essential and non-essential trace elements and their role in the development of exemplary pathophysiological processes in the cardiovascular system will be examined in more detail. Full article
(This article belongs to the Special Issue Cadmium and Trace Elements Toxicity)
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