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Special Issue "Relationships between Organ Toxicity and Metals"

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: 31 December 2021.

Special Issue Editors

Prof. Dr. Antonio Micali
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Guest Editor
Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
Interests: organ and tissue structure and ultrastructure
Prof. Dr. Letteria Minutoli
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Guest Editor
Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy
Interests: cadmium toxicity; varicocele; ischaemia and reperfusion of testis

Special Issue Information

Dear Colleagues,

It has been reported that metals such as cobalt, copper, chromium, iron, magnesium, manganese, molybdenum, nickel, selenium and zinc are essential nutrients required for various biochemical and physiological functions in plants and animals. Inadequate supply of these micro-nutrients results in a variety of deficiency diseases or syndromes. Their toxicity depends on several factors including dose, route of exposure, and chemical species, as well as age, gender, genetics, and nutritional status of exposed individuals. Metals, and in particular heavy metals, are considered systemic toxicants that are known to induce multiple-organ damage, even at lower levels of exposure and they are also classified as human carcinogens.

This Special Issue is focused on organ toxicity and it would include original articles and review on aspects related with molecular and pharmacological mechanisms of organ toxicity induced by different metals. Potential topics include, but are not limited to, intracellular targets, reactive oxygen species, apoptosis, and morphological aspects.

Prof. Dr. Antonio Micali
Prof. Dr. Letteria Minutoli
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 papers will be 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

  • Metals
  • Organ toxicity
  • Oxidative stress
  • Inflammation
  • Apoptosis
  • Carcinogenesis

Published Papers (1 paper)

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Research

Article
Increased Endocytosis of Cadmium-Metallothionein through the 24p3 Receptor in an In Vivo Model with Reduced Proximal Tubular Activity
Int. J. Mol. Sci. 2021, 22(14), 7262; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147262 - 06 Jul 2021
Viewed by 673
Abstract
Background: The proximal tubule (PT) is the major target of cadmium (Cd2+) nephrotoxicity. Current dogma postulates that Cd2+ complexed to metallothionein (MT) (CdMT) is taken up through receptor-mediated endocytosis (RME) via the PT receptor megalin:cubilin, which is the predominant pathway [...] Read more.
Background: The proximal tubule (PT) is the major target of cadmium (Cd2+) nephrotoxicity. Current dogma postulates that Cd2+ complexed to metallothionein (MT) (CdMT) is taken up through receptor-mediated endocytosis (RME) via the PT receptor megalin:cubilin, which is the predominant pathway for reuptake of filtered proteins in the kidney. Nevertheless, there is evidence that the distal parts of the nephron are also sensitive to damage induced by Cd2+. In rodent kidneys, another receptor for protein endocytosis, the 24p3 receptor (24p3R), is exclusively expressed in the apical membranes of distal tubules (DT) and collecting ducts (CD). Cell culture studies have demonstrated that RME and toxicity of CdMT and other (metal ion)–protein complexes in DT and CD cells is mediated by 24p3R. In this study, we evaluated the uptake of labeled CdMT complex through 24p3R after acute kidney injury (AKI) induced by gentamicin (GM) administration that disrupts PT function. Subcutaneous administration of GM at 10 mg/kg/day for seven days did not alter the structural and functional integrity of the kidney’s filtration barrier. However, because of PT injury, the concentration of the renal biomarker Kim-1 increased. When CdMT complex coupled to FITC was administered intravenously, both uptake of the CdMT complex and 24p3R expression in DT increased and also colocalized after PT injury induced by GM. Although megalin decreased in PT after GM administration, urinary protein excretion was not changed, which suggests that the increased levels of 24p3R in the distal nephron could be acting as a compensatory mechanism for protein uptake. Altogether, these results suggest that PT damage increases the uptake of the CdMT complex through 24p3R in DT (and possibly CD) and compensate for protein losses associated with AKI. Full article
(This article belongs to the Special Issue Relationships between Organ Toxicity and Metals)
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