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The Toxicity Mechanism of Cadmium on Organs
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The Toxicity Mechanism of Cadmium on Organs

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 (31 December 2023) | Viewed by 3505

Special Issue Editors

Dr. Yonggang Ma

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Guest Editor
College of Veterinary Medicine, Yangzhou University, Yangzhou, China
Interests: cadmium; toxicity; neurotoxicity
Dr. Hui Zou

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Guest Editor
College of Veterinary Medicine, Yangzhou Unicersity, Yangzhou, China
Interests: cadmium; autophagy; GJIC; apoptosis; mitochondria; oxidative stress
Prof. Dr. Zongping Liu

E-Mail Website
Guest Editor
College of Veterinary Medicine, Yangzhou University, Yangzhou, China
Interests: gut microbiota; cadmium; toxicity

Special Issue Information

Dear Colleagues,

Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism underlying this function of cadmium remains unclear. Therefore, new strategies for revealing the toxicity of cadmium are urgently needed. This Special Issue aims to present research exploring the effects of cadmium on organs.

Potential topics include, but are not limited to:

  • The toxicity of cadmium;
  • The mechanism of cadmium-induced cell death.
  • The mechanism of cadmium-induced osteoporosis;
  • The mechanism of cadmium-induced autophagy;
  • Target protection against cadmium toxicity;
  • Reproductive toxicity of cadmium.

Dr. Yonggang Ma
Dr. Hui Zou
Prof. Dr. Zongping Liu
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. 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

  • cadmium
  • apoptosis
  • pyroptosis
  • ferroptosis
  • autophagy

Published Papers (3 papers)

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Research

18 pages, 2251 KiB  
Article
Changes in Endogenous Essential Metal Homeostasis in the Liver and Kidneys during a Six-Month Follow-Up Period after Subchronic Cadmium Exposure
by Rafał Kusak, Marzenna Nasiadek, Joanna Stragierowicz, Wojciech Hanke and Anna Kilanowicz
Int. J. Mol. Sci. 2024, 25(7), 3829; https://doi.org/10.3390/ijms25073829 - 29 Mar 2024
Viewed by 419
Abstract
Cadmium (Cd) is one of the most dangerous environmental pollutants. Its mechanism of action is multidirectional; among other things, it disrupts the balance of key essential elements. The aim of this study was to assess how cumulative exposure to Cd influences its interaction [...] Read more.
Cadmium (Cd) is one of the most dangerous environmental pollutants. Its mechanism of action is multidirectional; among other things, it disrupts the balance of key essential elements. The aim of this study was to assess how cumulative exposure to Cd influences its interaction with selected essential elements (Cu, Zn, Ca, and Mg) in the kidney and liver during long-term observation (90 and 180 days) after subchronic exposure of rats (90 days) to Cd at common environmental (0.09 and 0.9 mg Cd/kg b.w.) and higher (1.8 and 4.5 mg Cd/kg b.w.) doses. Cd and essential elements were analyzed using the F-AAS and GF-AAS techniques. It was shown that the highest bioaccumulation of Cd in the kidney occurred six months after the end of exposure, and importantly, the highest accumulation was found after the lowest Cd dose (i.e., environmental exposure). Organ bioaccumulation of Cd (>21 μgCd/g w.w. in the kidney and >6 μgCd/g w.w. in the liver) was accompanied by changes in the other studied essential elements, particularly Cu in both the kidney and liver and Zn in the liver; these persisted for as long as six months after the end of the exposure. The results suggest that the critical concentration in human kidneys (40 μgCd/g w.w.), currently considered safe, may be too high and should be reviewed, as the observed long-term imbalance of Cu/Zn in the kidneys may lead to renal dysfunction. Full article
(This article belongs to the Special Issue The Toxicity Mechanism of Cadmium on Organs)
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12 pages, 2046 KiB  
Article
Taurine Alleviates Cadmium-Induced Hepatotoxicity by Regulating Autophagy Flux
by Yuntian Duan, Yumeng Zhao, Tao Wang, Jian Sun, Waseem Ali, Yonggang Ma, Yan Yuan, Jianhong Gu, Jianchun Bian, Zongping Liu and Hui Zou
Int. J. Mol. Sci. 2023, 24(2), 1205; https://doi.org/10.3390/ijms24021205 - 07 Jan 2023
Cited by 6 | Viewed by 1519
Abstract
Our previous studies have confirmed that cadmium (Cd) exposure causes hepatotoxicity; it also induces autophagy and blocks the autophagy flux. Therefore, we hypothesized that Cd hepatotoxicity could be alleviated through nutritional intervention. Taurine (Tau) has various biological functions such as acting as an [...] Read more.
Our previous studies have confirmed that cadmium (Cd) exposure causes hepatotoxicity; it also induces autophagy and blocks the autophagy flux. Therefore, we hypothesized that Cd hepatotoxicity could be alleviated through nutritional intervention. Taurine (Tau) has various biological functions such as acting as an antioxidant, acting as an anti-inflammatory, and stabilizing cell membranes. In order to explore the protective effect and internal mechanism of Tau on Cd-induced hepatotoxicity, normal rat liver cell line BRL3A cells were treated with Cd alone or in combination with Tau to detect cell injury and autophagy-related indexes in this study. We found that Tau can alleviate Cd-induced cell-proliferation decline and morphological changes in the cell. In addition, Tau activates autophagy and alleviates the blockage of Cd-induced autophagy flux. In this process, lysosome acidification and degradation were enhanced, and autophagosomes were further fused with lysosomes. Then, we found that Tau alleviated autophagic flux block by promoting the transfer of membrane fusion proteins STX17 and SNAP29 to autophagosomes and the translocation of VAMP8 to lysosomes, which in turn attenuated the hepatocyte injury induced by Cd exposure. This will further reveal the hepatotoxicity mechanism of Cd and provide the theoretical basis for the prevention and treatment of Cd poisoning. Full article
(This article belongs to the Special Issue The Toxicity Mechanism of Cadmium on Organs)
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14 pages, 6104 KiB  
Article
Rat Hepatocytes Mitigate Cadmium Toxicity by Forming Annular Gap Junctions and Degrading Them via Endosome–Lysosome Pathway
by Junzhao Yuan, Xiaoqian Huang, Yumeng Zhao, Jianhong Gu, Yan Yuan, Zongping Liu, Hui Zou and Jianchun Bian
Int. J. Mol. Sci. 2022, 23(24), 15607; https://doi.org/10.3390/ijms232415607 - 09 Dec 2022
Cited by 2 | Viewed by 932
Abstract
Gap junction protein connexin 43 (Cx43) plays a critical role in gap junction communication in rat hepatocytes. However, those located between hepatocytes are easily internalized following exposure to poisons. Herein, we investigated the potential of buffalo rat liver 3A (BRL 3A) cells to [...] Read more.
Gap junction protein connexin 43 (Cx43) plays a critical role in gap junction communication in rat hepatocytes. However, those located between hepatocytes are easily internalized following exposure to poisons. Herein, we investigated the potential of buffalo rat liver 3A (BRL 3A) cells to generate annular gap junctions (AGJs) proficient at alleviating cadmium (Cd) cytotoxic injury through degradation via an endosome–lysosome pathway. Our results showed that Cd-induced damage of liver microtubules promoted Cx43 internalization and increased Cx43 phosphorylation at Ser373 site. Furthermore, we established that Cd induced AGJs generation in BRL 3A cells, and AGJs were subsequently degraded through the endosome–lysosome pathway. Overall, our results suggested that Cx43 internalization and the generation of AGJs were cellular protective mechanisms to alleviate Cd toxicity in rat hepatocytes. Full article
(This article belongs to the Special Issue The Toxicity Mechanism of Cadmium on Organs)
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