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Cellular mechanisms of cadmium toxicity related to the homeostasis of essential metals

Biometals, 2010-10, Vol.23 (5), p.877-896 [Peer Reviewed Journal]

Springer Science+Business Media, LLC. 2010 ;Distributed under a Creative Commons Attribution 4.0 International License ;ISSN: 0966-0844 ;EISSN: 1572-8773 ;DOI: 10.1007/s10534-010-9336-y ;PMID: 20524046

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Title:
Cellular mechanisms of cadmium toxicity related to the homeostasis of essential metals
Author: Moulis, Jean-Marc
Subjects: Animals ; Binding Sites ; Biochemistry ; Biochemistry, Molecular Biology ; Biocompatibility ; Biological effects ; Biomedical and Life Sciences ; Cadmium ; Cadmium - pharmacokinetics ; Cadmium - toxicity ; Cations ; Cell Biology ; Cells ; Cellular ; copper ; Copper - metabolism ; Ecology, environment ; Environmental Pollutants - pharmacokinetics ; Environmental Pollutants - toxicity ; Health ; Homeostasis ; Homeostasis - drug effects ; Humans ; Intracellular Fluid - drug effects ; Intracellular Fluid - metabolism ; iron ; Iron - metabolism ; Life Sciences ; manganese ; Manganese - metabolism ; Materials handling ; Medicine/Public Health ; Metals ; Metals - metabolism ; Microbiology ; Models, Biological ; Models, Molecular ; Pharmacology/Toxicology ; Plant Physiology ; Protein Binding ; reactive oxygen species ; Regulation ; Resistance mechanism ; Toxicity ; Toxicology ; Transition Elements - metabolism ; Transition metals ; Zinc - metabolism
Is Part Of: Biometals, 2010-10, Vol.23 (5), p.877-896
Description: The widespread occurrence of cadmium in the environment continues to pose a threat to human health despite attempts at limiting its technological uses. The biologically significant ionic form of cadmium, Cd²⁺, binds to many bio-molecules and these interactions underlie the toxicity mechanisms of cadmium. Some of the molecules specialized in the handling of alkaline earth (Mg²⁺, Ca²⁺) and transition metal ions (e.g. Zn²⁺, Cu²⁺/⁺, Fe³⁺/²⁺) should be particularly sensitive to the presence of Cd²⁺, because they enclose cationic sites to which the toxic metal can bind. The possible molecular targets of this kind for cadmium are considered herein. Whereas in vitro evidence for native cation replacement by Cd²⁺ in bio-molecules has been largely provided, the demonstration of such occurrences in vivo is scarce, with the notable exception of metallothionein. One reason might be that realistic low-level Cd²⁺ contaminations involve cellular concentrations far smaller than those of endogenous cations that usually saturate their binding sites. It is very likely that cadmium toxicity is most often mediated by biological systems amplifying the signals triggered by the presence of Cd²⁺. The interference of Cd²⁺ with redox sensitive systems acting at the transcriptional and post-transcriptional levels is instrumental in such processes. A better understanding of cadmium toxicity to tackle the environmental challenges lying ahead thus requires properly designed studies implementing biologically relevant cadmium concentrations on different cell types, improved knowledge of the homeostasis of essential metals, and use of these data in a theoretical framework integrating all cellular aspects of cadmium effects.
Publisher: Dordrecht: Dordrecht : Springer Netherlands
Language: English;Dutch
Identifier: ISSN: 0966-0844
EISSN: 1572-8773
DOI: 10.1007/s10534-010-9336-y
PMID: 20524046
Source: AUTh Library subscriptions: ProQuest Central
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Cellular mechanisms of cadmium toxicity related to the homeostasis of essential metals

Springer Science+Business Media, LLC. 2010 ;Distributed under a Creative Commons Attribution 4.0 International License ;ISSN: 0966-0844 ;EISSN: 1572-8773 ;DOI: 10.1007/s10534-010-9336-y ;PMID: 20524046

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