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Inhibition of gap junctional intercellular communication by toxic metals.

Identifieur interne : 001905 ( Main/Exploration ); précédent : 001904; suivant : 001906

Inhibition of gap junctional intercellular communication by toxic metals.

Auteurs : RBID : pubmed:20866040

English descriptors

Abstract

As metals are ubiquitous in the environment, humans are continuously exposed to them. Although some metallic ions play key roles in human physiology, most metals are redundant and are actually hazardous to humans. A frequent event in the toxicological cascade triggered by nonessential metals concerns the abrogation of cellular signaling mediated by gap junctions. This paper provides a literature overview of the documented effects of mercury, cadmium, arsenic, aluminum, lead, nickel, vanadium, and indium on gap junctional intercellular communication. Whenever available, particular attention is paid to the mechanistic basis of this deleterious biological outcome, which may involve the gap junction activity level or may arise from modifications in the expression of the gap junction building stones, the connexins.

DOI: 10.1021/tx100276f
PubMed: 20866040

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Le document en format XML

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<div type="abstract" xml:lang="en">As metals are ubiquitous in the environment, humans are continuously exposed to them. Although some metallic ions play key roles in human physiology, most metals are redundant and are actually hazardous to humans. A frequent event in the toxicological cascade triggered by nonessential metals concerns the abrogation of cellular signaling mediated by gap junctions. This paper provides a literature overview of the documented effects of mercury, cadmium, arsenic, aluminum, lead, nickel, vanadium, and indium on gap junctional intercellular communication. Whenever available, particular attention is paid to the mechanistic basis of this deleterious biological outcome, which may involve the gap junction activity level or may arise from modifications in the expression of the gap junction building stones, the connexins.</div>
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