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Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.

The intracellular compartmentation of essential and toxic metals is of intense scientific interest because of its potential for adding to our understanding of both normal homeostatic mechanisms for metals and of the mechanisms which underlie metal-induced cell injury. High-affinity metal-binding pro...

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Detalles Bibliográficos
Autor principal: Fowler, B A
Formato: Texto
Lenguaje:English
Publicado: 1987
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1474359/
https://www.ncbi.nlm.nih.gov/pubmed/3297654
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author Fowler, B A
author_facet Fowler, B A
author_sort Fowler, B A
collection PubMed
description The intracellular compartmentation of essential and toxic metals is of intense scientific interest because of its potential for adding to our understanding of both normal homeostatic mechanisms for metals and of the mechanisms which underlie metal-induced cell injury. High-affinity metal-binding proteins, lysosomes, and precipitates such as inclusion bodies or concretions, play major roles in the regulation of divalent-metal cation bioavailability. The contribution of a given compartment toward metal homeostasis is dependent upon the level exposure, cell type, organ, species, and life cycle of the organism. Toxic metals may move between these compartments, but the rates and determinants of such exchanges have not been characterized. Available data clearly indicate that sequestration of toxic metals in these specialized compartments can produce profound disturbances in the subcellular handling of essential metals. Further studies of the mechanisms by which metals partition and/or transfer among these compartments are essential to understand and predict toxicity of this important class of toxic agents.
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spelling pubmed-14743592006-06-09 Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury. Fowler, B A Environ Health Perspect Research Article The intracellular compartmentation of essential and toxic metals is of intense scientific interest because of its potential for adding to our understanding of both normal homeostatic mechanisms for metals and of the mechanisms which underlie metal-induced cell injury. High-affinity metal-binding proteins, lysosomes, and precipitates such as inclusion bodies or concretions, play major roles in the regulation of divalent-metal cation bioavailability. The contribution of a given compartment toward metal homeostasis is dependent upon the level exposure, cell type, organ, species, and life cycle of the organism. Toxic metals may move between these compartments, but the rates and determinants of such exchanges have not been characterized. Available data clearly indicate that sequestration of toxic metals in these specialized compartments can produce profound disturbances in the subcellular handling of essential metals. Further studies of the mechanisms by which metals partition and/or transfer among these compartments are essential to understand and predict toxicity of this important class of toxic agents. 1987-04 /pmc/articles/PMC1474359/ /pubmed/3297654 Text en
spellingShingle Research Article
Fowler, B A
Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title_full Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title_fullStr Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title_full_unstemmed Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title_short Intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
title_sort intracellular compartmentation of metals in aquatic organisms: roles in mechanisms of cell injury.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1474359/
https://www.ncbi.nlm.nih.gov/pubmed/3297654
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