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Issue 5, 2012
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Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

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Aluminium (Al) is highly abundant in the environment and can elicit a variety of toxic responses in biological systems. Here we characterize the effects of Al on Caenorhabditis elegans by identifying phenotypic abnormalities and disruption in whole-body metal homeostasis (metallostasis) following Al exposure in food. Widespread changes to the elemental content of adult nematodes were observed when chronically exposed to Al from the first larval stage (L1). Specifically, we saw increased barium, chromium, copper and iron content, and a reduction in calcium levels. Lifespan was decreased in worms exposed to low levels of Al, but unexpectedly increased when the Al concentration reached higher levels (4.8 mM). This bi-phasic phenotype was only observed when Al exposure occurred during development, as lifespan was unaffected by Al exposure during adulthood. Lower levels of Al slowed C. elegans developmental progression, and reduced hermaphrodite self-fertility and adult body size. Significant developmental delay was observed even when Al exposure was restricted to embryogenesis. Similar changes in Al have been noted in association with Al toxicity in humans and other mammals, suggesting that C. elegans may be of use as a model for understanding the mechanisms of Al toxicity in mammalian systems.

Graphical abstract: Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

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Publication details

The article was received on 01 Sep 2011, accepted on 11 Apr 2012 and first published on 26 Apr 2012

Article type: Paper
DOI: 10.1039/C2MT00146B
Citation: Metallomics, 2012,4, 512-522
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    Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

    K. E. Page, K. N. White, C. R. McCrohan, D. W. Killilea and G. J. Lithgow, Metallomics, 2012, 4, 512
    DOI: 10.1039/C2MT00146B

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