Transferable properties of multi‐biological toxicity caused by cobalt exposure in <i>Caenorhabditis elegans</i>

Wang, Yang; Xie, Wei; Wang, Dayong

doi:10.1897/06-646r1.1

Cited by 50 publications

(16 citation statements)

References 27 publications

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“…This early exposure to Al appears to be enough to cause phenotypic abnormalities in later life since we found no evidence for elevated whole-body Al levels in the F 1 progeny when only the P 0 was exposed to Al. Similar transferable toxicity phenotypes have been reported for worms exposed to Zn, Ni, lead (Pb) and cobalt (Co) 29-32 and it has been suggested that this phenomenon could be due to the build-up of toxic metals inside the developing egg leading to Al toxicity during embryogenesis 29,32 —a process termed ’chemical legacy’. Maternal transfer of silver (Ag), selenium (Se) and Zn to developing embryos has been reported for the cuttlefish Sepia officinalis , indicating this as a possible mechanism of action.…”

Section: Discussionsupporting

confidence: 55%

Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

et al. 2012

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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.

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Section: Discussionsupporting

confidence: 55%

Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

et al. 2012

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“…The toxicities of a variety of metals and metalloids have been formally assayed in C elegans and include Ag, Al, Ar, Cd, Co, Cr, Cu, Hg, Pb, Ti, Ur, and Zn (Bruinsma et al , 2008; Calafato et al , 2008; Dhawan et al , 2000; Guo et al , 2009; Jiang et al , 2009; Liao and Yu, 2005; Ma et al , 2009; Roh et al , 2009; Wang et al , 2007, 2009; Ye et al , 2008). However, studies on the toxicity of selenium have not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

The Glutaredoxin GLRX-21 Functions to Prevent Selenium-Induced Oxidative Stress in Caenorhabditis elegans

Morgan

Estevez

Mueller

et al. 2010

Toxicological Sciences

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Selenium is an essential micronutrient that functions as an antioxidant. Yet, at higher concentrations, selenium is pro-oxidant and toxic. In extreme cases, exposures to excess selenium can lead to death or selenosis, a syndrome characterized by teeth, hair and nail loss, and nervous system alterations. Recent interest in selenium as an anti- tumorigenic agent has reemphasized the need to understand the mechanisms underlying the cellular consequences of increased selenium exposure. We show here, that in the nematode, Caenorhabditis elegans, selenium has a concentration range in which it functions as an antioxidant, but beyond this range it exhibits a dose- and time-dependent lethality. Oxidation-induced fluorescence emitted by the dye, carboxy-H2DCFDA, indicative of reactive oxygen species formation was significantly higher in animals after a brief exposure to 5mM sodium selenite. Longer-term exposures lead to a progressive selenium-induced motility impairment that could be partially prevented by coincident exposure to the cellular antioxidant–reduced glutathione. The C elegans glrx-21 gene belongs to the family of glutaredoxins (glutathione-dependent oxidoreductases) and the glrx-21(tm2921) allele is a null mutation that renders animals hypersensitive for the selenium-induced motility impairment, but not lethality. In addition, the lethality of animals with the tm2921 mutation exposed to selenium was unaffected by the addition of reduced glutathione, suggesting that GLRX-21 is required for glutathione to moderate this selenium-induced lethality. Our findings provide the first description of selenium-induced toxicity in C elegans and support its use as a model for elucidating the mechanisms of selenium toxicity.

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“…The locomotion behavior was assessed by the endpoints of head thrash and body bend, which have been successfully explored to evaluate the neurobehavioral toxicity induced by metal exposure [17]-[18]. The heat-shock is a commonly and extensively investigated stress in nematodes [9].…”

Section: Discussionmentioning

confidence: 99%

Metallothioneins Are Required for Formation of Cross-Adaptation Response to Neurobehavioral Toxicity from Lead and Mercury Exposure in Nematodes

Rui

et al. 2010

PLoS ONE

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Metallothioneins (MTs) are small, cysteine-rich polypeptides, but the role of MTs in inducing the formation of adaptive response is still largely unknown. We investigated the roles of metallothionein genes (mtl-1 and mtl-2) in the formation of cross-adaptation response to neurobehavioral toxicity from metal exposure in Caenorhabditis elegans. Pre-treatment with mild heat-shock at L2-larva stage effectively prevented the formation of the neurobehavioral defects and the activation of severe stress response in metal exposed nematodes at concentrations of 50 and 100 µM, but pre-treatment with mild heat-shock did not prevent the formation of neurobehavioral defects in 200 µM of metal exposed nematodes. During the formation of cross-adaptation response, the induction of mtl-1 and mtl-2 promoter activity and subsequent GFP gene expression were sharply increased in 50 µM or 100 µM of metal exposed Pmtl-1::GFP and Pmtl-2::GFP transgenic adult animals after mild heat-shock treatment compared with those treated with mild heat-shock or metal exposure alone. Moreover, after pre-treatment with mild heat-shock, no noticeable increase of locomotion behaviors could be observed in metal exposed mtl-1 or mtl-2 mutant nematodes compared to those without mild heat-shock pre-treatment. The defects of adaptive response to neurobehavioral toxicity induced by metal exposure formed in mtl-1 and mtl-2 mutants could be completely rescued by the expression of mtl-1 and mtl-2 with the aid of their native promoters. Furthermore, over-expression of MTL-1 and MTL-2 at the L2-larval stage significantly suppressed the toxicity on locomotion behaviors from metal exposure at all examined concentrations. Therefore, the normal formation of cross-adaptation response to neurobehavioral toxicity induced by metal exposure may need the enough accumulation of MTs protein in animal tissues.

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Transferable properties of multi‐biological toxicity caused by cobalt exposure in Caenorhabditis elegans

Cited by 50 publications

References 27 publications

Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

Aluminium exposure disrupts elemental homeostasis in Caenorhabditis elegans

The Glutaredoxin GLRX-21 Functions to Prevent Selenium-Induced Oxidative Stress in Caenorhabditis elegans

Metallothioneins Are Required for Formation of Cross-Adaptation Response to Neurobehavioral Toxicity from Lead and Mercury Exposure in Nematodes

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