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For instance, modes of toxicity have been identified that require covalent interactions between the toxicant and the target (Zhou et al. 2005) or that necessitate the redistribution of charge in both the toxicant and the target (Pardo et al. 1993).
Several sources have made definitive calls concerning particular modes of toxicity, for instance, labeling chemicals as being human carcinogens or developmental toxicants.
In this context, laboratory studies are extremely necessary to investigate the potential of an organism to be used as a bioindicator in field studies, and also enable a better understanding of chemical modes of toxicity.
The findings of the study suggest that in this size range and for the cell types studied, geometry does not play a dominant role in the modes of toxicity and uptake of these particles.
These data are used to assign gene expression profiles to specific modes of toxicity.
The modes of toxicity of weak acids are not easily elucidated.
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We refer to this as the 4-modes-of-toxicity (4MOT) model.
To decipher the mode of toxicity by different toxicants, powerful tools such as genomic phenotyping have been developed [ 1, 2, 11- 16].
The identification of the chemical species that are active toxicants and the mode of toxicity are both important components for accurately determining the full breadth of arsenic exposure.
Most important, a very clear dissimilarity from the control group indicated that the indomethacin-treated animals had been exposed to a toxic compound, although the mode of toxicity could not be unequivocally defined.
One key issue in the molecular understanding of pathogenicity, especially with mutations causing dominant forms of disease, is to determine the basic mode of toxicity that can be broadly predicted to be toxic gain of function, dominant negative and/or haploinsufficiency through partial loss of function.
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