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Integration of gene expression biomarkers and whole sediment toxicity identification evaluations
Citation:
BIALES, A. D., M. KOSTICH, R. M. BURGESS, AND K. T. HO. Integration of gene expression biomarkers and whole sediment toxicity identification evaluations. Presented at SETAC North America 2011, Boston, MA, November 13 - 17, 2011.
Impact/Purpose:
This work demonstrates the utility of incorporating gene expression endpoints to confirm and accentuate whole sediment TIEs.
Description:
Toxicity identification and evaluations (TIEs) use physical/chemical manipulation of a sample to isolate or change the potency of different groups of chemicals potentially toxic in a sample. Organisms are then exposed to these fractions pre- and post-manipulation to determine if the toxicity has changed. TIEs often focus on mortality to detect toxicity; however, this endpoint gives no definitive information as to the identity of the active toxicant(s). It has been suggested that gene expression profiles may be useful in identifying toxic substances from unknown samples. This is accomplished through the development of expression profiles, consisting of a number of genes, which respond in a specific manner to a given toxicant. Generally these expression profiles are established through the use of global transcriptional platforms, such as microarrays. For the current project, microarrays were constructed for the amphipod Ampelisca abdita, a model organism employed in sediment TIEs, which previously lacked any characterization on the molecular level. Exposures to eight model toxicants and mixtures were conducted at 10% of the LC50. Gene expression signatures were generated for individual exposures to specific toxicants or groups of toxicants. Using Elizabeth River VA sediments (ER), TIEs were conducted at two sediment dilutions, one toxic (40:60; ER:control sediment; 86.7% mortality) and one non-toxic (10:90; ER:control sediment; 0% mortality). A gene expression classifier was generated that would discriminate between ER and control sediment samples. Gene expression profiles of model toxicants, ER exposed organisms and control were clustered, with the idea that the model toxicant responsible for the observed mortality in the 40% ER sample would cluster more closely to the unmanipulated ER sediment relative to the other model toxicants. TIE results of the 40% ER samples indicated a large decrease in mortality rates with coconut charcoal addition and a moderate decrease with cation exchange resin addition. These results were compared with results obtained using gene expression as an endpoint. Comparisons were also made between results obtained using TIE and gene expression in the 10% ER sediment, where no significant results using the TIE process were obtained.