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Chronic Low-Level Domoic Acid Exposure Alters Gene Transcription and Impairs Mitochondrial Function in the CNS
Author(s): Hiolskia, Emma M.; Preston S. Kendrick; Elizabeth R. Frame; Mark S. Myers; Theo K. Bammler; Richard P. Beyer; Federico M. Farin; Hui-wen Wilkerson; Donald R. Smith; David J. Marcinek; Kathi A. Lefebvre
NCCOS Center: CSCOR
Name of Publisher: Elsevier
Publication Type: Journal Article
Journal Title: Aquatic Toxicology
Date of Publication: 2014
Reference Information: Vol. 155
Extent of Work: pp:151-159.
Keywords: domoic acid; chronic toxin exposure; microarray; subclinical effects; ECOHAB; central nervous system; vertebrates
Abstract: Domoic acid is an algal-derived seafood toxin that functions as a glutamate agonist and exerts excitotox-icity via overstimulation of glutamate receptors (AMPA, NMDA) in the central nervous system (CNS). Athigh (symptomatic) doses, domoic acid is well-known to cause seizures, brain lesions and memory loss;however, a significant knowledge gap exists regarding the health impacts of repeated low-level (asymp-tomatic) exposure. Here, we investigated the impacts of low-level repetitive domoic acid exposure ongene transcription and mitochondrial function in the vertebrate CNS using a zebrafish model in order to:(1) identify transcriptional biomarkers of exposure; and (2) examine potential pathophysiology that mayoccur in the absence of overt excitotoxic symptoms. We found that transcription of genes related to neu-rological function and development were significantly altered, and that asymptomatic exposure impairedmitochondrial function. Interestingly, the transcriptome response was highly variable across the expo-sure duration (36 weeks), with little to no overlap of specific genes across the six exposure time points(2, 6, 12, 18, 24, and 36 weeks). Moreover, there were no apparent similarities at any time point with thegene transcriptome profile exhibited by the glud1 mouse model of chronic moderate excess glutamaterelease. These results suggest that although the fundamental mechanisms of toxicity may be similar,gene transcriptome responses to domoic acid exposure do not extrapolate well between different expo-sure durations. However, the observed impairment of mitochondrial function based on respiration ratesand mitochondrial protein content suggests that repetitive low-level exposure does have fundamentalcellular level impacts that could contribute to chronic health consequences.
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