Journal
CHEMOSPHERE
Volume 309, Issue -, Pages -Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.chemosphere.2022.136464
Keywords
Saxitoxin; Paralytic shellfish poisoning; Nervous system; Copepod; Marine toxin
Categories
Funding
- KIOST
- [PEA0021]
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This study investigates the toxicity effects of Saxitoxin (STX) on the copepod Tigriopus japonicus and analyzes the transcriptome changes in response to STX exposure. The results demonstrate that the half-maximal lethal concentration of STX for Tigriopus japonicus is 12.35μM, causing rapid mortality at concentrations between 12 and 13μM. Transcriptome analysis reveals significant enrichment of genes involved in the nervous system and gene expression. Network analysis and toxicity pathway analysis identify congenital neurological disorders and oxidative stress pathways as the most significant effects of STX.
Saxitoxin (STX) is a highly toxic marine neurotoxin produced by phytoplankton and a growing threat to ecosystems worldwide due to the spread of toxic algae. Although STX is an established sodium channel blocker, the overall profile of transcriptional levels in STX-exposed organisms has yet to be described. Here, we describe a toxicity assay and transcriptome analysis of the copepod Tigriopus japonicus exposed to STX. The half-maximal lethal concentration of STX was 12.35 mu M, and a rapid mortality slope was evident at concentrations between 12 and 13 mu M. STX induced changes in swimming behavior among the copepods after 10 min of exposure. In transcriptome analysis, gene ontology revealed that the genes involved in nervous system and gene expression were highly enriched. In addition, the congenital neurological disorder and nuclear factor erythroid 2-related factor 2-mediated oxidative stress pathways were identified to be the most significant in network analysis and toxicity pathway analysis, respectively. This study provides valuable information about the effects of STX and related transcriptional responses in T. japonicus.
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