Transcriptional and toxic responses to saxitoxin exposure in the marine copepod Tigriopus japonicus. (December 2022)

• Record Type: Journal Article
• Authors: Kang, Hye-Min; Lee, Jihoon; Lee, Yeon-Ju; Park, Yeun; Lee, Euihyeon; Shin, A-Young; Han, Jeonghoon; Lee, Hyi-Seung; Lee, Jong Seok; Lee, Kyun-Woo
• Is Part Of: Chemosphere. Volume 309:Part 1(2022)
• Publication Date: 2022-12
• Subjects: Saxitoxin -- Paralytic shellfish poisoning -- Nervous system -- Copepod -- Marine toxin; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2022.136464
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: 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 μM, and a rapid mortality slope was evident at concentrations between 12 and 13 μM. 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 . Graphical abstract: Image 1 Highlights: Saxitoxin exposure induced mortality and behavioral changes in Tigriopus japonicus. Genes involved in neuron system-related pathways were deregulated. NRF2-mediated oxidative stress response was predicted as the main toxicity pathway.