Impact of the neurotoxin β-N-methylamino-L-alanine on the diatom Thalassiosira pseudonana using metabolomics

Sea-Yong Kim; Ulla Rasmussen; Sara Rydberg

doi:10.1016/j.marpolbul.2024.116299

Impact of the neurotoxin β-N-methylamino-L-alanine on the diatom Thalassiosira pseudonana using metabolomics

Mar Pollut Bull. 2024 Apr 5:202:116299. doi: 10.1016/j.marpolbul.2024.116299. Online ahead of print.

Authors

Sea-Yong Kim¹, Ulla Rasmussen², Sara Rydberg³

Affiliations

¹ Department of Ocean Environmental Sciences, Chungnam National University, Daejeon 34134, Republic of Korea.
² Department of Ecology, Environment and Plant Sciences, Stockholm University, SE 10691 Stockholm, Sweden.
³ Department of Ecology, Environment and Plant Sciences, Stockholm University, SE 10691 Stockholm, Sweden. Electronic address: sara.rydberg@su.se.

PMID: 38581736
DOI: 10.1016/j.marpolbul.2024.116299

Abstract

The neurotoxin β-N-methylamino-L-alanine (BMAA) has emerged as an environmental factor related to neurodegenerative diseases. BMAA is produced by various microorganisms including cyanobacteria and diatoms, in diverse ecosystems. In the diatom Phaeodactylum tricornutum, BMAA is known to inhibit growth. The present study investigated the impact of BMAA on the diatom Thalassiosira pseudonana by exposing it to different concentrations of exogenous BMAA. Metabolomics was predominantly employed to investigate the effect of BMAA on T. pseudonana, and MetaboAnalyst (https://www.metabo-analyst.ca/) was used to identify BMAA-associated metabolisms/pathways in T. pseudonana. Furthermore, to explore the unique response, specific metabolites were compared between treatments. When the growth was obstructed by BMAA, 17 metabolisms/pathways including nitrogen and glutathione (i.e. oxidative stress) metabolisms, were influenced in T. pseudonana. This study has further determined that 11 out of 17 metabolisms/pathways could be essentially affected by BMAA, leading to the inhibition of diatom growth.

Keywords: Algae; BMAA; Growth; Metabolomics; Toxin.