Perfluoroalkyl substances (PFAS) are widely dispersed persistent organic pollutants (POPs) throughout marine ecosystems. Due to ban of traditional long-chain PFAS, the emerging short-chain ones showed increased environmental detection as substitutes. As the foundation of aquatic food webs, microalgae play a pivotal role in the stability of marine environments. However, the toxicity of those short-chain PFAS was lack of investigation. Therefore, we chose 4C PFAS perfluorobutanoic acid (PFBA) and the marine model diatom Thalassiosira pseudonana as research targets, comprehensively studied the toxicity of PFBA to T. pseudonana in terms of the population growth, photosynthetic physiology and oxidative stress. Our results characterized the inhibited growth, inhibited photosynthetic parameters, increased reactive oxygen species (ROS) levels and activated antioxidant system under PFBA exposure. Further transcriptome analysis revealed the underlying molecular mechanisms: photosynthetic genes were slightly down-regulated and the expression of oxidative stress-related genes was enhanced; significant up-regulation of genes related to the DNA excision repair and replication-coupled DNA repair pathways; the expression of carbon metabolisms-related genes was increased, including the Calvin cycle, glycolysis, pentose phosphate pathway, tricarboxylic acid (TCA) cycle and fatty acid biosynthesis, that could provide sufficient energy for the recovery processes of microalgal cells. This study elucidated the underlying toxic mechanisms of PFBA on phytoplankton, and provided novel insights for assessing the environmental risks of PFAS.
Keyphrases
- oxidative stress
- dna damage
- dna repair
- induced apoptosis
- reactive oxygen species
- human health
- poor prognosis
- risk assessment
- fatty acid
- diabetic rats
- ischemia reperfusion injury
- genome wide
- drinking water
- climate change
- cell death
- binding protein
- bioinformatics analysis
- single cell
- long non coding rna
- transcription factor
- cell cycle arrest
- dna damage response
- cell proliferation
- loop mediated isothermal amplification
- genome wide identification
- endoplasmic reticulum stress
- label free
- anaerobic digestion
- cell free
- heat shock
- cell wall
- heat stress
- quantum dots