Stress response of rainbow trout fry after exposure to an elevated concentration of carbon dioxide based on transcriptome analysis

To investigate the mechanism of future predicted increases in carbon dioxide (CO2)-induced gill remolding in early life stages of fish, we evaluated physiological responses and performed transcriptome sequencing analysis of rainbow trout Oncorhynchus mykiss fry after 60 days of 1,000 ppm CO2 exposure. The malondialdehyde (MDA) content increased and key antioxidant enzymes were significantly inhibited, indicating that exposure to high CO2 may disrupt cellular redox homeostasis in the gill. The transcriptome sequencing analysis provided a list of possible stress responses of rainbow trout fry exposed to 1,000 ppm CO2. The upregulated uncoupling protein 2 and downregulated differentially expressed genes (DEGs) enriched in oxidative phosphorylation pathway tried to reduce oxidative stress. The upregulated DEGs enriched in ribosome biogenesis in eukaryotes pathway together with the induced heat shock proteins (HSPs) and ubiquitin-conjugated proteins occurred in treated fish to prevent the accumulation of aggregated proteins in gill tissue of the rainbow trout fry after the exposure of 1,000 ppm CO2.

Automated summary

This study investigated the mechanism of gill remodeling in early life stages of fish due to predicted increases in carbon dioxide (CO2). The findings suggest that high CO2 exposure disrupts cellular redox homeostasis in the gill and triggers stress responses to mitigate oxidative stress and prevent protein aggregation.