Zinc pollution impairs neural processes and protein function and also effects calcium-related transcriptional regulation and enzyme activity. In this study, we investigated pathways that potentially respond to calcium signaling under Zn2+ stress. Specifically we measured relative expressions of GeCNAα, GeCNB, GeMT, GeTNF-α, GeIL-1β, and GeHsp90 in gills, livers, and kidneys of the indicator species Gymnocypris eckloni and found wide variation in their expression between tissues during the course of Zn2+ exposure. Notably, GeCNAα, GeCNB, GeTNF-α, GeIL-1β, and GeMT were rapidly and strongly up-regulated in gills; GeIL-1β and GeHsp90 transcription was quickly induced in kidneys; and GeCNB, GeTNF-α, GeIL-1β, and GeHsp90 were most rapidly up-regulated in livers. GeCNAα and GeMT showed a contrasting late transcriptional up-regulation. These results suggest independent branches for chelation and immune responses during self-protection against Zn2+ toxicity, and the immune response appears to be faster than metal chelation.
Keywords: Calcineurin; Gymnocypris eckloni; Heavy-metal toxicity; Zinc pollution.