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.

锌污染会损害神经过程和蛋白质功能，还会影响钙相关的转录调节和酶活性。在这项研究中，我们调查了可能在Zn ²⁺胁迫下响应钙信号的途径。具体而言，我们测量了指示物种裸藻（Gymnocypris eckloni）的腮，肝和肾中GeCNAα，GeCNB，GeMT，GeTNF-α，GeIL-1β和GeHsp90的相对表达，并发现在Zn ²的过程中它们在组织之间的表达差异很大。⁺曝光。值得注意的是，GeCNAα，GeCNB，TNF中的GeTNF-α，GeIL-1β和GeMT迅速而强烈地上调。在肾脏中迅速诱导了GeIL-1β和GeHsp90的转录。和GeCNB，GeTNF-α，金邦-1β和GeHsp90最为迅速的肝脏上调。GeCNAα和GeMT显示出相反的后期转录上调。这些结果表明，在针对Zn ²⁺毒性的自我保护过程中，螯合和免疫反应具有独立的分支，并且免疫反应似乎比金属螯合要快。