Juvenile common carp were treated with Cd at a sublethal concentration for Cyprinidae (6.4 mg/L). The expression of N-methyl-D-aspartate receptor subunit genes (NR2A, NR2B) and ATP-binding cassette subfamily C member 1 gene (ABCC1) was compared between treated and untreated fish. In addition, cadmium accumulation in the fish tissues was assessed. NR2A was 18.9-fold upregulated by Cd in the eyes (choroid + retina), which accumulated Cd, and was not upregulated in brain, which didn't accumulate Cd. This may have been caused by the blocking of calcium channels by Cd, which has a very similar ionic radius to that of Ca. ABCC1 was 2.6-fold upregulated in gills and was not upregulated in liver; both tissues accumulated high levels of Cd. This difference may have been caused by the accumulation of predominantly previously inactivated Cd in liver or by some difference in the mechanisms of self-detoxification from Cd in fish gills and liver.
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