ISSN 1995-4301
(Print)

ISSN 2618-8406
(Online)

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1 issue of the journal in 2026

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2 issue of the journal in 2025

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Cd2+-induced tissue-specific expression of genes involved in cellular transportation in Eurasian carp (Cyprinus carpio)

K.V. Zolotarev, A.N. Mikhailov, M.V. Mikhailova, V.I. Nakhod, D.D. Zhdanov
Section: Ecotoxicology
Cd2+ is a heavy metal cation with some typical for heavy metals as well as unique toxic properties for live components of water ecosystems. The objective of this study was to analyze Cd2+-induced expression of genes of some cellular transportation proteins in several tissues of a fish and its possible correlation with Cd accumulation in tissues. Juvenile Cyprinus carpio were treated with Cd2+ at a preliminarily determinated 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 gene expression was 16.6-fold upregulated by Cd2+ 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 Cd2+, which has a very similar ionic radius to that of Ca2+. According to the result of the current study, it can be concluded that the similarity of the radius of a heavy metal cation to that of Ca2+ is a major factor contributing to its ability to irreversibly block calcium channels. ABCC1 gene expression was 2.0-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 Cd2+ in fish gills and liver.
Keywords: cadmium, accumulation, NR2A, calcium channels, ABCC1, self-detoxification
Article published in number 1 for 2026
DOI: 10.25750/1995-4301-2026-1-169-176
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