Atlantic salmon were held for 48 hours in water containing depleted uranium at three concentrations, and their liver gene expression was profiled with microarrays and confirmed by quantitative PCR. Hundreds of genes changed at each concentration, mapping to mitochondrial function, oxidative stress, nuclear receptor signaling and organ damage pathways. No micronuclei or changes in plasma stress markers were seen.
Key numbers
- Measured exposure water: 0.26, 0.53 and 1.0 mg/L uranium (nominal 0.25, 0.5 and 1.0 mg/L) (p. 3).
- Liver uranium after 48 h: 2.9 ± 1.5, 4.9 ± 1.9 and 7.5 ± 2.1 ng/g wet weight, n = 3 per group; not detected in controls (p. 3).
- Differentially expressed liver genes: 847, 891 and 766 at the three concentrations (abstract, p. 1).
Methods (brief)
Laboratory exposure in lake water; liver microarray analysis with pathway mapping to mammalian orthologs, quantitative PCR of eight genes, plasma variables and red blood cell micronucleus counts. Funded by the Norwegian University of Life Sciences, the Research Council of Norway and NIVA; the authors declare no competing interests.
Evidence fitness
Supports a mechanistic statement that the mitochondrion may be a target of uranium’s chemical toxicity in fish. Liver values come from experimental exposure and do not describe uranium in fish sold as food. It does not support human toxicity or dietary exposure claims.
Limitations
Short exposure, transcript-level endpoints without matching adverse physiological effects, three fish per group for tissue uranium, and depleted rather than natural uranium.
Related evidence
Update history
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