This preprint tests whether depleted uranium harms cells by disrupting mitochondria. In zebrafish exposed in water, larval movement fell and hatching was delayed at 18 ppb, below the United States drinking-water limit the authors cite, and DNA damage rose; cell reductive capacity fell without a classic oxidative-stress response. The authors link the effect to enrichment of a slingshot protein phosphatase and report partial rescue with an inhibitor. The work has not been peer reviewed.
Key numbers
- United States EPA maximum contaminant level for uranium in drinking water cited by the authors: 30 µg/L (abstract, p. 1).
- Reduced larval movement and delayed hatching at 18 ppb depleted uranium (abstract, p. 1).
- Dose-finding exposures: 0, 23.8, 238 and 2,380 ppb uranium (p. 11).
- Background cited by the authors: of 82 water sources sampled in the western Navajo Nation, nine exceeded the limit, with a maximum of 560.2 µg/L in groundwater (p. 6).
Methods (brief)
Waterborne exposure of zebrafish embryos and larvae, a shrapnel-implant model examined by electron microscopy with elemental analysis, behavioral and hatching assays, DNA-damage quantitative PCR, resazurin-based metabolic assays with antioxidant co-treatments, and transcript profiling. Funded by public and university research programs.
Evidence fitness
Supports a mechanistic, preliminary statement that depleted uranium can impair mitochondrial function at low waterborne concentrations in zebrafish. It does not support human health outcome or dietary exposure claims, and its conclusions are not peer reviewed.
Limitations
Preprint; fish and cell models; the depleted uranium form and exposure route differ from natural uranium that people drink; some mitochondrial DNA results varied between experiments.
Related evidence
Update history
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