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Depleted uranium (DU) is an emerging heavy metal pollutant with considerable environmental and occupational concerns. Its radiotoxicity is known to be low. However, its chemical toxicity should not be ignored. In order to explore the chemical toxicity of DU, the effects of uranyl nitrate, prepared from DU, on the model organism Caenorhabditis elegans were investigated. Chronic exposure to DU did not affect the lifespan or reproduction of the worm. DU had little effect on the physiological processes of C. elegans . Additionally, DU treatment did not make C. elegans more susceptible to UV, heat, or oxidative stress. Interestingly, chronic exposure of DU decreased the in vivo reactive oxygen species-scavenging ability through inhibiting the expression of antioxidant genes ctl -1, ctl -2, ctl -3, gst -7, and gst -10. Chronic but not acute exposure of DU induced a statistically significant degeneration of the dopaminergic (DAergic) neurons of treated worms and promoted the increase of α-synuclein aggregation and DAergic neurotoxicity. These findings may raise the public concerns regarding DU as an etiologic agent of Parkinson's disease and underline its potential neurotoxicity.

Exploring the Toxicology of Depleted Uranium with Caenorhabditis elegans