US EPA

1432342 

Journal Article 

Abstract 

Neurological Effects Of Acute Uranium Exposure 

Barber, D; Hancock, S; Mcnally, A; Hinckley, J; Binder, E; Ehrich, M; Jortner, B 

2005 

1 

Toxicological Sciences
ISSN: 1096-6080
EISSN: 1096-0929 

TOX/5000734 

84 

1-S 

123 

English 

We have previously shown that a single intraperitoneal exposure to depleted uranium increased regional brain uranium content. In the current study, we examined the neurological effects of a single intramuscular injection of 0, 0.1, 0.3, or 1 mg uranium/kg (as uranyl acetate, UA) in the presence and absence of stress. Stress treatments were applied for five days prior to injection and ceased just prior to injection. Animals that were stressed had four-fold higher plasma corticosterone levels at the time of uranium exposure (763 ? 131 vs. 189 ? 91 ng/ml). Treatment with UA produced time and dose-dependent increases in serum and brain uranium levels, with the highest levels observed on day 3. Exposure to UA decreased ambulatory activity, forelimb grip strength, and weight gain, regardless of stress treatment. Rats treated with 1 mg/kg UA exhibited a 30% decrease in striatal dopamine content 3 days after dosing (59 ?6 vs. 41? 5 ng/mg tissue). The effect on dopamine was ameliorated by prior application of stress. No effect of DU or stress was observed on levels of GABA, serotonin, norepinephrine, or GSH in the striatum, hippocampus, cerebellum, or cortex. These results indicate that single exposures to soluble uranium at doses as low as 0.1 mg/kg can have adverse neurological effects. However, uranium also produces renal toxicity (see Tobias et al., this meeting), so it is unclear if the neurological effects are a direct result of uranium or are secondary to renal injury.