作者: Krishnan Sriram , Gary X. Lin , Amy M. Jefferson , Jenny R. Roberts , Ronnee N. Andrews
DOI: 10.1016/J.TOX.2011.10.021
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摘要: Abstract Occupational exposure to welding fumes (WF) is thought cause Parkinson's disease (PD)-like neurological dysfunction. An apprehension that WF may accelerate the onset of PD also exists. Identifying reliable biomarkers and neurotoxicity are therefore critical for biomonitoring risk characterization exposure. Manganese (Mn) in consumables considered causative factor deficits seen welders. Hence, we sought determine if Mn accumulation blood or nail clippings can be a marker adverse neurotoxicity. To model this, rats were exposed by intratracheal instillation dissolved suspended fume components collected from gas metal arc-mild steel (GMA-MS) manual arc-hard surfacing (MMA-HS) welding. Trace element analysis revealed selective dopaminergic brain areas, striatum (STR) midbrain (MB), following two fumes. This caused abnormality as evidenced loss striatal tyrosine hydroxylase (Th; 25–32% decrease) Parkinson (autosomal recessive, early onset) 7 (Park7; 25–46% proteins. While was not detectable, levels nails strongly correlated with pattern (R2 = 0.9386) (R2 = 0.9332). Exposure manganese chloride (MnCl2) similar STR, MB nail. Our findings suggest has potential sensitive biomarker long-term associated The non-invasive means which collected, stored, transported relative ease, make it an attractive surrogate exposures occupational settings.