Abstract
Manganese (Mn) is an essential nutrient. However, a longitudinal study showed that exposure to Mn containing welding fumes under federal safety limits may cause a dose-dependent progression of Parkinsonism. Excess Mn causes neurotoxicity, however the underlying molecular mechanism remains unclear. Disrupted polyamine metabolism with increased putrescine levels was observed in suicidal cohorts and also occurs in multiple neurologic disorders, but no information is available on the possible effects of Mn on polyamine metabolism. To test the hypothesis that increased Mn causes increased putrescine and altered polyamine metabolism, human SH-SY5Y neuroblastoma cells were treated with MnCl2 (0,1,5,10,50,100μM for 5 hr; n=9/condition). Results showed that cellular Mn measured was representative of normal to pathological range (6 to 49 ng/mg protein) in the human brain. Putrescine and other untargeted metabolites were analyzed by liquid chromatography-ultra high-resolution mass spectrometry followed by metabolome-wide association study (MWAS) of putrescine. Results showed that cellular Mn caused a dose dependent increase in putrescine content (3.2 nmol/mg protein to 4.5 nmol/mg protein; p
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