Abstract
Chronic exposure to Manganese (Mn) causes manganism with symptoms similar to Parkinson's disease. The objective of this study was to determine the molecular targets of Mn in PC12 cells. We applied microarray technology to identify molecular targets of Mn and RT‐PCR/Western to validate results. Our results showed that Mn altered the expression of 223 genes; 146 were up regulated and 77 were down regulated. The sub‐lethal dose range (38–300 μM MnCl2) initiated metabolic stress, an induction of enolase/aldolase and hemeoxygenase 1 (HO‐1) (7.7 fold). Concentrations greater than 300 μM caused production of H2O2 concomitant to increase of gene expression of antioxidant enzymes; biliverdin reductase, arsenite inducible RNA associated protein, dithiolethione‐inducible gene‐1 (DIG‐1) and thioredoxin reductase 1 with reduced expression of mitochondrial glutaryl‐coenzyme A dehydrogenase (GCDH). In conclusion the results suggest that Mn toxicity is primarily associated with dose dependent induction of HO‐1 and elevated production of H2O2, along with a minor loss of mitochondrial function. (Supported by NIH grant NCRR G12 RR03020 and G12 MD007582).
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