Manganese produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this Parkinsonism-like disease. The Lewy bodies typical to PD are not seen in Mn-induced parkinsonism. Animal experiments have given the opportunity to examine the consequences of manganese overexposure under controlled conditions.
Manganese peroxidase the presence of O, can oxidize lignin or react with water to form HO. The Mn3+ ion itself can degrade lignin by catalyzing alkyl-aryl cleavages and α-carbon oxidation in phenols. MnP activity is controlled via transcriptional regulation. MnP is up-regulated by increases in extracellular Mn(II) and HO concentrations. It has been found that increased O concentration and heat stress also activate MnP. Manganese peroxidase In enzymology, a manganese peroxidase () is an enzyme that catalyzes the chemical reaction The 3 substrates of this enzyme are Mn(II), H, and HO, whereas its two products are Mn(III) and HO. This enzyme belongs