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 Manganese compounds where manganese is in oxidation state +7, which are mostly restricted to the unstable oxide MnO, compounds of the intensely purple permanganate anion MnO, and a few oxyhalides (MnOF and MnOCl), are powerful oxidizing agents. Compounds with oxidation states +5 (blue) and +6 (green) are strong oxidizing agents and are vulnerable to disproportionation. The most stable oxidation state for manganese is +2, which has a pale pink color, and many manganese(II) compounds are known, such as manganese(II) sulfate (MnSO) and manganese(II) chloride (MnCl). This oxidation state is also seen in the mineral rhodochrosite (manganese(II) carbonate). Manganese(II) most commonly