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 and copper. However, exposure to manganese dusts and fumes should not exceed the ceiling value of 5 mg/m even for short periods because of its toxicity level. Manganese poisoning has been linked to impaired motor skills and cognitive disorders. The permanganate exhibits a higher toxicity than the manganese(II) compounds. The fatal dose is about 10 g, and several fatal intoxications have occurred. The strong oxidative effect leads to necrosis of the mucous membrane. For example, the esophagus is affected if the permanganate is swallowed. Only a limited amount is absorbed by the intestines, but this small amount shows severe effects