Toxicity manganese

Graham, D.G. (1984). Catecholamines toxicity a proposal for the molecular pathogenesis of manganese toxicity and Parkinson s disease. Neurotoxicolc 5, 83-96. 

J. T. Moraghan, Manganese toxicity in flax growing on certain calcareous soils low in available iron. Soil Sci. Soc. Am. J. 43 177 (1979). 

Chandra SM Ara R, Nagar N et al Sterility in experimental manganese toxicity. Acta Biol Med 30 857-862, 1973... 

Petrov VV, Podosinovikova PP, Kubraskaya LG, Dolgo-Saburov VB (2004) Contribution of the pro-oxidant factor to the mechanism of heavy metals and manganese toxicity. Toksikologicheskii Vestnik (Russian Toxicological Reports ) 1 12-15... 

Manganese occurs in the liver of the animal body. Even though the amount ol manganese present in mammalian tissues is very small, its concentration seems to be accurately controlled by elaborate mechanisms These mechanisms function primarily by promoting the excretion of excesses of the element from the body rather than by regulating the amounts ol manganese the body absorbs. The mechanisms are located in the liver and on the mucosa of the gut. In cases of manganese toxicity, it is assumed that these mechanisms become saturated. 

Manganese toxicity is also known to represent a serious health hazard to humans, with toxic intakes of the element (either through the air or diet) resulting in severe pathologies, particularly of the central nervous system (15-19). The first observation of Mn toxicity in humans was made by Couper in 1837 (15) (Table II), who reported a paralytic disease in workers of a pyrolusite (Mn dioxide) mill. 

Table II. Selected Cases of Human Manganese Toxicity...

Manganese toxicity has been observed in miners exposed to high levels of Mn02 dust. The neurological symptoms mimic Parkinson s disease. Major changes were observed in the biogenic amines, dihydroxyphenylalanine (DOPA), and phenylalanine. Restoration of appropriate levels of these bioamines alleviated the symptoms. Chelation therapy has not been demonstrated as an effective strategy. ... 

When oral intake is precluded, the recommended daily parenteral supplementation of manganese is 0.15-0.8 mg. Manganese is mainly excreted in the bile during cholestasis serum manganese levels may rise, and manganese toxicity can result. Hjq)ermanganesemia after parenteral nutrition when first reported was linked to portosystemic encephalopathy. Patients with liver disease were particularly at risk. 

Taylor S, Manara AR. Manganese toxicity in a patient with cholestasis receiving total parenteral nutrition. Anaesthesia 1994 49(11) 1013. 

Many symptoms of manganese toxicity disappear after the victim is removed from the source of exposure. L-Dopa (levodopa) can reverse some symptoms, but complete recovery is not expected. Calcium-EDTA (the calcium disodium salt of ethylenediaminetetraacetic acid) will help improve an acute manganese-induced psychosis. 

FeU JM, Reynolds AP, Meadows N, Khan K, Long SG, Quaghebeur G et al. Manganese toxicity in children receiving long-term parenteral nutrition. Lancet 1996 347 1218-21. 

Butterworth RF, Spahr L, Fontaine S, Layrargues GP. Manganese toxicity, dopaminergic dysfunction and hepatic encephalopathy. Metab Brain Dis 1995 10 259-67. 

The central nervous system is the primary target of manganese toxicity. Although it is known that manganese is a cellular toxicant that can impair transport systems, enzyme activities, and receptor functions, the principal manner in which manganese neurotoxicity occurs has not been clearly established (Aschner and Aschner 1991). 

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