Manganese overload

The primary acute effects of manganese overload (intoxication) are manifested by dysfunction of the central and peripheral nervous systems [512,513], with symptoms that resemble Parkinson s disease and/or psychosis (schizophrenia) muscular rigidity, tremor, ataxia, flat affect, and hallucinations [14, 514-522] Damage to both white and grey matter of the CNS [523-525], as well as to motor neurons [526], has been documented. Chronic exposure to excess manganese (pre-conception, post-conception, and post-natal), by inhalation or other modes, causes developmental problems [527,528], involving especially the nervous system and mucopolysaccharide synthesis. Further studies on the metabolic fate and distribution of orally administered Mn(II) have been described [529]. 

In the diet and at the tissue level, ascorbic acid can interact with mineral nutrients. In the intestine, ascorbic acid enhances the absorption of dietary iron and selenium reduces the absorption of copper, nickel, and manganese but apparently has little effect on zinc or cobalt. Ascorbic acid fails to affect the intestinal absorption of two toxic minerals studied, cadmium and mercury. At the tissue level, iron overload enhances the oxidative catabolism of ascorbic acid. Thus, the level of dietary vitamin C can have important nutritional consequences through a wide range of inhibitory and enhancing interactions with mineral nutrients. 

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