Manganese ataxia

Manganese deficiency symptoms in animals affect three systems - bone, reproductive and brain (6,24). Impaired growth, skeletal abnormalities, depressed reproductive function and ataxia in newborn appear to be similar manganese symptoms in all species studied. 

The essentiality of manganese (Mn) for animals was established in 1931 by Orent and McCollum (1) who reported that this element is required for normal reproduction in the rat, and Kemmerer and colleagues (2) who showed that it was necessary for normal growth and reproduction in the mouse. Since then several investigators have verified the critical need of this nutrient for normal development (3). Manifestations of perinatal Mn deficiency in experimental animals include neonatal death, impaired growth, skeletal abnormalities, depressed reproductive function, congenital ataxia, and defects in protein, carbohydrate and lipid metabolism. 

In 1961 Hurley and coworkers ( 1) observed that congenitally ataxic rats were more susceptible to seizures induced by electroshock than were controls. This report followed closely a publication of preliminary findings (2) indicating that seizures induced in rats by hydralazine injection could be prevented by prior injection of manganese chloride. These preliminary findings were later confirmed (3) and indeed it was shown that it was the manganese deficiency that increased the seizure susceptibility of the rats independent of the ataxia (3). 

Manganese Skeletal deformities Gonadal and reproductive dysfunction Defective cholesterol metabolism Brain abnormalities Respiratory illness Ataxia Motor neuron diseases... 

Manganese Skelectal deformities Ataxia motor neurone... 

Manganese Nausea, vomiting, dermatitis, hair color changes, hypocholesterolemia, growth retardation, defective carbohydrate and protein metabolism Parkinsonian-like symptoms, hyper irritability, hallucinations, libido disturbances, ataxia Increased decreased biliary excretion high iron or vitamin C intake... 

Manganese at micromolar concentrations has long been recognized as essential for the proper development and normal function of the nervous system [1,5,8,188]. Recent reports add to the already abundant knowledge of the role of Mn(II) in neurochemistry of the whole organism. A deficiency or an excess of Mn(II) causes severe neurotoxic developmental and functional effects [188-190]. Exposure to abnormal levels of Mn(II) in the developmental stages of life may cause the mature animal to exhibit ataxia or startle responses [191], susceptibility to seizures or epilepsy [192-194]. In these reports most of the effects have been shown to correlate with or interrelate to levels of neurotransmitters or hormones, specific binding to receptors, abnormal diet, or stress [195-198]. 

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]. 

Manganese deficiency has been found in ruminants, pigs and poultry. The effects of acute deficiency are similar in all species and include retarded growth, skeletal abnormalities, ataxia of the newborn and reproductive failure. Manganese, through its activation of glycosyl transferases, is required for the formation of the mucopolysaccharide that forms the organic matrix of bone. 

Investigations of the mechanism of ataxia and incoordination in the offspring of manganese-deficient mothers revealed that the defects were due to the failure of otolith development in the maculae of the inner ear. Manganese deficiency impairs the devel-... 

Of the two remaining essential elements treated in the chapters of this work—selenium and manganese—no very specific effects of deficiency are seen in the brain. In fact, the ataxia of manganese deficiency turns out to arise from malformation of the otoliths of the inner ear. Selenium deficiency leads to reduced activity of glutathione peroxidase and may give rise to formation of lipid perxjxides, but such effects in brain are not well-documented. Frxjm the range of functions mentioned for the different trace elements, it is apparent that specificity rather than conformity is the key to the evolutionary roles of these substances. 

Manganese deficiency has been demonstrated in several species, including rats, mice, pigs, and cattle. Signs of manganese deficiency include impaired growth, skeletal abnormalities, impaired reproductive performance, ataxia, and defects in lipid and carbohydrate metabolism. 

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