Erythrocytes manganese

Hatano, S Nishi, Y., and Usui, T. (1983). Erythrocyte manganese concentration in healthy Japanese children, adults, and the elderly, and in cord blood. Am. f. Clin. Nutr. 37, 457-160. 

The possible hnk between hypermanganesemia and cholestasis has been investigated in patients receiving long-term parenteral nutrition (68). The authors concluded that cholestatic liver disease does not contribute to increased blood manganese concentrations in such patients, and that plasma concentrations reflect recent manganese exposure and impaired excretion when cholestasis is present. They also emphasized that serum concentrations are a poor marker and that erythrocyte manganese concentrations should be used instead. 

Olehy DA, Schmitt RA, Bethard WF. 1966. Neutron activation analysis of magnesium, calcium, strontium, barium, manganese, cobalt, copper, zinc, sodium, and potassium in human erythrocytes and plasma. J Nucl Med 6 917-927. 

In 1980 Hoffman (7) reported that serum manganese concentrations were the same in epileptics and non-epileptic controls in populations of both adults and children. This observation suggests that the differences reported by Tanaka (5) and by Papavasiliou, et al. (6) in whole blood were due to differences in manganese concentrations in the blood cells, probably erythrocytes. Whether this apparent deficiency in the erythrocytes of some epileptics translates into lower manganese concentrations in other tissues of these epileptics is unknown. 

Lombeck I, Wendel U, Versieck J, van Ballenberghe L, Bremer HJ, Duran R, Wadman S. Increased manganese content and reduced arginase activity in erythrocytes of a patient with prolidase deficiency (iminodipeptiduria), Eur J Pediatr 1986 144 571-3. 

Allain et al. (1987) issued a cautionary note about attempting to use acid precipitation in the measurement of manganese in whole blood. Low results were obtained which they suggested was because the manganese, bound to haem in erythrocytes, was precipitated with nitric acid and not released into solution. 

In the superoxide dismutase of bovine erythrocytes, and possibly elsewhere, zinc and copper are both linked to a histidine moiety. Analogous enzymes containing manganese instead of copper occur in both mammalian and bacterial organisms (Oberley and Buettner, 1979). For further reading on this highly unusual metalloenzyme, see Oberley (1982) and Rodgers and Powers (1981). 

ALA dehydratase, the second enzyme of the heme biosynthetic pathway, is inhibited in vitro by metals and other SH-directed agents. Inhibition of ALA dehydratase in liver and erythrocytes in vitro has been observed with silver, iron, manganese, copper, and zinc ions (Gibson et al. 1955) and in vivo with lead (Sassa 1978) and cobalt (Nakemura et al. 1975). The inhibition of ALA dehydratase in erythrocytes by lead in vivo is well established, and this effect is considered a highly sensitive measure of lead exposure in human subjects (considered further in Sect. D.I, below). 

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