Manganese concentration in mouse brain after intravenous injection.

Abstract

Abnormal deposit of manganese (Mn) in the basal ganglia is often observed in patients with chronic liver failure and patients receiving long-term parenteral nutrition. Based on the data that (54)Mn is transported into the brain efficiently via a transferrin-independent uptake system, Mn concentration in mouse brain was determined after intravenous (iv) injection (2 mg Mn/kg/day x 5 times) of either MnCl(2) or pH 8.6 buffer-treated MnCl(2), which has a higher affinity for transferrin than untreated MnCl(2). Brain Mn concentration was significantly increased in either case. Brain Mn concentration of MnCl(2) group was significantly higher than that of pH 8.6 buffer-treated MnCl(2) groups. Mn concentration in the caudate putamen of MnCl(2) group was also significantly higher than that of pH 8.6 buffer-treated MnCl(2) group. Ninety seconds after a single injection of MnCl(2) (2 mg Mn/kg), brain Mn concentration was remarkably increased with blood Mn level, but not 1 hr after injection. On the other hand, hepatic Mn concentration was remarkably high 1 hr after injection and the brain Mn concentration was increased again at 24 hr, followed by decrease of the hepatic Mn concentration. Relative Mn concentrations in the brain 90 sec after injection were different from those 24 hr after injection, suggesting that the mechanism of the increase of brain Mn concentration via blood Mn level is different from that via the redistribution from the liver. Mn ion and/or Mn bound to low molecular weight compounds may be involved in abnormal Mn uptake in the brain.