Developmental patterns of aluminum in mouse brain and effects of dietary aluminum excess on manganese deficiency.

Previous studies have shown that excess dietary Al during development can affect neurobehavioral measures and decrease tissue Mn of 21-day-old weanling mice without a corresponding increase in tissue Al concentrations. Al and Mn have similar tissue concentrations and similar affinities for transferrin, which is the major plasma transport protein for Al and Mn as well as Fe. In the present study, brain Al, Mn and Fe were studied at 6, 12, 18 and 24 days of age in offspring of Swiss Webster mice fed a semipurified diet containing excess Al (Al[+], 1000 micrograms Al/g diet, Al as Al lactate), marginal Mn (Mn[-], 3 micrograms Mn/g diet) or both excess Al and marginal Mn (Al[+]Mn[-]) from conception to day 24 postnatal (weaning on day 18). Brain Al concentrations were higher at 6 days of age than at later ages and were significantly elevated by the excess Al diet (P = 0.017) but returned to control levels by weaning. Brain Mn concentrations increased from day 6 to day 24 and were lower in the Mn deficient groups (P < 0.001) and also in the excess Al group (P = 0.024) than in controls. Brain Fe concentrations were not influenced by diet. Similar patterns were seen in liver as in brain. The marginal Mn diet led to postnatal growth retardation which was more severe in litters of dams fed Al[+]Mn[-] diets than in litters fed Mn[-] diet. These data suggest that excess Al in diet can interact specifically with Mn metabolism during development.