In order to determine sensitive periods for induction of neurodevelopmental effects of aluminum (Al), mice were fed either 25 (control) or 1000 (high Al) μg Al/g diet (as Al lactate) from conception through lactation and litters were fostered either within or between groups at birth. Birth parameters were not influenced by Al intake. Food intake and body weight were 10%-12% lower during lactation in dams fed the high Al diets. Both gestation and lactation high Al exposure led to growth retardation in offspring beginning on day 10 postnatal; combined gestation and lactation exposure led to the biggest weight differential at weaning (23%). For neurobehavioral measures obtained at weaning, forelimb grasp strength was influenced by gestation high Al exposure, whereas negative geotaxis was influenced by lactation exposure, and hindlimb grasp and temperature sensitivity were influenced by both gestation and lactation exposure. Pup liver and brain manganese (Mn) and liver iron (Fe) concentrations at weaning were lower after high Al lactation exposure than in controls. Pup brain and liver Al concentrations were similar among the groups. These data show that mice are susceptible to neurodevelopmental effects of high maternal dietary Al intake during both gestation and lactation, and that high maternal intake can result in altered essential trace element metabolism in the offspring.
- Aluminum lactate
- Growth retardation
- Trace metals
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience