Rat dams received lanthanum chloride in drinking water, and their offspring were exposed through the placenta and milk and then directly for 28 days after weaning. Exposed offspring showed impaired spatial learning in a water maze, dose-dependent lanthanum accumulation in the hippocampus, neuronal damage and apoptosis, with cell experiments pointing to a microRNA-124 and PI3K/Akt mechanism.
Key numbers
- Drinking water lanthanum chloride concentrations: 0.25%, 0.5% and 1% (low, medium, high); six breeding pairs per group (Methods, p. 2).
- Hippocampal lanthanum in offspring increased stepwise from control to low, medium and high groups, each step statistically significant; values are shown only in a figure (Figure 2, p. 5).
- Escape latency and swim distance were longer in all exposed groups, and time in the target quadrant shorter in the medium and high groups (p. 4).
Methods (brief)
Pregnant rats and offspring were exposed via drinking water; spatial memory was tested with a Morris water maze; hippocampal lanthanum was measured by ICP-MS; histology, TUNEL, RT-qPCR, luciferase reporter and western blots, plus HT22 cell culture with mimics and inhibitors of microRNA-124.
Evidence fitness
Supports statements that high-concentration lanthanum chloride exposure during development reaches the rat hippocampus and impairs learning in rats. It does not establish effects at dietary exposure levels relevant to people.
Limitations
Doses are very high relative to any food exposure described in the cited evidence; hippocampal concentrations shown only graphically; water intake and absorbed dose not reported.
Related evidence
Update history
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