The effects of aluminum ingestion on intestinal cadmium absorption, lipid peroxidation and alkaline phosphatase activity.

Consumption of dietary aluminum (A1, 2000 or 4000 ppm) for 1 month did not influence mouse body weight. In order to estimate an absorption of cadmium (Cd) from the gastrointestinal tract, mice were intubated twice every 24 h with Cd (CdCl2). In the A1-supplemented mice, Cd absorption increased rather than decreased. Intestinal Cd and metallothionein concentrations were increased by the A1 supplement. Intestinal alkaline phosphatase activity and lipoperoxide concentrations were also enhanced by A1 ingestion. Of course, intestinal A1 concentration was at a high level in the A1-supplemented groups. However, A1 accumulation was not observed in the liver. The increase of Cd absorption may be due to an abnormality of the gut wall caused by the A1. Our results suggest that A1 is not inert for animals, even though A1 absorption is poor.