In mice the oral LD50 values of aluminium chloride and aluminium sulphate were 0·77 ± 0·12 and 0·98 ± 0·09 g. Al/kg. (± S.E.) respectively.
Mice and rats were fed on a normal diet containing about 170 p.p.m. of aluminium. Doubling this concentration caused a decrease in growth in the second and third generations of mice. A high intake of aluminium sulphate (2,835 p.p.m.) caused a 20-fold increase of aluminium retention in white rats. Aluminium accumulated in various tissues, especially in the skeleton, liver, and testes. A high rate of intake (2,665 p.p.m.) caused a negative phosphorus balance in the rat, with an increased output of phosphorus in the faeces. The lower absorption of phosphorus was also demonstrated with Na2H32PO4. Chronic and acute poisoning by aluminium chloride caused, after intraperitoneal Na2H32PO4, decreased incorporation of 32P into the phospholipids and nucleic acids of various tissues in the rat. It also caused a fall in the adenosinetriphosphate acid-levels in plasma, and a rise in the adenosine diphosphate level.
The results suggest that the toxic effects of aluminium salts result both from decreased absorption of phosphorus and from interference with phosphorylation processes in the tissues.
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