Oral aluminum administration to rats with normal renal function. 1. Impairment of erythropoiesis

Abstract

Aluminum (Al) toxicity has been mainly investigated in uremic patients although healthy subjects and patients without renal insufficiency are not exempt from its potential deleterious effects. This experimental study aims to elucidate the action of different doses of Al citrate on in vivo erythropoiesis and find out whether the metal exerts a local toxic effect upon the bone marrow late erythroid progenitor cells. The groups in the first experimental series were: C 1 (n=5) controls and T Al-1 (n=5) rats receiving 1 mmol Al citrate/g body weight/day by gavage. Colony-forming units-erythroid (CFU-E) development was inhibited in the T Al-1 group, but the median osmotic fragility (MOF) and hematocrit (Ht) values were similar to those of the C 1 group. The groups in the second series were C 2 (n=5) controls and T Al-2 (n=5) rats receiving Al citrate in drinking water (100 mmol/l). The T Al-2 group showed decreased Ht, hemoglobin concentration, MOF and red blood-cell life-span values (P50.05), and a marked inhibition of the CFU-E development (P50.01). Serum and bone Al concentrations were increased in both Al-treated groups (P50.01). There was a dose-dependent increase in bone Al levels (P50.01) and a dose-dependent decrease of CFU-E development (P50.05). The CFU-E development was inversely correlated with the bone Al content (r=70.79; P50.05). The results demonstrate that even very low doses of Al citrate impair erythropoiesis in vivo and higher doses exert a deleterious action on both CFU-E and mature erythrocytes. This might show a local effect of Al on CFU-E caused by the bone sensitivity to the metal accumulation.