Analysis of urinary porphyrins in rats exposed to aluminum and iron

The mechanism by which excess aluminum induces anemia may be aluminum overload resulting from a reversible block in heme synthesis due either to a defect in porphyrin synthesis or to impaired iron utilization. Studies were conducted to define the specific changes in the urinary porphyrin excretion pattern (porphyrin profile) and the time course of those changes in rats exposed to aluminum. In these studies, aluminum chloride (AlCl3) was orally administered to female Wistar rats at the dose of 100 mg Al/kg for 35 days with or without FeCl2 (4 mg Fe/kg). Control rats were treated with 0.9% NaCl or with FeCl2 (4 mg/kg). The dynamics of urine porphyrins (8-, 7-, 6-, 5-, and 4-carboxyporphyrins) was determined by HPLC on the 7th, 14th, 21st, 28th, and 35th days in both exposed and control groups of rats. The results of the experiment indicate that aluminum induced a statistically significant increase in the percentage of uroporphyrin and a decrease in coproporphyrin in urine (cumulative dose, 2100 mg Al/kg). Changes in urinary porphyrins were observed when the concentration of aluminum in serum was at 48 microg Al/L on average. Administration of iron together with aluminum diminished the described changes in porphyrins metabolism caused by aluminum itself.