Effect of Prenatal Administration of Aluminum and Parathyroid Hormone on Fetal Development in the Rat

Summary Oral aluminum (Al) exposure is a consequence of the element's presence in food, cosmetics, drinking water and its use in preparations administered therapeutically in large quantities as antacids or phosphate binders. Al is neurotoxic in animals and elevated concentrations of Al have been detected in brains of patients with certain encephalopathies. Protein synthesis, ribosomal RNA content and microtubular polymerization may be altered by Al. Since there are critical periods of protein synthesis and cellular division during embryonic development it was of interest to determine the teratogenic potential of Al. Since parathyroid hormone (PTH) increases tissue Al concentrations the effects of combined treatment of Al and PTH were also evaluated. Rats were maintained on diet supplemented with Al and/or calcium and treated with PTH or vehicle from day 6 of pregnancy through day 19, when fetuses were removed by Caesarean section. Combined or separate treatment with PTH and Al did not alter the number of live fetuses, fetal size, incidence of gross, soft-tissue or skeletal anomalies. Al concentration in whole fetal carcass was not affected. Combined treatment was accompanied by a significant increase in resorption rate. Histopathological alterations were not detected in animals from any treatment group. These results suggest that although combined maternal treatment with PTH and 1000 ppm Al may increase embryolethality, it may not enhance the potential for Al-induced toxic effects in surviving rat fetuses.