OBSERVATIONS ON THE EFFECTS OF BERYLLIUM ON ALKALINE PHOSPHATASE

Abstract

Listen

Translate article

In the past 5 years a number of papers have dealt with the clinical aspects of exposure to various beryllium compounds (l-4). Because of these reports several laboratories (5) have attempted to reproduce in animals the lesions seen in the human cases but with only partial success. In 1946, Dr. Leroy Gardner (6) noted that the intravenous injection of zinc-beryllium silicate or beryllium oxide into rabbits resulted in the development of osteogenic sarcomas after a latent period as short as 5$ months or as long as 1 year. This observation has been confirmed in this laboratory and will be described in a later paper. Several authors (7-10) have reported that the addition of beryllium carbonate to the diet of young rats led to the development of rachitic changes which have been termed “beryllium rickets.” Extremely low levels of serum phosphate and a marked lowering of the alkaline phosphatase content of the kidney accompanied the development of this lesion. Furthermore, this lesion could not be prevented by cod liver oil or irradiated ergosterol, though Kay and Skill (10) were able to prevent it by the daily parenteral administration of glycerophosphate. These authors think that the lesion, at least in part, is due to the precipitation of beryllium phosphate in the intestine, making the phosphate unavailable for absorption. However, Sobel, Goldfarb, and Kramer (11) in studying in vitro the calcifying power of ordinary rachitic bone and beryllium rachitic bone in normal serum noted a markedly diminished calcifying power in the latter compared to the former. They also noted that, although the addition of viosterol to the beryllium rachitogenic diet produced a rise in the calcium and phosphorus product in the serum, the rickets was not prevented and the defect in the calcifying power in vitro was still present. This work suggested that in addition to the factor of poor absorption of phosphate from the intestine there was also a local factor which interfered with calcification. In 1943, Hyslop et al. (12) presented evidence that beryllium tends to be stored in bone.