A study of gastric secretion and kidney function in chronic fluorosis in experimental animals

Abstract

Observations have been made on experimental animals subjected to short- and long-term ingestion of fluorides. These included renal function tests and the cytology and histochemistry of the kidney and gastric mucosa. Rats given fluorides in the drinking-water showed albuminuria, glycosuria and a rise in urea output that increased steadily during the three weeks of the experiment. That fluorides interfere with tubular reabsorption was shown in an experiment in which rats on a sodium-free diet excreted sodium when given a fluoride (KF) solution to drink. Kidney clearance values were greatly reduced. Kidney lesions appeared, and activities of the enzymes succinic dehydrogenase and alkaline phosphatase were negligible. The gastric mucosa was similarly affected. For long-term fluoride administration to rats NaF solution was mixed with the food. Within a few months kidney clearance values were reduced and the kidneys contained non-functioning renal parenchyma. The surviving renal epithelium showed normal succinic dehydrogenase activity. Casts noticed previously have been identified. The suggestion is made that it is the glomerulus which, primarily, is attacked by fluoride. In chronic fluorosis the fundic mucosa of the rat stomach was found to be thin, due to the disappearance of many of the parietal cells. Peptic cells were apparently unaffected and mucoid cells were stimulated. The histological changes confirm previous observations (Bowie, Darlow and Murray) that HCl secretion, but not pepsin secretion, is suppressed by fluoride. Bogs, apart from reduced alkaline phosphatase activity in some kidneys, showed no kidney or stomach lesions after two years' fluoride feeding. Rabbit kidneys and stomachs remained apparently normal after the animals had been drinking NaF solution for up to four years. The results of some acute experiments included show that injection of NaF solution into rabbits raises the citric acid content of the kidney. In view of this, the possibility that it is due to the synthesis of a fluoro-fatty acid and provides a biochemical lesion (R.A. Peters) has been considered.