Effect of sodium fluoride administration to rats on bone phosphorous content and phosphatemia.
Fluoride (F) has a known mitogenic effect on bone cells. The daily administration of 40 micromol NaF per 100 g of body weight (bw) increases bone mass in rats. Nevertheless, the quality and composition of bone formed under F stimulus is still matter of study. The objective of this work was to investigate the effect of sodium fluoride (NaF, CAS 7681-49-4) administration on phosphate metabolism and its impact on bone. Experiments were carried out in female fasted 50-day-old rats. Unless otherwise stated, NaF dose was 40 micromol NaF/day . 100 g bw, administered by gastric tube. Four groups of 4 rats each were given the following daily NaF doses: Group A: 0, B: 20, C: 40 and D: 60 micromol NaF/day x 100 g bw. After 30 days rats were killed saving their femora and plasma. Bone phosphorous contents (BPC) and phosphatemia (mg/dl) were measured. BPC decreased significantly as a function of NaF dose. A: 93.3+/-14.1; B: 78.7+/-15.5; C: 61.1+/-14.7**; D: 59.6+/-8.6 **mg P/g dry bone (** significant difference to group A, p < 0.01). Phosphatemia (mg/dl) increased significantly with a peak at 90 min after NaF dose (basal: 5.34+/-0.06; 90 min: 8.15 +/-0.43, p < 0.001). Phosphaturia (microg/min) increased though differences were not significant (basal: 46.7+/-42.8; 4 h: 1275 +/-757, p > 0.05). In thyroparathyroidectomized rats, plasma phosphate increased continuously for at least 240 min. Renal plasmatic flow, glomerular filtration rate and renal blood flow were not affected by NaF treatment. In isolated perfused rat kidneys, urinary phosphate excretion remained unaffected after NaF administration. Phosphate concentration was measured in the plasma and erythrocytes of rats after one dose of NaF (n = 8). Phosphate content of erythrocyte was not affected by NaF, in spite of the concurrent increase in phosphatemia. It is concluded that the treatment with NaF causes a transitory increase in plasma phosphate levels. Neither renal hemodynamic factors nor the inhibitory effect on parathormone actions appear to be the causes of hyperphosphatemia. Efflux of phosphate from cells might not be the cause of the increase in phosphatemia. The loss of phosphorous from bone appears as the most probable determinant of hyperphosphatemia after fluoride administration.
Di Loreto
Verónica
V
Laboratorio de Biología Osea, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Rosario, Argentina.
Rigalli
Alfredo
A
Puche
Rodolfo
R
D000818:Animals; D001842:Bone and Bones / Q000737:chemistry* / Q000187:drug effects*; D004912:Erythrocytes / Q000737:chemistry / Q000378:metabolism; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D066298:In Vitro Techniques; D010281:Parathyroid Hormone / Q000097:blood; D016105:Parathyroidectomy; D010477:Perfusion; D010758:Phosphorus / Q000032:analysis* / Q000097:blood / Q000652:urine; D051381:Rats; D012079:Renal Circulation / Q000187:drug effects; D012969:Sodium Fluoride / Q000494:pharmacology*; D013965:Thyroidectomy
D010281:Parathyroid Hormone; D010758:Phosphorus; D012969:Sodium Fluoride