Effect of crystallization inhibitors on vascular calcifications induced by vitamin D: a pilot study in Sprague-Dawley rats.
BACKGROUND
Pathological calcification in soft tissues (ie, ectopic calcification) can have severe consequences. Hydroxyapatite is the common mineral phase present in all tissue calcifications. In general, the development of tissue calcifications requires a pre-existing injury as an inducer (heterogeneous nucleant), whereas further progression requires the presence of other promoter factors (such as hypercalcemia and/or hyperphosphatemia) and/or a deficiency in calcification repressor factors (crystallization inhibitors and cellular defense mechanisms). The present study investigated the capacity of etidronate (a bisphosphonate used in osteoporosis treatment) and phytate (a natural product) to inhibit vascular calcification in rats.


RESULTS
Six male Sprague-Dawley rats in each of the 3 treatment groups were subcutaneously injected with either a placebo (physiological serum solution), etidronate (0.825 micromol x kg(-1) x day (-1)) or phytate (0.825 micromol x kg (-1) x day(-1)) for 8 days. Four days into this regimen, calcinosis was induced by subcutaneous injections of 500,000 IU/kg vitamin D at 0 h, 24 h and 48 h. Ninety-six hours after the final vitamin D injection, the rats were killed and aortas and their hearts were removed for histological and calcium analyses. The data showed that phytate-treated rats had lower levels of aortic calcium than placebo-treated rats. All groups had similar heart calcium levels.


CONCLUSIONS
The present study found that phytate acted as a vascular calcification inhibitor. Thus, the action of polyphosphates could be important in protecting against vascular calcification.
Grases
Félix
F
Laboratory of Renal Lithiasis Research, University Institute of Health Sciences Research (IUNICS), University of Balearic Islands, Palma of Mallorca, Spain. fgrases@uib.es
Sanchis
Pilar
P
Perelló
Joan
J
Isern
Bernat
B
Prieto
Rafel M
RM
Fernández-Palomeque
Carlos
C
Torres
José J
JJ
D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology; D050197:Atherosclerosis / Q000188:drug therapy* / Q000517:prevention & control; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D002114:Calcinosis / Q000139:chemically induced / Q000188:drug therapy* / Q000517:prevention & control; D002118:Calcium / Q000378:metabolism; D003460:Crystallization; D012968:Etidronic Acid / Q000627:therapeutic use*; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010833:Phytic Acid / Q000627:therapeutic use*; D010865:Pilot Projects; D011122:Polyphosphates / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D014807:Vitamin D
D050071:Bone Density Conservation Agents; D011122:Polyphosphates; D014807:Vitamin D; D010833:Phytic Acid; D012968:Etidronic Acid; D002118:Calcium