By Geoffrey H. Bourne
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Additional resources for Calcification and Physiology
The function of the vesicles in muscle contraction, as in calcification, is not altogether clear; some investigators believe that mitochondria, not the vesicles, control the relaxing factor. In pathological calcification of heart muscle in vitamin D-intoxicated rats, Bonucci and Sadun (1973) observed calcium phosphate within mitochondria in undamaged as well as degenerated myocardial cells. The deposits consisted either of needle-shaped or granular aggregates having the histochemical properties and X-ray diffraction pattern of apatite.
When the capacity of the mitochondria to store calcium in the myocardium is overloaded, and when the concentration of calcium in the microfibrils increases, calcification follows. Normally, the calcium deposits are confined to the SR vesicles and the mitochondria are involved to a much lesser extent. Under pathological conditions, calcification is initiated by myofilament-protein binding of calcium. Speer and Urist ( 1965 ) suggest that the increased calcium concentration in myofilament may lead to protein-calcium phosphate ion association for nucleation and growth of apatite crystals.
More important, the period of synthesis of alkaline phosphatase activity was prolonged by E H D P which suggested that the enzyme activity was correlated with the synthesis of large quantities of noncalcifiable matrix rather than with the mechanism of calcification. However, these experiments confirmed observations of Francis et al. (1969) and Fleish et al. (1973) demonstrating that alkaline phosphatase fails to cleave the Ρ—C—Ρ bonds of diphosphonate, a powerful nonphysiological inhibitor of mineralization.
Calcification and Physiology by Geoffrey H. Bourne