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The aim of this research was to evaluate the effect of dietary phytate on cardiovascular calcification in rats during aging. Male Wistar rats (10 weeks old) were randomly assigned to four diet groups. The control group was fed with a balanced diet (UAR-A04) containing phytate. The AIN group was fed a purified diet (AIN-76A) with an undetectable level of phytate. The PHY group was fed with a purified diet (AIN-76A) enriched with phytate (phytin, as the calcium magnesium salt). The MOD group was fed with the AIN-76A diet (phytate undetectable) enriched with MgO, inositol and CaHPO4. At 76 weeks of age all rats were sacrificed, and the aortas, hearts, kidneys, livers and femurs were removed for chemical analysis. The most significant differences were found in the aorta calcium content. Phytate-treated rats (the control and PHY groups) had significantly lower levels of calcium in the aorta compared to nonphytate-treated rats (AIN and MOD groups). The present study demonstrated that dietary phytate treatment significantly reduced age-related aorta calcification.

The aim of this study was to assess the inhibitory action of phytate in formation of renal calculi. Hypertension (induced by nicotine) combined with hypercalcemia (induced by D vitamin) was used to induce calcification in renal tissue in male Wistar rats that were fed a purified phytate free diet. Phytate non-treated rats developed significant calcium deposits in kidneys and papillae, as well as in kidney tubules and vessels, whereas calcium deposits were absent in control and phytate treated rats. Fragments of hydroxyapatite (HAP) calculi exhibited the capacity to induce the growth of calcium salts on their surfaces. Presence of 1.5 mg/L of phytate in the synthetic urine inhibited the formation of calcium oxalate monohydrate on HAP renal calculi in normocalciuric conditions. The findings show that the action of phytate as a crystallization inhibitor takes place both in the intrapapillary tissue and urine.

Calcification is an undesirable disorder, which frequently occurs in the heart vessels. In general, the formation of calcific vascular lesions involves complex physicochemical and molecular events. Calcification (hydroxyapatite) is initiated by injury and is progressed by promoter factors and/or the deficit of inhibitory signals. Myo-inositol hexakisphosphate (phytate, InsP6) is found in organs, tissues and fluids of all mammals and exhibits an important capacity as a crystallization inhibitor of calcium salts in urine and soft tissues. The levels found clearly depend on the dietary intake but it can also be absorbed topically. In this paper, the capacity of InsP6 as a potential inhibitor of cardiovascular calcifications was assessed in Wistar rats. Three groups were included, a control group, an InsP6 treated group (subjected to calcinosis induction by Vitamin D and nicotine and treated with standard cream with a 2% of InsP6 as potassium salt) and an InsP6 non-treated group (only subjected to calcinosis induction). All rats were fed AIN 76-A diet (a purified diet in which InsP6 is undetectable). Animals were monitorized every 12 hours. After 60 hours of calcinosis treatment, all rats of the InsP6 non-treated group died and the rest were sacrificed. Aortas and hearts were removed. A highly significant increase in the calcium content of aorta and heart tissue was observed in the InsP6 non-treated rats (21 +/- 1 mg calcium/g dry aorta tissue, 10 +/- 1 mg calcium/g dry heart tissue) when compared with controls (1.3 +/- 0.1 mg calcium/g dry aorta tissue, 0.023 +/- 0.004 mg calcium/g heart dry tissue) and InsP6 treated (0.9 +/- 0.2 mg calcium/g dry aorta tissue, 0.30 +/- 0.03 mg calcium/g dry heart tissue) animals. Only InsP6 non-treated rats displayed important mineral deposits in aorta and heart. These findings are consistent with the action of InsP6, as an inhibitor of calcification of cardiovascular system.

Urine contains variable amounts of organic matter derived from cell degradation. The cellular detritus is composed by membranous and cytosolic glycoproteins, etc. The aim of this paper was to study the role of organic matter in calcium oxalate crystal development and to evaluate the action of some crystallization inhibitors on this process. Crystallization studies were carried out on urine in stagnant urine as well as under flow conditions, in presence and absence of cellular debris. Low amounts of cellular debris (when batch conditions were used), exhibited some inhibitory activity on heterogeneous nucleation of calcium oxalate monohydrate crystals, probably due to glycoproteins. Increasing amounts of cellular debris, however, promoted the nucleation of calcium oxalate monohydrate crystals. When cellular debris was retained in a cavity with a urine flow, this organic matter effectively induced the development of primary aggregates of calcium oxalate monohydrate crystals (crystallization range 2.8 mg/h per mg of organic matter). Presence of crystallization inhibitors prevented or minimized crystal development. These findings show that cell debris provides the necessary elements for the development of oxalate crystals and that this process can be effectively inhibited by presence of crystallization inhibitors.

Myo-inositol hexakisphosphate (InsP6, phytate) is a molecule to which diverse beneficial properties have been attributed. Some of these properties are related to its dermatological use as discolouring agent, on preventing calcinosis cutis or due to its important role on premature aging. Other studies also seem to demonstrate a capacity of InsP6 to inhibit skin cancer. In this paper, the effect of the vehicle of topical administration of phytate is studied, using four groups of male Wistar rats (n = 6) fed with an InsP6 defficient diet and treated with a hydrophyl gel or an O/W moisturizing cream with two different concentrations of InsP6. Due to the correlation between InsP6 absorption and its urinary excretion, these last values were used to evaluate this process. It was found that phytate was absorbed through the skin using both a gel or a cream, demonstrating that its absorption is independent on the matrix used for topical treatment. However, urinary InsP6 values were slightly higher when using the gel, but in all cases values were much higher than those found with oral InsP6 treatment, due to the formation of insoluble species in the gastrointestinal tract when InsP6 is administered orally.