The article gives an overview of phytic acid in food and of its significance for human nutrition. It summarises phytate sources in foods and discusses problems of phytic acid/phytate contents of food tables. Data on phytic acid intake are evaluated and daily phytic acid intake depending on food habits is assessed. Degradation of phytate during gastro-intestinal passage is summarised, the mechanism of phytate interacting with minerals and trace elements in the gastro-intestinal chyme described and the pathway of inositol phosphate hydrolysis in the gut presented. The present knowledge of phytate absorption is summarised and discussed. Effects of phytate on mineral and trace element bioavailability are reported and phytate degradation during processing and storage is described. Beneficial activities of dietary phytate such as its effects on calcification and kidney stone formation and on lowering blood glucose and lipids are reported. The antioxidative property of phytic acid and its potentional anticancerogenic activities are briefly surveyed. Development of the analysis of phytic acid and other inositol phosphates is described, problems of inositol phosphate determination and detection discussed and the need for standardisation of phytic acid analysis in foods argued.

https://wiebaktmee.nl/cms/pdf/Schlemmer%20_Mol_Nutr_Food_res_2009_Phytate_in_foods_and_significance_for_humans.pdf

Phytate in foods and significance for humans: food sources, intake, processing, bioavailability, protective role and analysis.

Phytic acid (PA) is the primary storage compound of phosphorus in seeds accounting for up to 80% of the total seed phosphorus and contributing as much as 1.5% to the seed dry weight. The negatively charged phosphate in PA strongly binds to metallic cations of Ca, Fe, K, Mg, Mn and Zn making them insoluble and thus unavailable as nutritional factors. Phytate mainly accumulates in protein storage vacuoles as globoids, predominantly located in the aleurone layer (wheat, barley and rice) or in the embryo (maize). During germination, phytate is hydrolysed by endogenous phytase(s) and other phosphatases to release phosphate, inositol and micronutrients to support the emerging seedling. PA and its derivatives are also implicated in RNA export, DNA repair, signalling, endocytosis and cell vesicular trafficking. Our recent studies on purification of phytate globoids, their mineral composition and dephytinization by wheat phytase will be discussed. Biochemical data for purified and characterized phytases isolated from more than 23 plant species are presented, the dephosphorylation pathways of phytic acid by different classes of phytases are compared, and the application of phytase in food and feed is discussed.

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Phytate: impact on environment and human nutrition. A challenge for molecular breeding

https://www.kidney-international.org/article/S0085-2538(15)46509-3/pdf

Nanobacteria: An infectious cause for kidney stone formation

Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants.

https://www.kidney-international.org/article/S0085-2538(15)30495-6/pdf

Control of calcium oxalate crystal structure and cell adherence by urinary macromolecules

Biopathological crystallization : a general view about the mechanisms of renal stone formation

The effects of free radicals on the development of crystals attached to the living epithelium have been studied using an experimental model that enables close simulation of the conditions prevailing in the kidney. The results obtained clearly demonstrate that free radical-damaged cells produce a favorable environment for crystal development. At low free radical concentrations, crystals develop on calcium-enriched zones, whereas at higher concentrations, crystals develop on areas with a destroyed monolayer of superficial cells. Evaluation of the action of some products with antioxidant action and/or crytallization-inhibitory capacity is also included. Antioxidants, such as ascorbic acid and mannitol, exerted the most remarkable effects in avoiding calcium oxalate crystal development, whereas crystal inhibitors, such as citric acid, did not produce any remarkable reduction in calcium oxalate crystallization. Phytic acid notably decreased calcium oxalate crystal development. The ability of phytic acid to diminish calcium oxalate crystallization must be attributed to the combination of its inhibitory capacity of calcium oxalate crystallization and its preventive antioxidant action.

Development of calcium oxalate crystals on urothelium: effect of free radicals.

Biopathological Crystallization: A General View About the Mechanism of Renal Stone Formation

An experimental model that enables the close simulation of conditions prevailing in the kidney during the formation of stones, using living tissue of pig urinary bladder, was developed. The results obtained clearly confirmed the importance of the antiadherent glycosaminoglycan (GAG) layer in preventing the development of solid concretions on the urothelium. Of importance was the capacity of the necrosed urothelium to act as a heterogeneous nucleant of calcium oxalate monohydrate (COM) and dihydrate (COD) crystals, demonstrating the major urolithiasic risk factor that alterations of the healthy epithelium covering the renal papilla may pose in humans. The significant increase in brushite and hydroxyapatite crystals detected on the urothelium when the pH of the artificial urine was 6.5, and the protective GAG layer was reduced or the tissue was necrosed, was also notable. The crystallization inhibitory effects caused by citrate and phytate were also studied. It was found that whereas citrate, at normal urinary concentrations, caused a slight reduction in crystallization, with phytate there was total elimination of crystallization-when it was present at very low concentrations such as 1.0 microgram/ml.

Study of the early stages of renal stone formation: experimental model using urothelium of pig urinary bladder

We have studied the early stages of calcium oxalate monohydrate (COM) crystallization, mainly heterogeneous nucleation, on fixed particles. Experiments were performed using a flow system that closely

L. García-Ferragut

Papers

Biopathological crystallization : a general view about the mechanisms of renal stone formation

Development of calcium oxalate crystals on urothelium: effect of free radicals.

Biopathological Crystallization: A General View About the Mechanism of Renal Stone Formation

Study of the early stages of renal stone formation: experimental model using urothelium of pig urinary bladder

Study of the effects of different substances on the early stages of papillary stone formation