The influences of chondroitin sulfate C (C6S) on size, aggregation, sedimentation, and Zeta potential of sub-micron calcium oxalate monohydrate (COM) and calcium oxalate dihydrate (COD) crystallites with mean sizes of about 330？nm were investigated using an X-ray diffractometer, nanoparticle size Zeta potential analyzer, ultraviolet spectrophotometer, and scanning electron microscope, after which the results were compared with those of micron-grade crystals. C6S inhibited the conversion of COD to COM and the aggregation of COM and COD crystallitesis; it also decreased their sedimentation rate, thus increasing their stability in aqueous solution. The smaller the size of the COD crystallites, the easier they can be converted to COM. The stability of sub-micron COD was worse than that of micron-grade crystals. C6S can inhibit the formation of calcium oxalate stones. 1. Introduction The formation of urinary stones is closely related to supersaturation, nucleation, growth, and aggregation of stone salt. Compared with the urine of stone patients, normal urine has more types of inhibitors with higher concentration and stronger activity. These inhibitors include some small-molecule inorganic salts such as citrate and pyrophosphate and urinary macromolecules such as glycosaminoglycan (GAG), nephrocalcin, Tamm-Horsfall protein, and prothrombin fragment 1 [1–5]. As the main component of urinary stones, calcium oxalate (CaOxa) mainly exists in the form of calcium oxalate monohydrate (COM) and calcium oxalate dehydrate (COD). In the urine of patients afflicted with urinary stones, the existing probability of COM crystallites is much higher than that in healthy controls [6]. A study showed that CaOxa crystals in urine only take 3？min to 4？min to flow through the nephron [7] and about 12？min to pass through the pelvis. Within such a short time, the crystal could not grow into a pathological size (larger than tens of microns). Rapid aggregation of the crystals is an important factor in CaOxa stone formation [8, 9]. GAG is an important urinary macromolecule that inhibits urinary stone formation [2]. Urinary GAGs originate from two sources. The first source of urinary GAGs is the serum, which is filtered through the kidney into the urine. The electrophoretic types of GAGs in urine are similar to those present in the serum; moreover, the excretion of urinary GAGs increases along with the increment of GAG concentration in the serum [10–12]. The GAGs in the serum originate from degradation products of proteoglycans in connective tissues, such as the cartilage,
References
[1]
C. Mechlin, C. Kalorin, J. Asplin, and M. White, “Splenda improves tolerance of oral potassium citrate supplementation for prevention of stone formation: results of a randomized double-blind trial,” Journal of Endourology, vol. 25, no. 9, pp. 1541–1545, 2011.
[2]
J. P. Lulich, C. A. Osborne, M. Carvalho, and Y. Nakagawa, “Effects of a urolith prevention diet on urine compositions of glycosaminoglycans, Tamm-Horsfall glycoprotein, and nephrocalcin in cats with calcium oxalate urolithiasis,” American Journal of Veterinary Research, vol. 73, no. 3, pp. 447–451, 2012.
[3]
P. Viswanathan, J. D. Rimer, A. M. Kolbach, M. D. Ward, J. G. Kleinman, and J. A. Wesson, “Calcium oxalate monohydrate aggregation induced by aggregation of desialylated Tamm-Horsfall protein,” Urological Research, vol. 39, no. 4, pp. 269–282, 2011.
[4]
W. Chiangjong and V. Thongboonkerd, “A novel assay to evaluate promoting effects of proteins on calcium oxalate crystal invasion through extracellular matrix based on plasminogen/plasmin activity,” Talanta, vol. 101, pp. 240–245, 2012.
[5]
D. Webber, A. L. Rodgers, and E. D. Sturrock, “Glycosylation of prothrombin fragment 1 governs calcium oxalate crystal nucleation and aggregation, but not crystal growth,” Urological Research, vol. 35, no. 6, pp. 277–285, 2007.
[6]
J.-Y. He, S.-P. Deng, and J.-M. Ouyang, “Morphology, particle size distribution, aggregation, and crystal phase of nanocrystallites in the urine of healthy persons and lithogenic patients,” IEEE Transactions on Nanobioscience, vol. 9, no. 2, pp. 156–163, 2010.
[7]
W. G. Robertson, “Kidney models of calcium oxalate stone formation,” Nephron Physiology, vol. 98, no. 2, pp. p21–p30, 2004.
[8]
J.-Y. He, J.-M. Ouyang, and R.-E. Yang, “Agglomeration of urinary nanocrystallites: key factor to formation of urinary stones,” Materials Science and Engineering C, vol. 30, no. 6, pp. 878–885, 2010.
[9]
N. K. Saw, P. N. Rao, and J. P. Kavanagh, “A nidus, crystalluria and aggregation: key ingredients for stone enlargement,” Urological Research, vol. 36, no. 1, pp. 11–15, 2008.
[10]
S. D. Roberts and M. I. Resnick, “Glycosaminoglycans content of stone matrix,” Journal of Urology, vol. 135, no. 5, pp. 1078–1083, 1986.
[11]
N. W. Poon and M. D. I. Gohel, “Urinary glycosaminoglycans and glycoproteins in a calcium oxalate crystallization system,” Carbohydrate Research, vol. 347, no. 1, pp. 64–68, 2012.
[12]
I. D. Thorne and M. I. Resnick, “A methodology for the characterization of urinary glycosaminoglycans,” Journal of Urology, vol. 131, no. 5, pp. 995–999, 1984.
[13]
W. Bodenstab, J. Kaufman, and C. L. Parsons, “Inactivation of antiadherence effect of bladder surface glycosaminoglycan by a complete urinary carcinogen (N-methyl-N-nitrosourea),” Journal of Urology, vol. 129, no. 1, pp. 200–201, 1983.
[14]
T. Schwend, R. J. Deaton, Y. Zhang, B. Caterson, and G. W. Conrad, “Corneal sulfated glycosaminoglycans and their effects on trigeminal nerve growth cone behavior in vitro: roles for ECM in cornea innervation,” Investigative Ophthalmology & Visual Science, vol. 53, no. 13, pp. 8118–8137, 2012.
[15]
N. Volpi, A. Mucci, and L. Schenetti, “Stability studies of chondroitin sulfate,” Carbohydrate Research, vol. 315, no. 3-4, pp. 345–349, 1999.
[16]
B. Erkurt, Y. Ilker, Y. Budak, B. ？zveren, L. Türkeri, and A. Akda？, “Effect of urinary stone disease and extracorporeal shockwave lithotripsy on excretion of glycosaminoglycans,” Journal of Endourology, vol. 13, no. 8, pp. 553–557, 1999.
[17]
Y. M. Michelacci, R. Q. Glashan, and N. Schor, “Urinary excretion of glycosaminoglycans in normal and stone forming subjects,” Kidney International, vol. 36, no. 6, pp. 1022–1028, 1989.
[18]
S. Srinivasan, P. Kalaiselvi, R. Sakthivel, V. Pragasam, V. Muthu, and P. Varalakshmi, “Uric acid: an abettor or protector in calcium oxalate urolithiasis? biochemical study in stone formers,” Clinica Chimica Acta, vol. 353, no. 1-2, pp. 45–51, 2005.
[19]
O. Miyake, K. Yoshimura, M. Tsujihata et al., “Possible causes for the low prevalence of pediatric urolithiasis,” Urology, vol. 53, no. 6, pp. 1229–1234, 1999.
[20]
S.-P. Deng and J.-M. Ouyang, “Effects of dipalmitoylphosphatidylcholine monolayers to the crystallization of calcium oxalate monohydrate from the solution containing chondroitin sulfate C,” Colloids and Surfaces A, vol. 257-258, pp. 47–50, 2005.
[21]
M. Masui, M. Suzuki, Y. Fujise, and N. Kanayama, “Calcium-induced changes in chondroitin sulfate chains of urinary trypsin inhibitor,” Biochimica et Biophysica Acta, vol. 1546, no. 2, pp. 261–267, 2001.
[22]
H. Peng, J.-M. Ouyang, X.-Q. Yao, and R.-E. Yang, “Interaction between sub-micron COD crystals and renal epithelial cells,” International Journal of Nanomedicine, vol. 7, no. 8, pp. 4727–4737, 2012.
[23]
J.-M. Ouyang, Z.-Y. Xia, G.-N. Zhang, and H.-Q. Chen, “Nanocrystallites in urine and their relationship with the formation of kidney stones,” Reviews in Inorganic Chemistry, vol. 32, no. 2-4, pp. 101–110, 2012.
[24]
S. Kulaksizoglu, M. Sofikerim, and C. Cevik, “Impact of various modifiers on calcium oxalate crystallization,” International Journal of Urology, vol. 14, no. 3, pp. 214–218, 2007.
[25]
M. Donnet, N. Jongen, J. Lemaitre, and P. Bowen, “New morphology of calcium oxalate trihydrate precipitated in a segmented flow tubular reactor,” Journal of Materials Science Letters, vol. 19, no. 9, pp. 749–750, 2000.
[26]
S. C. Lee, H. W. Choi, H. J. Lee et al., “In-situ synthesis of reactive hydroxyapatite nano-crystals for a novel approach of surface grafting polymerization,” Journal of Materials Chemistry, vol. 17, no. 2, pp. 174–180, 2007.
[27]
X.-J. Xu, Y.-M. Liu, H.-Y. Yu, and J.-M. Ouyang, “Thermodynamical transformation of calcium oxalate dihydrate and its stabilization by algal sulfated polysaccharide,” Chinese Journal of Inorganic Chemistry, vol. 23, no. 4, pp. 640–644, 2007.
[28]
M.-E. Laurence, P. Levillain, B. Lacour, and M. Daudon, “Advantage of zero-crossing-point first-derivative spectrophotometry for the quantification of calcium oxalate crystalline phases by infrared spectrophotometry,” Clinica Chimica Acta, vol. 298, no. 1-2, pp. 1–11, 2000.
[29]
A. Gul and P. Rez, “Models for protein binding to calcium oxalate surfaces,” Urological Research, vol. 35, no. 2, pp. 63–71, 2007.
[30]
R. L. Ryall, M. C. Chauvet, and P. K. Grover, “Intracrystalline proteins and urolithiasis: a comparison of the protein content and ultrastructure of urinary calcium oxalate monohydrate and dihydrate crystals,” BJU International, vol. 96, no. 4, pp. 654–663, 2005.
[31]
M. Q. Ge and W. Y. Liang, “Adsorption of sodium dodecylbenzenesulfate (SDBS) on nanosized CaCO3 and dispersion of nanosized CaCO3 in water,” Journal of Dispersion Science and Technology, vol. 31, no. 8, pp. 1157–1162, 2010.
[32]
J. M. Baumann, B. Affolter, U. Caprez, C. Clivaz, Z. Gluck, and R. Weber, “Stabilization of calcium oxalate suspension by urinary macromolecules, probably an efficient protection from stone formation,” Urologia Internationalis, vol. 79, no. 3, pp. 267–272, 2007.
[33]
C.-Y. Duan, Z.-Y. Xia, G.-N. Zhang, B.-S. Gui, J.-F. Xue, and J.-M. Ouyang, “Changes in urinary nanocrystallites in calcium oxalate stone formers before and after potassium citrate intake,” International Journal of Nanomedicine, vol. 8, no. 1, pp. 909–918, 2013.
[34]
M. Tsujihata, C. Momohara, I. Yoshioka, A. Tsujimura, N. Nonomura, and A. Okuyama, “Atorvastatin inhibits renal crystal retention in a rat stone forming model,” Journal of Urology, vol. 180, no. 5, pp. 2212–2217, 2008.
[35]
K. Fong-Ngern, P. Peerapen, S. Sinchaikul, S.-T. Chen, and V. Thongboonkerd, “Large-scale identification of calcium oxalate monohydrate crystal-binding proteins on apical membrane of distal renal tubular epithelial cells,” Journal of Proteome Research, vol. 10, no. 10, pp. 4463–4477, 2011.
[36]
K. G. Christmas, L. B. Gower, S. R. Khan, and H. El-Shall, “Aggregation and dispersion characteristics of calcium oxalate monohydrate: effect of urinary species,” Journal of Colloid and Interface Science, vol. 256, no. 1, pp. 168–174, 2002.
[37]
J.-M. Ouyang, S.-P. Deng, J.-P. Zhong, B. Tieke, and S.-H. Yu, “Crystallization of calcium oxalate monohydrate at dipalmitoylphosphatidylcholine monolayers in the presence of chondroitin sulfate A,” Journal of Crystal Growth, vol. 270, no. 3-4, pp. 646–654, 2004.
[38]
J.-M. Ouyang, M. Wang, P. Lu, and J. Tan, “Degradation of sulfated polysaccharide extracted from algal Laminaria japonica and its modulation on calcium oxalate crystallization,” Materials Science and Engineering C, vol. 30, no. 7, pp. 1022–1029, 2010.
[39]
A. Hesse, H. Wuzel, and W. Vahlensieck, “Significance of glycosaminoglycans for the formation of calcium oxalate stones,” American Journal of Kidney Diseases, vol. 17, no. 4, pp. 414–419, 1991.
[40]
J.-M. Ouyang , “Chemical basis in the investigation of calcium oxalate stones,” Chemistry, vol. 65, no. 5, pp. 326–332, 2002.
[41]
B. Fellstom, U. Backman, B. Danielson, and B. Wikstr？m, “Treatment of renal calcium stone disease with the synthetic glycosaminoglycan pentosan polysulphate,” World Journal of Urology, vol. 12, no. 1, pp. 52–54, 1994.
[42]
S.-S. Zhang, G.-D. Liu, and J.-Y. He, “The experimental result and clinical observation of Sterculia lychnophora Hance inhibiting the formation of calcium oxalate crystals,” Chinese Journal of Urology, vol. 17, pp. 51–53, 1996.
[43]
X.-L. Kang, J.-Y. He, Y.-R. Chen, and G.-D. Liu, “The effect of wuIing powder on inhibition of calcium oxalate crystallization and urinary GAGs excretion,” Chinese Journal of Urology, vol. 12, no. 3, pp. 227–230, 1991.
