scholarly journals Flagellum Is Responsible for Promoting Effects of Viable Escherichia coli on Calcium Oxalate Crystallization, Crystal Growth, and Crystal Aggregation

2019 ◽  
Vol 10 ◽  
Author(s):  
Rattiyaporn Kanlaya ◽  
Orapan Naruepantawart ◽  
Visith Thongboonkerd
Keyword(s):  
Escherichia Coli ◽  
Crystal Growth ◽  
Calcium Oxalate ◽  
Calcium Oxalate Crystallization ◽  
Crystal Aggregation

Exploring the Molecular Level Interaction of Human Serum Albumin with Calcium Oxalate Monohydrate Crystals

2021 ◽  
Vol 28 ◽  
Author(s):  
Priyadarshini ◽  
Abhishek Negi ◽  
Chetna Faujdar ◽  
Lokesh Nigam ◽  
Naidu Subbarao
Keyword(s):  
Amino Acids ◽  
Crystal Growth ◽  
Human Serum Albumin ◽  
Serum Albumin ◽  
Calcium Oxalate ◽  
Human Serum ◽  
Stone Formation ◽  
Calcium Oxalate Monohydrate ◽  
Calcium Oxalate Crystallization ◽  
In Silico Docking

Background: Human serum albumin (HSA) is one of the most abundant proteins in the blood plasma, urine as well as in the organic matrix of renal calculi. Macromolecules present in the urine modulate kidney stone formation either by stimulating or inhibiting crystallization process. Objective: In the present study, effect of HSA protein on the growth of calcium oxalate monohydrate crystal (COM) was investigated. Methods: Crystal growth assay was used to measure oxalate depletion in the crystal seeded solution in the presence of HSA. HSA concentrations exhibiting effect on crystal growth were selected for FTIR and XRD analysis. In silico docking was performed on seven different binding sites of HSA. Results: Albumin is playing dual role in growth of calcium oxalate crystallization. FTIR and XRD studies further revealed HSA exerted strain over crystal thus affecting its structure by interacting with amino acids of its pocket 1. Docking results indicate that out of 7 binding pocket in protein, calcium oxalate interacts with Arg-186 and Lys-190 amino acids of pocket 1. Conclusion: Our study confirms the role of HSA in calcium oxalate crystallization where acidic amino acids arginine and lysine are binding with COM crystals, revealing molecular interaction of macromolecule and crystal in urolithiasis.

Inhibition of calcium oxalate monohydrate crystal aggregation by urine proteins

1989 ◽  
Vol 257 (1) ◽  
pp. F99-F106 ◽  
Author(s):  
B. Hess ◽  
Y. Nakagawa ◽  
F. L. Coe
Keyword(s):  
Crystal Growth ◽  
Calcium Oxalate ◽  
Renal Stones ◽  
Calcium Oxalate Monohydrate ◽  
Assay Method ◽  
Crystal Aggregation ◽  
Stone Formers ◽  
Aggregation Inhibitors ◽  
Normal Urine

Normal urine inhibits both the growth and the aggregation of calcium oxalate monohydrate (COM) crystals but the molecules that inhibit aggregation are not well defined. We have developed a spectrophotometric assay method to measure the aggregation of COM crystals in vitro under conditions that avoid simultaneous crystal growth. At pH 7.2 and 90 mM NaCl, Tamm-Horsfall glycoprotein (THP) and nephrocalcin (NC), a major urinary inhibitor of COM crystal growth, inhibit COM crystal aggregation at concentrations as low as 2 X 10(-9) and 1 X 10(-8) M, respectively. When increasing NaCl to 270 mM or lowering pH to 5.7, inhibition by both glycoproteins, but more markedly by THP, is decreased. Urinary NC from calcium oxalate renal stone formers (SF NC) and NC isolated from calcium oxalate renal stones (stone NC) both inhibit COM crystal aggregation 10-fold less than NC from normal urine. Citrate is ineffective even at millimolar concentrations. Thus THP and NC are two major inhibitors of COM crystal aggregation in normal urine; SF NC and stone NC are defective aggregation inhibitors.

Tamm-Horsfall Mucoprotein Reduces Promotion of Calcium Oxalate Crystal Aggregation Induced by Urate in Human Urine In Vitro

1994 ◽  
Vol 87 (2) ◽  
pp. 137-142 ◽  
Author(s):  
Phulwinder K. Grover ◽  
Villis R. Marshall ◽  
Rosemary L. Ryall
Keyword(s):  
Calcium Oxalate ◽  
Stone Formation ◽  
Urine Samples ◽  
Urine Specimen ◽  
Calcium Oxalate Crystal ◽  
Physiological Concentration ◽  
Calcium Oxalate Crystallization ◽  
Crystal Aggregation

1. Increasing the concentration of dissolved urate promotes calcium oxalate crystallization in urine from which Tamm-Horsfall mucoprotein, an inhibitor of calcium oxalate crystal aggregation, has almost completely been removed. This study aimed to determine whether the effect of urate could be reduced or abolished by a physiological concentration of Tamm-Horsfall mucoprotein. This was approached in two ways. 2. The effect of Tamm-Horsfall mucoprotein on calcium oxalate crystallization induced by urate was tested in ultrafiltered (10 kDa) urine samples from 10 healthy men. Tamm-Horsfall mucoprotein (35 mg/l) was added to half of each specimen, the urate concentration was increased by the addition of sodium urate solution and crystallization was induced by a standard load of oxalate. The remainder of each urine specimen was used as a control; these specimens were treated with an identical amount of urate solution, but contained no Tamm-Horsfall mucoprotein. Tamm-Horsfall mucoprotein had no effect on the urinary metastable limit or on the deposition of calcium oxalate, but significantly reduced the size of the particles precipitated. 3. The effect of increasing the urate concentration in the presence of Tamm-Horsfall mucoprotein was tested. Tamm-Horsfall mucoprotein (35 mg/l) was added to 10 ultrafiltered urine samples as before, the samples were divided, and the concentration of urate was increased in half of each specimen. Compared with the control to which no urate was added, urate significantly reduced the amount of oxalate required to induce spontaneous calcium oxalate nucleation and increased the median volume and the particle size of the material deposited. 4. It was concluded that, in vivo, (a) hyperuricosuria would encourage the formation of calcium oxalate stones by promoting calcium oxalate crystallization, (b) Tamm-Horsfall mucoprotein would not lessen the effect of urate on calcium oxalate nucleation or bulk deposition but would reduce its effect on crystal aggregation; it could therefore reduce the likelihood of stone formation in patients with hyperuricosuria.

scholarly journals Tetrazoles: calcium oxalate crystal growth modifiers

CrystEngComm ◽  
2015 ◽  
Vol 17 (13) ◽  
pp. 2675-2681 ◽  
Author(s):  
Calum J. McMulkin ◽  
Massimiliano Massi ◽  
Franca Jones
Keyword(s):  
Crystal Growth ◽  
Calcium Oxalate ◽  
Calcium Oxalate Crystal ◽  
Calcium Oxalate Crystallization

Metabolically stable tetrazole molecules are shown to impact calcium oxalate crystallization, thus tetrazoles can be used in investigating biological crystallization processes.

scholarly journals Elongation factor Tu on Escherichia coli isolated from urine of kidney stone patients promotes calcium oxalate crystal growth and aggregation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Piyawan Amimanan ◽  
Ratree Tavichakorntrakool ◽  
Kedsarin Fong-ngern ◽  
Pipat Sribenjalux ◽  
Aroonlug Lulitanond ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Crystal Growth ◽  
Calcium Oxalate ◽  
Kidney Stone ◽  
Elongation Factor ◽  
Elongation Factor Tu ◽  
Calcium Oxalate Crystal

scholarly journals Antiurolithiatic activity of Berberis asiatica by In vitro calcium oxalate crystallization methods

2020 ◽  
Vol 11 (4) ◽  
pp. 6233-6237
Author(s):  
Kishore Bandarapalle ◽  
Prasanna Raju Yalavarthi ◽  
Chandra Sekhar Kothapalli Bannoth
Keyword(s):  
Crystal Growth ◽  
Calcium Oxalate ◽  
Positive Control ◽  
Primary Objective ◽  
Crystal Nucleation ◽  
Standard Drug ◽  
Crystal Aggregation ◽  
Ic50 Values ◽  
Growth Assay

The primary objective of this research was to investigate the antiurolithiatic effect of the aqueous Heartwood extract of Berberis asiatica (AEBA) on in vitro crystallization methods. The antiurolithiatic behaviour was carried out in the presence and absence of AEBA at the concentration range of 100-1000 μg/ml by employing crystal nucleation, crystal aggregation, and crystal growth assay methods. Standard drug Cystone was made use of positive control in the concentration range of 100-1000 μg/ml. Inhibition efficiency of AEBA on crystal nucleation, crystal aggregation and crystal growth was spectrophotometrically validated. The percentage inhibition rate of crystal nucleation, crystal aggregation and crystal growth by AEBA and standard drug cystone was endorsed to be dose-dependent in nature. The half maximal inhibitory concentration (IC50) values of standard drug cystone on crystal nucleation, crystal aggregation and crystal growth were estimated to be 415.30±21.35, 573.7±65.53 and 566.20±62.06 μg/ml, respectively, while the AEBA, IC50 values were reckoned to be 839±69.13, 927.10±69.98 and 851±86.60 μg/ml, respectively. The findings of in vitro crystallization study disclosed that an aqueous Heartwood extract of Berberis asiatica possesses calcium oxalate crystal inhibition activity on crystal nucleation, crystal aggregation, and crystal growth recommended it as a potent and promising antiurolithiatic activity.

scholarly journals Escherichia coli Aggravates Calcium Oxalate Stone Formation via PPK1/Flagellin-Mediated Renal Oxidative Injury and Inflammation

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Lingyue An ◽  
Weizhou Wu ◽  
Shujue Li ◽  
Yongchang Lai ◽  
Dong Chen ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Calcium Oxalate ◽  
Stone Formation ◽  
Bacterial Species ◽  
Oxidative Injury ◽  
Wild Type ◽  
E Coli ◽  
Crystal Aggregation ◽  
Stone Formers

Escherichia coli (E. coli) is closely associated with the formation of kidney stones. However, the role of E. coli in CaOx stone formation is not well understood. We explored whether E. coli facilitate CaOx stone formation and its mechanism. Stone and urine cultures were reviewed from kidney stone formers. The ability of calcium oxalate monohydrate (COM) aggregation was detected to evaluate the influence of uropathogenic E. coli, then gel electrophoresis and nanoLC-MS/MS to detect the crystal-adhered protein. Flagellin (Flic) and polyphosphate kinase 1 (PPK1) were screened out following detection of their role on crystal aggregation, oxidative injury, and inflammation of HK-2 cell in vitro. By transurethral injection of wild-type, Ppk1 mutant and Flic mutant strains of E. coli and intraperitoneally injected with glyoxylate in C57BL/6J female mice to establish an animal model. We found that E. coli was the most common bacterial species in patients with CaOx stone. It could enhance CaOx crystal aggregation both in vitro and in vivo. Flagellin was identified as the key molecules regulated by PPK1, and both of them could facilitate the crystal aggregation and mediated HK-2 cell oxidative injury and activated the inflammation-related NF-κB/P38 signaling pathway. Wild-type strain of E. coli injection significantly increased CaOx deposition and enhanced oxidative injury and inflammation-related protein expression, and this effect could be reversed by Ppk1 or Flic mutation. In conclusion, E. coli promotes CaOx stone formation via enhancing oxidative injury and inflammation regulated by the PPK1/flagellin, which activated NF-κB/P38 pathways, providing new potential drug targets for the renal CaOx calculus precaution and treatment.

Urine osmolality predicts calcium-oxalate crystallization risk in patients with recurrent urolithiasis

Urolithiasis ◽  
2021 ◽  
Author(s):  
Stavros A. Kavouras ◽  
Hyun-Gyu Suh ◽  
Marion Vallet ◽  
Michel Daudon ◽  
Andy Mauromoustakos ◽  
...  
Keyword(s):  
Calcium Oxalate ◽  
Urine Osmolality ◽  
Calcium Oxalate Crystallization ◽  
Crystallization Risk
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