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L C Cao

Publications and source records attributed to L C Cao.

27 records · Page 2Linked to original sources
PubMed1993

An ultrastructural study of experimentally induced microliths in rat proximal and distal tubules.

Calcium oxalate stone formation was induced in rats by oral application of ethylene glycol and ammonium chloride for 4, 8 and 24 days. After each induction period, light-microscopically, birefringent crystals were seen in the tubular lumen and, intracellularly, in proximal and distal tubular cells. After a postfixation which partially removed the crystalline material crystal ghosts were seen by electron microscopy. In the lumen, crystal ghosts were observed ranging from single crystals to crystal agglomerates. The large intraluminal agglomerates were surrounded by epithelial cells and cellular debris. Both crystal types had an organic interior. In the cytoplasm of ultrastructurally changed proximal tubular cells, small (200 to 600 nm. in diameter) single crystal ghosts were present in the terminal web at the basis of the microvilli. Others were present in large vacuolar structures, with a fine granular matrix. After the prolonged microlith induction periods, such vacuolar structures were seen throughout the cell. The organic matrix of the crystal ghosts therein had acquired a more aggregated and complex structure.

Ammonium Chloride↗
PubMed1993

Electron energy-loss spectroscopical and image analysis of experimentally induced rat microliths. II.

Following a microlith-inducing diet of ethylene glycol plus ammonium chloride, intraluminal and intracellular crystals are observed in aldehyde-fixed rat proximal and distal tubule cells by light and electron microscopy. Qualitative, in-situ analysis with electron-probe X-ray microanalysis (EPMA) of these intraluminal and intracellular crystals shows the presence of calcium, a trace of magnesium, some chlorine and the virtual absence of phosphorus and sulphur. Electron energy-loss spectroscopical element (EELS) analysis and electron-spectroscopic imaging (ESI) confirm, at both sites, the presence of calcium. Selected area electron diffraction (a) confirmed the crystallinity of both the intracellular and intraluminal crystals; (b) produced identical diffractograms from intracellular crystals in proximal tubule cells and deliberately internalized exogenous COM-crystals in cultured LLC-PK1 cells and (c) produced mean dhkl-values, identical to the dhkl-values from calcium oxalate monohydrate (14-771) in the ASTM index, from 4 different intracellular crystals in proximal-tubule cells.

Ammonium Chloride↗
PubMed1993

Absence of a transcellular oxalate transport mechanism in LLC-PK1 and MDCK cells cultured on porous supports.

Transepithelial oxalate transport across polarized monolayers of LLC-PK1 cells, grown on collagen-coated microporous membranes in Transwell culture chambers, was studied in double-label experiments using [14C]-oxalate together with [3H]-D-mannitol as an extracellular marker. The [14C]-labeled glucose analog alpha-methyl-glucoside (alpha-MG) was used as functional marker for active proximal tubular sugar transport. Cellular uptake of oxalate and alpha-MG at both the apical and basolateral plasma membrane was determined. When added to the upper compartment, alpha-MG was actively taken up at the apical membrane, directed through the cells to the basolateral membrane and transported to the lower compartment, indicating functional epithelial sugar transport by LLC-PK1 cells. In LLC-PK1 cells, the uptake of alpha-MG at the apical membrane was approximately 50 times higher than that at the basolateral membrane. In contrast to this active transport of sugar, LLC-PK1 cells did not demonstrate oxalate uptake either at the apical or basolateral plasma membrane. The apical-to-basolateral (A- > B) flux of oxalate in LLC-PK1 cells was identical to the basolateral-to-apical (B- > A) oxalate flux in these cells. Moreover these flux characteristics were similar to those found for D-mannitol, indicating paracellular movement for both compounds. From these data, it is concluded that, under the experimental conditions used, LLC-PK1 cells do not exhibit a specific transcellular transport system for oxalate.

Animals↗
PubMed1993

A review of new concepts in renal stone research.

Clinical and basic research in the field of urolithiasis has developed rapidly in recent years. Progress in extracorporeal shock wave lithotripsy (ESWL) and percutaneous nephrolithotomy (PNL) has brought about a revolution in the surgical treatment of urolithiasis and research at the cellular and molecular level is now expanding. In spite of these advances, however, clinical treatment of urolithiasis remains far from satisfactory. Stone recurrence in many patients cannot be predicted and is beyond control of urologists mainly because the mechanisms of stone formation are still not fully understood. It is necessary to study the process of stone-formation more intensely at the cellular and molecular level, and to strengthen the links between basic and clinical research in the field. In this review, the processes involved in the formation of stones are compared with those involved in normal bio-mineralization and a model of urolithiasis is put forward based on modern systems science. Attention is concentrated on: (a) Directions of research based on physico-chemical theories of stone formation; (b) The role of renal tubular defects in urolithiasis; (c) The role of free radical reactions in stone formation; and (d) Macromolecular abnormalities and their correction.

Biological Transport, Active↗
PubMed1992

The effect of two new semi-synthetic glycosaminoglycans (G871, G872) on the zeta potential of calcium oxalate crystals and on growth and agglomeration.

The effects of two new semisynthetic glycosaminoglycans (GAGs), G871 and G872, on the crystal growth and agglomeration of calcium oxalate monohydrate (COM) were studied in artificial urine in vitro. A constant composition crystallization system and a seeded crystal growth system were used to measure the rate of crystal growth and degree of agglomeration. The zeta potential on the crystal surface was measured using a Coulter DELSA 440 doppler electrophoretic light scattering analyzer. The previously reported GAG analogue, sodium pentosan polysulphate (SPP or SP54), was studied as a reference inhibitor of crystallization using the same systems. All three substances had a concentration-dependent effect on the zeta potential and on the rate of crystal growth and agglomeration of COM in artificial urine. G872 had a significantly greater effect than either G871 or SPP on all the measured parameters. It is suggested that semisynthetic GAGs, such as those reported in this paper may be of use in the prevention of the recurrence of calcium oxalate stones.

Calcium Oxalate↗
PubMedDate not supplied

Oxalate-induced redistribution of phosphatidylserine in renal epithelial cells: implications for kidney stone disease.

AIMS: The present studies assessed the possibility that exposure to oxalate leads to alterations in membrane structure that promote crystal binding to renal epithelial cells. Specifically, we determined whether oxalate exposure produces a redistribution of membrane phosphatidylserine (PS) and an increase in the binding of (14)C-oxalate crystals to renal epithelial cells. METHODS: PS distribution was monitored in MDCK cells and in phospholipid-containing vesicles using NBD-PS, a fluorescent derivative of PS. Superficial PS was also detected by monitoring the binding of annexin V to MDCK cells. RESULTS: Oxalate exposure rapidly increased the abundance of superficial NBD-PS and increased the binding of annexin V to MDCK cells. Oxalate exposure also increased PS at the surface of phospholipid vesicles, suggesting that oxalate may interact directly with PS. The oxalate concentrations that increased superficial PS also increased binding of (14)C-oxalate crystals to MDCK cells, and the increased crystal binding was blocked by annexin V. CONCLUSIONS: These findings provide direct evidence that oxalate exposure promotes both a redistribution of PS and an increase in crystal binding in renal epithelial cells and support the notion that oxalate toxicity may contribute to the development of stone disease by altering the properties of the renal epithelial cell membrane.

Animals↗