Renal epithelial cell injury and its promoting role in formation of calcium oxalate monohydrate

Abstract

The injurious effect of hydrogen peroxide (H(2)O(2)) on renal epithelial cells of the African green monkey (Vero cells) and the difference in the modulation of Vero cells on crystal growth of calcium oxalate (CaOxa) before and after injury were investigated. The degree of injury of Vero cells was proportional to the concentration and action time of H(2)O(2). After the cells had been injured, the released amount of malonaldehyde in the culture medium increased, the superoxide dismutase activity decreased, the expression quantity of osteopontin on the surface of Vero cells increased significantly, the zeta potential became more negative, and the amount of CaOxa crystals adhering to cells increased. The CaOxa crystals induced by the cells in the control group were round and blunt; however, those induced by the injured cells had irregular shapes with sharp edges and corners. As the crystallization time increased from 6 to 24 h, the size of the crystals induced by the injured cells increased accordingly, whereas that of crystals induced by the control cells did not increase significantly. The injured cells could promote the growth of CaOxa crystals and their adhesion to the cells; thus, the formation of CaOxa stones was promoted. The cells in the control group could also be injured after being incubated with supersaturated CaOxa solution for a long time, which promoted the crystallization of CaOxa. The results suggest that the retention of supersaturated CaOxa solution or CaOxa crystals in the urinary tract for a long time is a risk factor for the formation of kidney stones.

Reinjury risk of nano-calcium oxalate monohydrate and calcium oxalate dihydrate crystals on injured renal epithelial cells: aggravation of crystal adhesion and aggregation

“…36 H 2 O 2 causes various changes in renal epithelial cells, such as the increased free radical generation, increased lipid peroxidation, and the decreased cellular antioxidant status, which induces cell injury and eventual cell death. 37,38 H 2 O 2 could cause oxidative stress by reacting with transition metals, thereby damaging cell components, such as proteins, lipids, and DNA, and leading to cell death. 39 The toxic effect of H 2 O 2 has been suggested to occur via hydroxyl radicals, which are generated by the Fenton or Haber-Weiss reactions.…”

Interaction between submicron COD crystals and renal epithelial cells

“…15 The cell suspension was inoculated in suitable plates and incubated at 37°C for 24 hours, with 5% carbon dioxide and saturated humidity. After 24 hours, the media were changed to serum-free culture media and the cells were incubated for 12 hours to achieve synchronization (the total incubation time was 36 hours).…”

“…OPN expression was observed via LSM with OPN primary antibody and fluorescein isothiocyanate secondary antibody as previously described. 15 …”

Injury Difference of the Un-Aggregated and Aggregated Calcium Oxalate Monohydrate on Human Kidney Proximal Tubular Epithelial Cells

“…It had 300 amino-acid residues, among which negatively charged aspartate, serine and glutamic acid had a high proportion [9] . Therefore, OPN could not only adsorb the calcium ions in solution, but also adhere to the positively charged COM crystals [10] .…”