1. Oxidative stress in a novel model of chronic acidosis in LLC-PK1 cells.
- Author
-
Rustom R, Wang B, McArdle F, Shalamanova L, Alexander J, McArdle A, Thomas CE, Bone JM, Shenkin A, and Jackson MJ
- Subjects
- Acids pharmacology, Ammonia metabolism, Animals, Biomarkers analysis, Cell Division drug effects, Cell Survival drug effects, Chaperonin 60 metabolism, Chronic Disease, Epithelial Cells cytology, Epithelial Cells drug effects, Glutathione metabolism, Glutathione Peroxidase metabolism, HSC70 Heat-Shock Proteins, HSP70 Heat-Shock Proteins metabolism, Hydrogen-Ion Concentration, Kidney cytology, Kidney drug effects, LLC-PK1 Cells, Models, Biological, Permeability drug effects, Proteins metabolism, Sulfhydryl Compounds metabolism, Swine, Acidosis metabolism, Epithelial Cells metabolism, Kidney metabolism, Oxidative Stress
- Abstract
Chronic metabolic acidosis occurs commonly in chronic renal failure (CRF). The proximal renal tubular cell is the site in the kidney of high oxidative metabolic activity and in CRF is associated with adaptive hypertrophy and hypermetabolism. We hypothesised that chronic acidosis may lead to increased generation of reactive oxygen species due to increased oxidative activity. We developed a novel model of chronic acidosis in LLC-PK1 cells and measured markers of oxidative stress and metabolism. Acidosis led to a reduction in cellular total glutathione and protein thiol content and an increase in glutathione peroxidase activity and NH3 generation. The expression of constitutively expressed heat stress protein (HSP) HSC70 and HSP60 increased at pH 7.0., (Copyright 2003 S. Karger AG, Basel)
- Published
- 2003
- Full Text
- View/download PDF