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
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acidosis / metabolism*
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Acids / pharmacology
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Ammonia / metabolism
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Animals
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Biomarkers / analysis
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Cell Division / drug effects
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Cell Survival / drug effects
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Chaperonin 60 / metabolism
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Chronic Disease
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Epithelial Cells / cytology
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Epithelial Cells / drug effects
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Epithelial Cells / metabolism*
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Glutathione / metabolism
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Glutathione Peroxidase / metabolism
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HSC70 Heat-Shock Proteins
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HSP70 Heat-Shock Proteins / metabolism
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Hydrogen-Ion Concentration
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Kidney / cytology
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Kidney / drug effects
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Kidney / metabolism*
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LLC-PK1 Cells
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Models, Biological
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Oxidative Stress*
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Permeability / drug effects
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Proteins / metabolism
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Sulfhydryl Compounds / metabolism
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Swine
Substances
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Acids
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Biomarkers
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Chaperonin 60
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HSC70 Heat-Shock Proteins
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HSP70 Heat-Shock Proteins
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Proteins
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Sulfhydryl Compounds
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Ammonia
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Glutathione Peroxidase
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Glutathione