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Oxidative stress in a novel model of chronic acidosis in LLC-PK1 cells.

作者信息

Rustom Rana, Wang Bohan, McArdle Frank, Shalamanova Liliana, Alexander John, McArdle Anne, Thomas Carol E, Bone J Michael, Shenkin Alan, Jackson Malcolm J

机构信息

Department of Medicine, Liverpool University, Liverpool, UK.

出版信息

Nephron Exp Nephrol. 2003;95(1):e13-23. doi: 10.1159/000073019.

DOI:10.1159/000073019
PMID:14520010
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.

摘要

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