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Antioxidant enzyme gene expression in rats with remnant kidney induced chronic renal failure

C Van Den Branden1, B Ceyssens, D De Craemer

  • 1Department of Human Anatomy, Vrije Universiteit Brussel and Academic Hospital, Brussel, Belgium. cvdbrand@minf.vub.ac.be

Insights

Reactive oxygen intermediates impact chronic kidney disease. In rats, catalase gene expression and activity decrease during kidney failure, unlike other antioxidant enzymes, indicating its vulnerability.

Area of Science:

  • Nephrology
  • Biochemistry
  • Molecular Biology

Background:

  • Reactive oxygen intermediates (ROIs) are implicated in chronic kidney injury and glomerulosclerosis.
  • Understanding antioxidant enzyme responses is crucial for managing renal failure.

Purpose of the Study:

  • To investigate changes in renal cortex antioxidant enzyme gene expression in a rat remnant-kidney model.
  • To compare gene expression data with previously published enzyme activity data.

Main Methods:

  • Utilized Northern blot analysis to evaluate antioxidant enzyme gene expression (catalase, copper/zinc-containing superoxide dismutase, glutathione peroxidase) in rat renal cortex mRNA.
  • Compared findings with existing data on enzyme activities in the same model.

Main Results:

  • Catalase gene expression and activity decreased during the progression of renal failure and glomerulosclerosis.
  • Copper/zinc superoxide dismutase and glutathione peroxidase gene expression remained normal, though their activities showed a transient decrease.
  • Catalase appeared more susceptible to ROIs than superoxide dismutase and glutathione peroxidase.

Conclusions:

  • Antioxidant enzyme activity and gene expression do not always correlate in direction or timing during chronic kidney disease development.
  • Catalase is particularly vulnerable to oxidative stress in the remnant-kidney model.
  • Different antioxidant enzymes exhibit distinct responses to reactive oxygen intermediates in chronic renal failure.

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