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Related Experiment Videos

Gamma-glutamyltransferase release by the post ischemic kidney: multiple forms and cellular pH.

T C Welbourne, T Phifer, M Thomas

    Life Sciences
    |September 19, 1983
    PubMed
    Summary

    Following kidney ischemia, gamma-glutamyltransferase release shifts from membrane-bound to soluble forms. This change, linked to cellular recovery, may serve as a clinical indicator of kidney health.

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    Area of Science:

    • Nephrology
    • Biochemistry
    • Cell Biology

    Background:

    • Kidney ischemia can lead to cellular damage and altered enzyme release.
    • Gamma-glutamyltransferase (GGT) is a key enzyme found in renal tubule cells.
    • Understanding GGT release dynamics is crucial for assessing kidney injury and recovery.

    Purpose of the Study:

    • To investigate the release patterns and forms of gamma-glutamyltransferase (GGT) from renal tubule cells after ischemia-reperfusion.
    • To determine the relationship between GGT release, cellular conditions (pH, ATP), and its physical state (membrane-bound vs. soluble).
    • To explore the potential of GGT excretion forms as a clinical biomarker for kidney injury and recovery.

    Main Methods:

    • In situ study of gamma-glutamyltransferase (GGT) release from renal tubule cells following 30 minutes of ischemia.

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  • Measurement of GGT levels in kidney tissue and urine during a 30-minute reflow period.
  • Analysis of the enzyme's form (membrane-bound vs. soluble) in kidney and urine samples.
  • Correlation of GGT changes with cellular pH, urinary pH, and ATP levels.
  • In vitro alkalinization of renal homogenates to assess its effect on soluble GGT.

    • Main Results:

    • Kidney GGT levels decreased by 33% after 15 minutes of reflow, with minimal urinary recovery (1.2%) and no renal vein release.
    • Initially, GGT was predominantly membrane-bound in both kidney and urine.
    • Over subsequent reflow, renal GGT continued to decline, with 5% of the loss excreted in urine.
    • A shift to a soluble GGT form occurred, coinciding with cellular alkalosis, urinary alkalinization, and increased ATP levels.
    • Alkalinization of renal homogenates doubled the amount of soluble GGT.

    Conclusions:

    • Immediate GGT loss post-ischemia involves cellular uptake or urinary release, with cellular uptake being dominant.
    • The later appearance of soluble GGT suggests intracellular alkaline proteinase activity and exocytosis during cellular recovery.
    • The form of excreted GGT (membranous vs. soluble) may serve as a valuable clinical index for differentiating cellular necrosis from cellular recovery.