The effect of glutathione content on renal function following warm ischemia

Harold C. Yang, Vincent H. Gattone, Louis F. Martin, Lee W. Grotyohann, Jay McElroy, Russell C. Scaduto

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


Reperfusion after ischemia produces tissue injury due to free radicals generated during the reflow period. Glutathione (GSH) mediates against this oxidant damage by scavenging free radicals and protecting cells against injury. In an attempt to reduce the injury caused by free radicals, rat kidneys were pretreated with GSH monoethyl ester to elevate renal GSH fivefold. Previous studies in a renal artery occlusion model showed that pretreated kidneys in comparison to untreated controls were functionally impaired as measured by glomerular filtration rate, urine flow rate, and histology. To eliminate systemic effects of the pretreatment, kidneys were subjected to a fixed period of warm ischemia but flushed of blood and transplanted into nonpretreated syngeneic recipients. As before, pretreated kidneys exhibited marked functional impairment. We conclude that (i) elevation of renal GSH with GSH monoethyl ester enhances rather than prevents renal dysfunction and (ii) the enhancement of renal ischemic injury following pretreatment is not due to nonspecific systemic effects of GSH monoethyl ester pretreatment.

Original languageEnglish (US)
Pages (from-to)633-636
Number of pages4
JournalJournal of Surgical Research
Issue number6
StatePublished - Jun 1989

All Science Journal Classification (ASJC) codes

  • Surgery


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