Effect of aging on intestinal ischemia and reperfusion injury

Pritesh C. Shah, Robert E. Brolin, Peter S. Amenta, Devendra R. Deshmukh

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Intestinal ischemia/reperfusion (I/R) is a serious disorder that is prevalent in elderly patients. Reactive oxygen species are implicated in the pathogenesis of intestinal I/R injury. Reactive oxygen species are also implicated in cellular senescence and aging. To test the hypothesis that aging exacerbates intestinal I/R injury, the effects of intestinal I/R on tissue injury were compared between young (3 month old) and aged (12 month old) mice. Intestinal ischemia was induced by occluding the superior mesenteric artery with a microbulldog clamp. Reperfusion was initiated by removing the clamp. Mortality due to intestinal ischemia followed by reperfusion was significantly higher in aged mice. There were no differences in the baseline levels of malondialdehyde or myeloperoxidase activity (indicators of lipid peroxidation and neutrophil infiltration, respectively) between young and aged mice. Although intestinal I/R caused a significant increase in malondialdehyde levels and myeloperoxidase activity in aged mice, similar increases were also observed in young mice. There were no significant differences in the activities of antioxidant enzymes including superoxide dismutase, glutathione peroxidase and catalase between young and aged mice that underwent sham operation. Intestinal I/R caused a significant decrease in catalase activity only in aged mice. In conclusion, our results indicate that aged mice are more susceptible to mortality due to intestinal I/R and that an age-dependent decrease in catalase activity may contribute to the observed mortality.

Original languageEnglish (US)
Pages (from-to)37-50
Number of pages14
JournalMechanisms of Ageing and Development
Volume107
Issue number1
DOIs
StatePublished - Feb 1 1999
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Aging
  • Developmental Biology

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