Original contribution
Evidence that the large loss of glutathione observed in ischemia/reperfusion of the small intestine is not due to oxidation to glutathione disulfide

https://doi.org/10.1016/0891-5849(93)90092-9Get rights and content

Abstract

Reperfusion injury following ischemia is thought to be the consequence of reactive oxygen species possibly generated either by xanthine oxidase activity or by processes associated with neutrophil activation in the affected organ or tissue. The conversion of xanthine dehydrogenase to the oxidase as well as the interactions between endothelium and neutrophils in the margination and activation of the latter are all considered to be results of conditions resulting from the ischemic episode. Determination of the redox status of glutathione in an ischemic/reperfused organ is frequently employed as an indicator of oxidative stress created by the production of oxygen free radicals during the reperfusion period. In this procedure, the ratio of oxidized glutathione (GSSG) to total glutathione (GSH + GSSG) is utilized to demonstrate the proportion of glutathione oxidized during reperfusion. We determined this ratio in the rat small intestine during ischemia and reperfusion and found that while the ratio of GSSG/(GSH + GSSG) does increase, this increase was the result of GSH disappearance rather than an increase in GSSG, and that essentially all of this loss occurred during the ischemic episode. We demonstrated that no oxidation of GSH occurred that was attributable to reperfusion per se; nor was there an increase of GSSG during this reoxygenation period.

References (44)

  • J.M. McCord

    Superoxide dismutase: Rationale for use in reperfusion injury and inflammation

    J. Free Radic. Biol. Med.

    (1986)
  • R.H. Turnage et al.

    Hepatocellular oxidant stress following intestinal ischemia-reperfusion injury

    J. Surg. Res.

    (1991)
  • E.J. Lesnefsky et al.

    Oxidation and release of glutathione from myocardium during early reperfusion

    Free Radic. Biol. Med.

    (1989)
  • M.W. Fariss et al.

    High-performance liquid chromatography of thiols and disulfides: Dinitrophenol derivatives

    Methods Enzymol.

    (1987)
  • H.J. Stein et al.

    Oxygen free radicals and glutathione in hepatic ischemia/reperfusion injury

    J. Surg. Res.

    (1991)
  • A. Meister

    Methods for the selective modification of glutathione metabolism and study of glutathione transport

    Methods Enzymol.

    (1985)
  • E.K. Abdalla et al.

    Arterial levels of oxidized glutathione (GSSG) reflect oxidant stress in vivo

    J. Surg. Res.

    (1990)
  • U.A. Nilsson et al.

    Detection of oxygen radicals during reperfusion of intestinal cells in vitro

    Free Radic. Biol. Med.

    (1989)
  • B.J. Zimmerman et al.

    Mechanisms of oxidant-mediated microvascular injury followng reperfusion of the ischemic intestine

    Basic Life Sci.

    (1988)
  • P.N. Rao et al.

    Purine nucleoside phosphorylase: A new marker for free oxygen radical injury to the endothelial cell

    Hepatology

    (1990)
  • J.M. McCord

    Oxygen-derived free radicals in postichemic tissue injury

    N. Engl. J. Med.

    (1985)
  • M.L. Myers et al.

    Enhancement of recovery of myocardial function by oxygen free-radical scabengers after Reversible Regional Ischemia

    Circulation

    (1985)
  • Cited by (37)

    • Protective effects of green tea on intestinal ischemia-reperfusion injury

      2011, Nutrition
      Citation Excerpt :

      It is interesting to note that although there was a mild to moderate expression of GPx in the intestinal mucosa of control sham I/R animals, the expression of GPx was negative in group I (I/R) and group II (green tea + I/R) animals. Our results are in agreement with the studies of Gibson et al. [31] who showed a large loss of glutathione in the small intestine of rats after I/R. Green tea, red wine, cocoa, olive oil, soya beans, and turmeric contain high concentrations of polyphenols, which have strong antioxidant properties.

    • Glutathione synthesis in intestinal ischaemia-reperfusion injury: effects of moderate hypothermia

      2009, Journal of Pediatric Surgery
      Citation Excerpt :

      The actions of these deleterious reactive species can be prevented by antioxidants, either those occurring naturally such as glutathione (GSH) or powerful xenobiotic antioxidants such as FeTMPyP [1,3]. Glutathione is a particularly important intracellular antioxidant that has been shown to have dramatically decreased levels in the intestine after intestinal I/R [2,4,5]. We have shown that hypothermia prevents liver bioenergetic failure and mortality during experimental intestinal I/R injury [6] and that this benefit persists even when hypothermia is applied at the time of reperfusion [7].

    • Reduced glutathione oxidation ratio and 8 ohdG accumulation by mild ischemic pretreatment

      2000, Brain Research
      Citation Excerpt :

      A representative HPLC chromatogram obtained from NEM-pretreated samples presented in the current study clearly demonstrated that a special care needs to be taken to correct for the artifactual oxidation of glutathione. It is also conceivable that GSH can decrease independently of GSSG as suggested in the rat intestine ischemia model [20]. Since changes in the total glutathione levels as well as its redox states contribute to the glutathione oxidation ratio, the degree of the glutathione oxidation ratio was employed as a measure of the ischemia-induced oxidative stress in the current study.

    View all citing articles on Scopus
    View full text