The role of xanthine oxidase in ischemia/reperfusion damage of rat liver

Histol Histopathol. 1995 Jan;10(1):111-6.

Abstract

Oxygen radicals have been proposed to be involved in the induction of liver cell damage during reperfusion after ischemia. The role of xanthine oxidase in this process and the potential of the antioxidant system have been studied in a model of in vivo ischemia of rat liver followed by 1 h reperfusion by the use of enzyme histochemistry. Based on decreased lactate dehydrogenase activity in certain areas of liver parenchyma, cell damage could already be detected at 1 h reperfusion after ischemia. Incubations performed on serial sections showed that the same areas contained decreased activities of xanthine oxidoreductase, xanthine oxidase, catalase and glucose-6-phosphate dehydrogenase. Some individual cells in the undamaged liver parenchyma expressed a very high glucose-6-phosphate dehydrogenase, which suggests that these cells have a good defence against oxidative stress. It is concluded that oxygen radicals derived from xanthine oxidase do not play a decisive role in the induction of cell damage immediately at reperfusion after ischemia. However, it cannot be excluded that xanthine oxidase present in the blood stream can give rise to the development of additional damage later on.

MeSH terms

  • Animals
  • Disease Models, Animal
  • Glucosephosphate Dehydrogenase / metabolism
  • Histocytochemistry
  • Kupffer Cells / enzymology
  • Kupffer Cells / pathology
  • L-Lactate Dehydrogenase / metabolism
  • Liver / enzymology*
  • Liver / injuries*
  • Liver / pathology
  • Male
  • Monocytes / enzymology
  • Monocytes / pathology
  • Oxidative Stress
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / metabolism
  • Reperfusion Injury / enzymology*
  • Reperfusion Injury / pathology
  • Xanthine Oxidase / metabolism*

Substances

  • Reactive Oxygen Species
  • L-Lactate Dehydrogenase
  • Glucosephosphate Dehydrogenase
  • Xanthine Oxidase