Oxidative injury and other metabolic disorders in hepatic encephalopathy

Rom J Physiol. 1999 Jan-Jun;36(1-2):29-36.

Abstract

Within the complex mechanism of hepatic encephalopathy resulting from alcohol poisoning, a significant pathogenic role seems to relate to lipid peroxides (free radicals generated by chronic alcohol poisoning itself). Oxidative aggression is emphasized by the diminishing antioxidative capacity of the body resulting from serious liver injury brought about by chronic ethyl poisoning. The poisoning influences the whole functional capacity of the liver, hepatic protein synthesis included, which also means ceruloplasmin and siderophilin synthesis; the two latter elements make up AOS Cp-Tr which neutralizes the harmful activity of Cu and Fe excess and stimulates release of free radicals of oxygen. The purpose of our research was to study the redox balance alteration in blood in a group of patients who were in a critical condition and had been admitted to the somatic patients ward of the "Prof. Dr. Alexandru Obregia" Neurology and Psychiatry Hospital and who were suffering from hepatic encephalopathy resulting from ethyl poisoning.

MeSH terms

  • Alcoholic Intoxication
  • Alcoholism / metabolism
  • Ceruloplasmin / analysis
  • Glutathione / blood
  • Hepatic Encephalopathy / chemically induced
  • Hepatic Encephalopathy / metabolism*
  • Humans
  • Iron / blood
  • Lipid Peroxides / blood
  • Middle Aged
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism
  • Superoxide Dismutase / blood
  • Transferrin / analysis

Substances

  • Lipid Peroxides
  • Reactive Oxygen Species
  • Transferrin
  • Iron
  • Superoxide Dismutase
  • Ceruloplasmin
  • Glutathione