[The role of paracetamol in transition reactions of alpha-nitrogen and oxidative stress in the liver]

Pol Merkur Lekarski. 2012 Dec;33(198):346-8.
[Article in Polish]


Paracetamol (Acetaminophen, PC) is metabolized in liver to N-acetyl-p-benzoquinon-imine (NAPQI), that is in turn conjugated by glutathione S-transferase with glutathione. NAPQI inhibits the respiratory chain. It may cause a 90% decrease of ATP concentration in mitochondria of hepatocytes. The oxidation of paracetamol to quinine form can also generate free radicals. Both above mentioned processes, can injure the mitochondria and cells. There have not been found in accessible literature any data dealing with paracetamol influence on the process elimination of the alpha nitrogen in the liver. The ATP concentration decline may lead to disturbances in mitochondrial enzymes. There are discrepant data of the role of free radicals in the mechanism of toxic action of paracetamol.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Acetaminophen / metabolism*
  • Acetaminophen / toxicity*
  • Adenosine Triphosphate / metabolism
  • Animals
  • Liver / drug effects
  • Liver / metabolism*
  • Mitochondria / drug effects
  • Mitochondria / metabolism
  • Nitrogen / metabolism
  • Oxidative Stress


  • Acetaminophen
  • Adenosine Triphosphate
  • Nitrogen