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

Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego (2013-02-27)
Renata Polaniak, Rafał Jakub Bułdak, Ewa Birkner, Dorota Karbowska, Karol Ochocki, Ryszard Szkilnik
ABSTRACT

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.

MATERIALS
Product Number
Brand
Product Description

Paracetamol, European Pharmacopoeia (EP) Reference Standard
Supelco
Acetaminophen, Pharmaceutical Secondary Standard; Certified Reference Material
Sigma-Aldrich
Acetaminophen, BioXtra, ≥99.0%
Sigma-Aldrich
Acetaminophen, meets USP testing specifications, 98.0-102.0%, powder
Sigma-Aldrich
Acetaminophen, analytical standard
USP
Acetaminophen, United States Pharmacopeia (USP) Reference Standard
Supelco
Acetaminophen solution, 1.0 mg/mL in methanol, ampule of 1 mL, certified reference material, Cerilliant®