Abstract
The most serious complication after ingestion of a toxic dose of acetaminophen is liver damage. The aim of study was to review the research on the biochemical and molecular mechanisms of acetaminophen hepatotoxicity. It was shown that effect of the acetaminophen metabolism is the production of N-acetyl-p-benzoquinone, which is formed by bioactivation with the participation of cytochrome P450 enzymes. The combination of N-acetyl-p-benzoquinone and proteins can cause a disruption in protein homeostasis in cell membrane and mitochondrion. It may interfere with cellular signal process. Small and chronic doses of acetaminophen lead to damage of the cell nucleus. These effects can explain the mechanism of hepatotoxicity. N- acetyl- pbenzoquinone can cause an increase in oxidative stress. Lipids peroxidation and proteins oxidation are the main factors, which lead to necrosis of hepatocytes. It was shown that N-acetyl-p-benzoquinone can cause a decrease in GSH level and SH groups. For this reason, N-acetyl-p-benzoquinone was recognized as a key factor of the acetaminophen hepatotoxicity.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
