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Updated: May 30, 2026

Partial Lobular Hepatectomy: A Surgical Model for Morphologic Liver Regeneration

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Published on: May 31, 2018

Paracetamol hepatotoxicity and microsomal function.

R Kaushal¹, K R Dave, S S Katyare

¹Department of Biochemistry, Faculty of Science, M.S. University of Baroda, Vadodara, Gujarat 390002, India.

Environmental Toxicology and Pharmacology

|July 26, 2011

Summary

This summary is machine-generated.

Paracetamol overdose in rats impairs microsomal function by altering enzyme activity and membrane composition. This leads to increased membrane fluidity and reduced sulfhydryl groups, indicating cellular damage.

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An Intestine/Liver Microphysiological System for Drug Pharmacokinetic and Toxicological Assessment

An Intestine/Liver Microphysiological System for Drug Pharmacokinetic and Toxicological Assessment

Published on: December 3, 2020

Area of Science:

Biochemistry
Toxicology
Cell Biology

Background:

Paracetamol (acetaminophen) is a common analgesic with known hepatotoxicity at high doses.
Microsomal function is crucial for cellular metabolism and detoxification processes.
Understanding paracetamol's effects on microsomes is vital for managing overdose toxicity.

Purpose of the Study:

To investigate the impact of paracetamol-induced hepatotoxicity on rat liver microsomal function.
To analyze alterations in enzyme kinetics, membrane lipid composition, and membrane fluidity.

Main Methods:

Rats were administered a hepatotoxic dose of paracetamol (650 mg/kg).
Microsomal fractions were isolated and analyzed for Na(+),K(+)-ATPase activity, V(max), and temperature kinetics.
Lipid peroxidation, phospholipid, and cholesterol content were quantified.
Changes in specific phospholipids, lysophosphoglycerides, and sulfhydryl groups were assessed.

Main Results:

Paracetamol significantly reduced Na(+),K(+)-ATPase activity and V(max) in component II.
Microsomal membrane fluidity increased, with a 50% decrease in acidic phospholipids (phosphatidylserine, phosphatidylinositol) and a 12-fold increase in lysophosphoglycerides.
Sphingomyelin content increased reciprocally.
A significant reduction in sulfhydryl groups was observed, while lipid peroxidation remained unchanged.

Conclusions:

Paracetamol-induced hepatotoxicity alters rat liver microsomal function.
Changes in phospholipid composition lead to increased membrane fluidity and impaired enzyme activity.
Reduced sulfhydryl groups suggest oxidative stress or direct interaction with paracetamol metabolites.