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Updated: Jun 20, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Gentamicin induced lipid peroxidation and its control with ascorbic acid.

Pritesh Devbhuti¹, Achintya Saha, Chandana Sengupta

¹Division of Medicinal and Pharmaceutical Chemistry, Dept. of Pharmaceutical Technology, Jadavpur University, Kolkata-700032, India. priteshdevbhuti@yahoo.co.in

Acta Poloniae Pharmaceutica

|August 26, 2009

Summary

Ascorbic acid inhibits gentamicin-induced lipid peroxidation by reducing harmful byproducts like malonyldialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE). This antioxidant action helps protect against drug-induced cellular damage.

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Published on: October 13, 2010

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Last Updated: Jun 20, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Gramicidin-based Fluorescence Assay; for Determining Small Molecules Potential for Modifying Lipid Bilayer Properties

Gramicidin-based Fluorescence Assay; for Determining Small Molecules Potential for Modifying Lipid Bilayer Properties

Published on: October 13, 2010

Area of Science:

Biochemistry
Pharmacology
Toxicology

Background:

Lipid peroxidation, the oxidative degradation of polyunsaturated fatty acids (PUFAs), is implicated in various diseases.
Reactive oxygen species (ROS) drive lipid peroxidation, producing toxic end products such as malonyldialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE).
Drug-induced lipid peroxidation is a significant source of cellular toxicity.

Purpose of the Study:

To investigate the inhibitory effect of ascorbic acid on gentamicin-induced lipid peroxidation in vivo.
To assess the impact of gentamicin and ascorbic acid co-administration on key oxidative stress markers.

Main Methods:

An in vivo study using rabbits divided into experimental groups.
Treatment with gentamicin (an aminoglycoside antibiotic) and co-administration with ascorbic acid.
Measurement of malonyldialdehyde (MDA), 4-hydroxy-2-nonenal (HNE), reduced glutathione (GSH), and nitric oxide (NO) levels in blood.

Main Results:

Gentamicin significantly increased MDA and HNE levels, indicating elevated lipid peroxidation.
Gentamicin administration led to a significant decrease in reduced glutathione (GSH) and nitric oxide (NO) levels.
Co-administration of ascorbic acid effectively inhibited the gentamicin-induced increase in MDA and HNE, and mitigated the decrease in GSH and NO.

Conclusions:

Ascorbic acid demonstrates a significant inhibitory effect against gentamicin-induced lipid peroxidation.
Ascorbic acid may serve as a protective agent against the oxidative stress caused by gentamicin toxicity.