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Microscopic Analysis of Oxidative Stress in Cultured Cells. I. Confocal Microscopy

Published online by Cambridge University Press:  02 July 2020

Beverly E. Maleeff
Affiliation:
Department of Safety Assessment, GlaxoSmithKline, King of Prussia, PA
Tracy L. Gales
Affiliation:
Department of Safety Assessment, GlaxoSmithKline, King of Prussia, PA
Padma K. Narayanan
Affiliation:
Department of Safety Assessment, GlaxoSmithKline, King of Prussia, PA
Mark A. Tirmenstein
Affiliation:
Department of Safety Assessment, GlaxoSmithKline, King of Prussia, PA
Timothy K. Hart
Affiliation:
Department of Safety Assessment, GlaxoSmithKline, King of Prussia, PA
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Abstract

Cellular oxidative stress, a common mechanism of drug-induced toxicity, is a result of the formation of reactive oxygen species (ROS) in response to chemical stimuli. An endpoint of ROS production is lipid peroxidation, which can in turn lead to disruption of cellular membranes, loss of mitochondrial function, protein oxidation and DNA damage. This toxicity can be organ-specific due to the varying capacities of tissues to handle oxidative events. Liver is particularly sensitive to the effects of oxidative stress, and hepatic toxicity is seen clinically. HepG2 cells are an immortalized human hepatoma cell line used as an in vitro model for mammalian hepatotoxicity studies. The purpose of this study was to characterize the effects of chemically induced oxidative stress in this cultured cell model.

HepG2 cells were grown to subconfluence in poly-L-lysine coated 4-well LabTek II chambered coverglasses (Nalge Nunc International).

Type
Microscopy, Microanalysis and Imaging in the Pharmaceutical Industry (Organized by S. Samuelsson and B. Maleeff)
Copyright
Copyright © Microscopy Society of America 2001

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