This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Canuto, R. A. Articles by Dianzani, M. U. Search for Related Content PubMed PubMed Citation Articles by Canuto, R. A. Articles by Dianzani, M. U.

Lipid Peroxidation in Rat AH-130 Hepatoma Cells Enriched in Vitro with Arachidonic Acid¹

Department of Experimental Medicine and Oncology, University of Turin, Corso Raffaello 30, 10125 Turin, Italy

Tumor cells generally display low lipid peroxidation. A low content of polyunsaturated fatty acids in membrane phospholipids is a possible cause of their decreased susceptibility to lipid peroxidation.

To investigate the importance of substrate availability in eliciting lipid peroxidation and to study cell viability in conditions of stimulated lipid peroxidation, AH-130 hepatoma cells were enriched with arachidonic acid. The enriched hepatoma cells showed increased mortality correlated with the increased incorporation of arachidonic acid in membrane phospholipids. When 0.5 mM arachidonic acid was added to hepatoma cells, this fatty acid reached a percentage content similar to that found in hepatocytes.

Hepatoma cells enriched with this concentration were further incubated to determine their susceptibility to lipid peroxidation; mortality increased in parallel with increased thiobarbituric acid-reactive substance production. The highest mortality was in hepatoma cells treated with ascorbate/FeSO₄. Mortality in normal cells was low, although they had a high production of thiobarbituric acid-reactive substances. The high capability of normal cells to metabolize the products of lipid peroxidation might explain the different viabilities of normal cells and hepatoma cells.

It may therefore be possible to modify the composition of fatty acids of hepatoma cells in order to sensitize them to the toxic effect of prooxidant agents.

¹ This study was supported by a grant from the Ministry for University, Scientific and Technological Research, Rome, Italy.

² To whom requests for reprints should be addressed.

Received 2/20/90. Accepted 6/18/91.

This article has been cited by other articles:

				D. Siegel, E. M. Bolton, J. A. Burr, D. C. Liebler, and D. Ross The Reduction of alpha -Tocopherolquinone by Human NAD(P)H:Quinone Oxidoreductase: The Role of alpha -Tocopherolhydroquinone as a Cellular Antioxidant Mol. Pharmacol., August 1, 1997; 52(2): 300 - 305. [Abstract] [Full Text]

				Q. Chen, M. Galleano, and A. I. Cederbaum Cytotoxicity and Apoptosis Produced by Arachidonic Acid in Hep G2 Cells Overexpressing Human Cytochrome P4502E1 J. Biol. Chem., June 6, 1997; 272(23): 14532 - 14541. [Abstract] [Full Text] [PDF]