HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: M200312-JLR200v1 44/1/118    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Berge, K. Articles by Berge, R. K. Search for Related Content PubMed PubMed Citation Articles by Berge, K. Articles by Berge, R. K. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 44, 118-127, January 2003
Copyright © 2003 by Lipid Research, Inc.

Impact of mitochondrial ß-oxidation in fatty acid-mediated inhibition of glioma cell proliferation

Kjetil Berge^1,*, Karl Johan Tronstad^*, Pavol Bohov^*,, Lise Madsen^* and Rolf K. Berge^*

^* Department of Clinical Biochemistry, Haukeland Hospital, University of Bergen, N-5021 Bergen, Norway
Institute of Experimental Endocrinology, Slovak Academy of Sciences, SK-83101 Bratislava, Slovak Republic

¹ To whom correspondence should be addressed. e-mail: kjetil.berge{at}ikb.uib.no

Tetradecylthioacetic acid (TTA), which cannot be ß-oxidized, exerts growth-limiting properties in glioma cells. In order to investigate the importance of modulated lipid metabolism and alterations in mitochondrial properties in this cell death process, we incubated glioma cells both with TTA and the oxidizable fatty acid palmitic acid (PA), in the presence of L-carnitine and the carnitine palmitoyltransferase inhibitors etomoxir and aminocarnitine. L-carnitine partly abolished the PA-mediated growth reduction of glioma cells, whereas etomoxir and aminocarnitine enhanced the antiproliferative effect of PA. The production of acid-soluble products increased and the incorporation of PA into glycerolipids decreased after L-carnitine supplementation. L-carnitine was found to enhance the antiproliferative effect of TTA, but did not affect the incorporation of TTA into glycerolipids, or ceramide. PDMP, sphingosine 1-phosphate, desipramine, fumonisin B₁, and L-cycloserine were able not to rescue the glioma cells from PA and TTA-induced growth inhibition, suggesting that increased ceramide production is not important in the growth reduction. TTA-mediated growth inhibition was accompanied with an increased uptake of PA and increased incorporation of PA into triacylglycerol (TG).

Our data suggest that mitochondrial functions are involved in fatty acid-mediated growth inhibition. Whether there is a causal relationship between TG accumulation and the apoptotic process remains to be determined.

Abbreviations: CPT, carnitine palmitoyltransferase; _m, mitochondrial membrane potential; PA, palmitic acid; PL, phospholipid; TG, triacylglycerol; TTA, tetradecylthioacetic acid

Supplementary key words triacylglycerol • phospholipids • fatty acid oxidation • growth regulation • apoptosis • tetradecylthioacetic acid • palmitic acid • ceramide

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				M. F. Cury-Boaventura, R. Gorjao, T. M. de Lima, T. M. Piva, C. M. Peres, F. G. Soriano, and R. Curi Toxicity of a Soybean Oil Emulsion on Human Lymphocytes and Neutrophils JPEN J Parenter Enteral Nutr, March 1, 2006; 30(2): 115 - 123. [Abstract] [Full Text] [PDF]

				K. Ravnskjaer, M. Boergesen, B. Rubi, J. K. Larsen, T. Nielsen, J. Fridriksson, P. Maechler, and S. Mandrup Peroxisome Proliferator-Activated Receptor {alpha} (PPAR{alpha}) Potentiates, whereas PPAR{gamma} Attenuates, Glucose-Stimulated Insulin Secretion in Pancreatic {beta}-Cells Endocrinology, August 1, 2005; 146(8): 3266 - 3276. [Abstract] [Full Text] [PDF]