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Original Article

Measurement of plasma F2-isoprostanes as an index of lipid peroxidation does not appear to be confounded by diet

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Pages 115-127 | Received 26 Aug 1999, Published online: 07 Jul 2009
 

Abstract

F2-isoprostanes (F2-IPs) are formed by the free radicalcatalysed oxidation of arachidonic acid. The measurement of F2-IPs, especially 8-epi-PGF, is recognised as a reliable marker of lipid peroxidation and is currently used as a sensitive index of oxidative stress in vivo. The majority of 8-epi-PGF present in the circulation occurs in association with lipoproteins which are synthesised in the liver. Since lipoproteins are derived from dietary fatty acids and triglycerides, it is possible that 8-epi-PGF generated in polyunsaturated fatty acid-rich food (during initial processing/packaging or during meal preparation) may become incorporated within these lipoproteins during synthesis. In view of the growing use of 8-epi-PGF as a marker of lipid peroxidation in vivo in nutritional or clinical studies, it is therefore important to investigate the possibility that the circulating levels measured could be confounded by the presence of 8-epi-PGF in food. In this study we evaluated the levels of 8-epi-PGF present in several popular fastfoods, using a combination of solid phase extraction and gas chromatography-mass spectrometry. Fastfoods were selected to represent meals prepared from vegetable-, chicken-, fish- and meat-derived ingredients. Total (free + esterified) 8-epi-PGF levels ranged from 0.09 to 0.73 pmol/g (122–644 pmol/mmol arachidonic acid), with the highest levels present in beef-derived meals. Further investigation of hamburgers and cheeseburgers revealed 8-epi-PGF levels of 1.83 ± 0.24 and 0.84 ± 0.03 nmol/mmol arachidonic acid, respectively. Lower concentrations of vitamin E were found in the hamburgers. The postprandial contribution to plasma 8-epi-PGF levels following ingestion of 100 g portions of these fast-foods would therefore be expected to be no greater than the low picomole range, and would be unlikely to influence the normal endogenous levels of 8-epi-PGF, and those produced during oxidative stress.

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