Measurement of plasma F-2-isoprostanes as an index of lipid peroxidation does not appear to be confounded by diet

F-2-isoprostanes (F-2-IPs) are formed by the free radical-catalysed oxidati on of arachidonic acid. The measurement of F-2-IPs, especially 8-epi-PGF(2 alpha), is recognised as a reliable marker of lipid peroxidation and is cur rently used as a sensitive index of oxidative stress in vivo. The majority of 8-epi-PGF(2 alpha) present in the circulation occurs in association with lipoproteins which are synthesised in the liver. Since lipoproteins are de rived from dietary fatty acids and triglycerides, it is possible that 8-epi -PGF(2 alpha) generated in polyunsaturated fatty acid-rich food (during ini tial processing/packaging or during meal preparation) may become incorporat ed within these lipoproteins during synthesis. In view of the growing use o f 8-epi-PGF(2 alpha) as a marker of lipid peroxidation in vivo in nutrition al or clinical studies, it is therefore important to investigate the possib ility that the circulating levels measured could be confounded by the prese nce of 8-epi-PGF(2 alpha) in food. in this study we evaluated the levels of 8-epi-PGF(2 alpha) present in several popular fast-foods, using a combinat ion of solid phase extraction and gas chromatography-mass spectrometry Fast -foods were selected to represent meals prepared from vegetable-, chicken-, fish- and meat-derived ingredients. Total (free + esterified) 8-epi-PGF(2 alpha) levels ranged from 0.09 to 0.73 pmol/g (122-644 pmol/mmol arachidoni c acid), with the highest lea els present in beef-derived meals. Further in vestigation of hamburgers and cheeseburgers revealed 8-epi-PGF(2 alpha) lev els 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 postp randial contribution to plasma 8-epi-PGF(2 alpha) levels following ingestio n of 100 g portions of these fast-foods would therefore be expected to be n o greater than the low picomole range, and would be unlikely to influence t he normal endogenous levels of 8-epi-PGF(2 alpha) and those produced during oxidative stress.