1998
DOI: 10.1016/s0009-3084(98)00021-8
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Lipid oxidation in unfractionated serum and plasma

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Cited by 98 publications
(70 citation statements)
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“…In vitro antiatherogenic activity was evaluated by the human plasma oxidation inhibition assay according to Schnitzer et al (1998) with minor modifications using a Spectrophotometer Lambda 25 (Perkin-Elmer, Norwalk, USA) equipped with an 8 position thermostated sample changer. Aliquots of raw and roasted pumpkin seed extracts (0.020 to 0.030 µL) were placed in UV-transparent disposable cuvettes (Brand, Wertheim, Germany) and dried under a stream of nitrogen.…”
Section: In Vitro Anti-atherogenic Activitymentioning
confidence: 99%
“…In vitro antiatherogenic activity was evaluated by the human plasma oxidation inhibition assay according to Schnitzer et al (1998) with minor modifications using a Spectrophotometer Lambda 25 (Perkin-Elmer, Norwalk, USA) equipped with an 8 position thermostated sample changer. Aliquots of raw and roasted pumpkin seed extracts (0.020 to 0.030 µL) were placed in UV-transparent disposable cuvettes (Brand, Wertheim, Germany) and dried under a stream of nitrogen.…”
Section: In Vitro Anti-atherogenic Activitymentioning
confidence: 99%
“…The oxidation of plasma lipoproteins was determined by the method of Schnitzer et al (1998). Reaction mixure (2 ml) contained 20 μl of plasma, CuCl 2 ·2H 2 O (100 μmol/l), phosphate buffer (3.3 × 10 -3 mol/l, pH 7.4).…”
Section: Oxidation Of Plasma Lipoproteinsmentioning
confidence: 99%
“…Moreover, the smoking status was not found to affect oxidation parameters by multivariate analysis; (4) most medications have been added during hospitalization, so that most of their effects should have been observed during hospitalization; specifically, statin therapy was found to carry no effect on t max by multivariate analysis; (5) thrombolysis cannot be considered to be a major confounder, as none of the oxidation parameters differed significantly between admission (before thrombolysis) and repeated measurements during hospitalization (after thrombolysis); (6) the putative effect of heparin has been excluded (see Methods) by analysis of the effect of adding heparin to serum samples in vitro. Furthermore, the values of the measured oxidation parameters did not differ significantly between admission (before heparin therapy) and the repeated measurements during hospitalization (during heparin treatment), indicating that heparin treatment cannot explain the differences observed in oxidation parameters at the different time points after MI; (7) the possibility that freezing and thawing of serum samples had a significant effect on the reported results has been excluded by comparing the kinetic parameters of oxidation on paired samples, frozen and unfrozen 14,16 (Methods).…”
Section: Discussionmentioning
confidence: 94%
“…14 The absorbance at 245 nm is attributed to dienic hydroperoxides and 7-ketocholesterol, whereas the absorbance at 268 nm is attributed mostly to dienals and other final products of decomposition of hydroperoxides. 14,15 This method has been shown to correlate strongly with copper-mediated oxidation of LDL, as reported by Schnitzer et al 16 The kinetics of oxidation ( Fig. 1) was analyzed in terms of (1) the maximal rate of accumulation of absorbing products (V max ), (2) the time at which the rate of peroxidation achieved its maximal value (t max )-this parameter is in good correlation with the "lag" preceding oxidation and reflects the resistance of serum lipids to oxidative stress 15 -, and (3) the maximal accumulation of absorbing products (OD max ).…”
Section: Copper-induced Oxidation Of Serum Lipidsmentioning
confidence: 99%