A thromboxane effect of a hydroxytyrosol-rich olive oil wastewater extract in patients with uncomplicated type I diabetes.

OBJECTIVE: To assess the antioxidant/non-antioxidant effects of a hydroxytyrosol (HT)-rich phenolic extract from olive mill wastewaters administered with a breakfast. DESIGN, SETTING AND SUBJECTS: Five type I diabetic patients received 25 mg of HT the first day and 12.5 mg/day the following 3 days. Blood sampling was carried out at T(0) (baseline) and T(4d) just before the breakfast + HT administration and at time points 1, 2, 3 and 4 h after T(0). Urines (24-h) were collected from T(0) to T(4d). Baseline HbA1c was generally inferior to 10%, glycemia was within the range 6-24 mmol/l, whereas total cholesterol, HDL-chol and triglycerides were normal. RESULTS: The major finding was the 46% decrease in the serum TXB(2) production after blood clotting at T(4d). Plasma vitamin A, E, beta-carotene were not changed. Vitamin C tended to increase (P = 0.075). Plasma antioxidant capacity was enhanced at T(0)+1 h only, whereas its main determinants (albumin, bilirubin, uric acid) were not modified. Urinary 8-isoPGF(2alpha) levels were highly variable and were not affected significantly by HT administration. CONCLUSION: The major effect of HT accounts for an antiaggregating platelet action, leading to a possible prevention of thrombotic and microthrombotic processes.

Wine phenolic antioxidants inhibit AP-1 transcriptional activity.

Some of the beneficial effects of moderate wine consumption may be related to the antioxidant properties of polyphenolic compounds containing tannins, flavonoids, and phenolic acids. Cellular actions have recently been reported and may involve the modulation of transcriptional factors such as AP-1 (activator protein-1), which controls the expression of various genes implicated in inflammation processes, cell differentiation, and proliferation. The aim of this study was to evaluate the modulation of AP-1 activity by the phenolic acids (gallic, caffeic, protocatechic, paracoumaric, sinapic, and ferulic acids) that are present in wine and to compare their modulating pathways to those of lipophilic or hydrophilic "chain-breaking" antioxidants (such as DL-alpha-tocopherol or trolox) vitamin C, nitric oxide, and reduced glutathione. AP-1 response was studied on a cell line (MTLN) derived from MCF-7 cells transfected with luciferase gene under TRE sequence control. After stimulation by phorbol 12-myristate 13-acetate (PMA; 100 nM, 6 h, 10(-7) M), luciferase activity was determined by a luminescence method in the presence of luciferine/coenzyme A solution using a luminometer (LKB 1251, Finland). Antioxidants to be tested were incubated with cells in the presence or absence of PMA. Stimulation with PMA resulted in an AP-1-mediated increase in luciferase gene expression corresponding to an 8-fold increase in luciferase activity. After stimulation by PMA, a dose-dependent inhibition of AP-1 was observed with the six phenolic acids in the 20 nM-20 microM concentration range: gallic acid > caffeic > protocatechic, paracoumaric, sinapic acids > ferulic acid. Inhibition was more pronounced with phenolic acids than with DL-alpha-tocopherol (IC(50) = 5 +/- 4.5 microM for gallic acid vs 85 +/- 11 microM for vitamin E). None of the hydrophilic antioxidants inhibited PMA-induced AP-1 activation. None of the antioxidants tested in the absence of PMA stimulation induced any activation or inhibition of AP-1. Our results suggest that phenolic acids may act directly on cell signaling via inhibition of AP-1 transcriptional activity. In addition to preventing LDL oxidation in the arterial wall, our observations indicate that phenolic acids have a cell-mediated capacity to prevent some of the processes involved in atherosclerosis in a plasma concentration range compatible with nutritional intakes.

Specific antioxidant activity of caffeoyl derivatives and other natural phenolic compounds: LDL protection against oxidation and decrease in the proinflammatory lysophosphatidylcholine production.

Specific antioxidant activity (SAA) (i.e., activity related to the molar or gallic acid equivalent amount of antioxidant) of natural polyphenolic mixtures or pure phenolic compounds was studied using their capacity to delay the conjugated diene production brought about by in vitro LDL copper-mediated or AAPH-mediated oxidation. The cinnamic acid series (caffeic, sinapic, ferulic acids) displayed a constant SAA over a large range of concentrations, whereas the benzoic acid series (gallic and protocatechuic acids) showed much higher SAA at low concentrations. The natural phenolic mixtures had a constant SAA. The highest SAA was obtained with caffeoyl esters (caffeoylquinic, rosmarinic, and caffeoyltartaric acids) and catechin for the copper-oxidation and the AAPH-oxidation system, respectively. Phenolic mixtures and acids delayed vitamin E depletion and decreased proinflammatory lysophosphatidylcholine production. As with polyphenols, probucol delayed lysophosphatidylcholine and conjugated dienes production, at higher concentrations, but was not effective at preventing vitamin E depletion. Polyphenols prevent the oxidation of LDL and its constituents (vitamin E, phosphatidylcholine), which is compatible with an antiinflammatory and antiatherosclerotic role in pathophysiological conditions.

Decreased superoxide anion production in cultured human promonocyte cells (THP-1) due to polyphenol mixtures from olive oil processing wastewaters.

The purpose of this study was to examine whether human monocytic line THP-1 after differentiation into adherent macrophages, taken as a model of human macrophages implicated in atheroma, is able to produce lower quantities of O(2)(*)(-) either in the presence of polyphenol-rich olive oil wastewater (OWW) fractions or after OWW preincubation and withdrawal from the medium. In these respective conditions, the purpose was to examine the scavenging activity and the cell action of OWW toward O(2)(*)(-) production. It was clearly seen that OWW fractions lowered the O(2)(*)(-) production in both conditions, leading to the conclusion that they were able to scavenge O(2)(*)(-) and to depress O(2)(*)(-) production in the cell. Given the role of O(2)(*)(-) in LDL oxidation and oxidized LDL in atheroma, these results support an antiatherogenic role of OWW and its potential utilization as a food complement.

Risk factors for cortical, nuclear, and posterior subcapsular cataracts: the POLA study. Pathologies Oculaires Liées à l'Age.

The POLA (Pathologies Oculaires Liées à L'Age) Study is a population-based study of cataract and age-related macular degeneration and their risk factors being carried out among 2,584 residents of Sète, southern France, aged 60-95 years. Recruitment took place between June 1995 and July 1997. Cataract classification was based on a standardized lens examination by slit lamp, according to Lens Opacities Classification System III. This paper presents results obtained from cross-sectional analysis of the first phase of the study. In polytomous logistic regression analyses, an increased risk of cataract was found for female sex (cataract surgery: odds ratio (OR) = 3.03; cortical cataract: OR = 1.67), brown irises (cortical, nuclear, and mixed cataracts: OR = 1.61), smoking (cataract surgery: OR = 2.34 for current smokers and OR = 3.75 for former smokers), known diabetes of 10 or more years' duration (posterior subcapsular, cortical, and mixed cataracts and cataract surgery: OR = 2.72), use of oral corticosteroids for at least 5 years (posterior subcapsular cataract: OR = 3.25), asthma or chronic bronchitis (cataract surgery: OR = 2.04), cancer (posterior subcapsular cataract: OR = 1.92), and cardiovascular disease (cortical cataract: OR = 1.96). Decreased risk of cataract was found with higher education (all types of cataract and cataract surgery: OR = 0.59), hypertension (cataract surgery: OR = 0.57), and high plasma retinol levels (nuclear and mixed cataracts and cataract surgery: OR = 0.75 for a 1-standard-deviation increase). Most of the risk factors identified in this study confirm the findings of other studies. The association of cataract with plasma retinol level requires further investigation.

Age-related macular degeneration and antioxidant status in the POLA study. POLA Study Group. Pathologies Oculaires Liées à l'Age.

OBJECTIVE: To give the levels of antioxidant nutrients in relation to age-related macular degeneration (AMD). METHODS: Pathologies Oculaires Liees a l'Age is a population-based study on cataract and AMD and their risk factors, carried out on 2584 inhabitants of Sete, France. Age-related macular degeneration was defined by findings from fundus photographs according to an international classification. Biological measurements were taken from fasting blood samples. RESULTS: After multivariate adjustment, plasma alpha-to-copherol levels showed a weak negative association with late AMD (P = .07). Lipid-standardized plasma alpha-tocopherol levels showed a significant negative association with late AMD (P= .003): the risk of late AMD was reduced by 82% in the highest quintile compared with the lowest. Similarly, lipid-standardized plasma alpha-tocopherol levels were inversely associated with early signs of AMD (odds ratio, 0.72 [95% confidence interval, 0.53-0.98]; P=.04). No associations were found with plasma retinol and ascorbic acid levels or with red blood cell glutathione values. COMMENT: These results suggest that vitamin E may provide protection against AMD. Only randomized interventional studies could prove the protective effect of vitamin E on AMD.

Effects of dietary crude palm oil, fish oil and their association on cholesterol and lipoprotein constants in rats which could be beneficial in humans.

The aim was first to examine the differential effects of crude and refined palm oil (CPO and RPO) on the lipid and lipoprotein constants of plasma in rats and to compare the effect of crude palm oil to that of fish oil. Secondarily, it was to know whether one can take advantage from the association of CPO with FO. Twenty-four-day-old weaning rats were divided into five experimental groups, each receiving a purified diet containing 10% oil as either a single oil or an equal amount of two oils. After a feeding period of 36 days, the main results were as follows. As compared to the rats fed the RPO diet, those fed the CPO diet had lower total cholesterol, LDL-C, VLDL-C and apoB and higher HDL-C/LDL-C and apoA1/apoB ratios. Those fed the FO diet had only lower VLDL-C and triglycerides and higher HDL-C and HDL-C/LDL-C ratio. Whereas FO associated with RPO in the same diet had the same effect as FO alone, FO associated with CPO tends to reinforce the effect of CPO. This is particularly true for the effects on apoB and apoA1 which were found to be synergistically depressed and enhanced, respectively. Given the role played by these biological constants as predictors of CVD in humans, and in spite of the fact that these predictors are not relevant in rats, these results would suggest the potential interest of CPO or the association of CPO with FO in human nutrition.

Differences between polyunsaturated fatty acid status of non-institutionalised elderly women and younger controls: a bioconversion defect can be suspected.

OBJECTIVE: To evaluate the polyunsaturated fatty acid (PUFA) status in non-institutionalised elderly women and to detect a possible essential fatty acid bioconversion defect. DESIGN AND SUBJECTS: The fatty acid composition of total plasma lipids, plasma triglycerides (TG), cholesterol esters (CE), phospholipids (PL), and erythrocytes was determined by capillary column gas-liquid chromatography in a sample of 200 non-institutionalised healthy elderly women over 75 years of age. The data were compared with those of a control group of 50 young female volunteers aged 20-48 y. RESULTS: In elderly women, the n-6 series precursor, linoleic acid (18:2 n-6), was lower in TG and CE (P = 0.029 and 0.014, respectively). In CE, this fatty acid was highly correlated with vegetable and vegetal fat intakes (P < 0.0001), suggesting a lower dietary supply than in controls. Higher percentages of 16:1 n-7 were found in all the plasma lipid fractions in elderly women, especially in CE (P < 0.0001). The ratios 20:4 n-6/20:3 n-6 and 22:6 n-3/20:5 n-3 were significantly lower in PL from elderly women (P < 0.005 and P < 0.002, respectively), raising the question of the efficiency of the terminal steps of 20:4 n-6 and 22:6 n-3 biosynthesis. Dietary investigations in elderly women indicated that a high dietary protein intake via meat probably contributed to the supply of 20:4 n-6 and thus maintained the status of this fatty acid, despite the suspected altered biosynthesis. CONCLUSION: The PUFA status in the elderly women group could be more fragile and dependent on exogenous supply of long-chain PUFAs than previously suspected.

Differential effect of N-ethyl maleimide on delta6-desaturase activity in human fetal liver toward fatty acids of the n-6 and n-3 series.

The effect of N-ethyl-maleimide (NEM) on delta5- and delta6-desaturase activities and the incorporation of substrates and products into different microsomal lipid classes and phospholipid (PL) subclasses were studied in human fetal liver microsomes, obtained after legally approved therapeutic abortion. Desaturase activities were measured by a radiochemical method using reversed-phase high-performance liquid chromatography (HPLC). After nonphospholipid (NPL) and PL separation on silica cartridges, the radioactivity in different lipids of the NPL group was assessed by two-dimensional thin-layer chromatography, and their fatty acid (FA) composition by gas-liquid chromatography. The PL subclasses were separated, and the distribution of radioactivity between products and substrates was determined in PL subclasses. NEM inhibited the delta5- and delta6-desaturase activities in the n-6 series of FA but not the delta6-desaturase activity in the n-3 series, which suggests the existence of two distinct delta6-desaturases, one for the n-6 series and another for the n-3 series. Whether NEM was present or absent, most of the radioactivity was recovered in the free FA form (about 80%). The desaturation products, obtained in the presence or absence of NEM, were preferentially incorporated into PL, suggesting a channeling of the newly synthesized FA toward microsomal PL. The comparison of the distribution of substrates and products incorporated into the different PL classes showed that most of the labeled FA were incorporated into phosphatidylcholine and to a lesser degree into phosphatidylethanolamine.

Associations of antioxidant enzymes with cataract and age-related macular degeneration. The POLA Study. Pathologies Oculaires Liées à l'Age.

OBJECTIVE: Oxidative mechanisms may play an important role in the etiology of cataract and age-related macular degeneration (AMD). The authors present the level of two antioxidant enzymes in relation to cataract and AMD. DESIGN: Population-based, cross-sectional study on cataract and AMD and their risk factors. PARTICIPANTS: This study includes 2584 participants recruited among the residents of the town of Sète (in the south of France), who were 60 years of age or older. INTERVENTION/METHODS: Cataract was defined on the basis of slit-lamp examination, according to the Lens Opacities Classification System III, and AMD on the basis of fundus photographs according to an international classification. Biologic measurements were made centrally from blood samples for which the patient fasted. MAIN OUTCOME MEASURES: The presence of early and late AMD and of subcapsular, cortical, nuclear, and mixed cataracts was assessed and related to the levels of plasma glutathione peroxidase and erythrocyte superoxide dismutase. RESULTS: After multivariate adjustment, higher levels of plasma glutathione peroxidase (pIGPx) were significantly associated with a ninefold increase in late AMD prevalence, a sixfold increase in cortical cataract, and a twofold increase in nuclear and mixed cataracts. High levels of erythrocyte superoxide dismutase (SOD) activity were not associated with late AMD and early signs of AMD but were associated with a twofold increase in nuclear cataract. CONCLUSION: The authors show here, for the first time, a strong association of high levels of pIGPx with age-related eye diseases. High levels of SOD also are associated with increased risk of nuclear cataract. More data are needed at the biochemical and epidemiologic levels for a better understanding of these findings.

alpha-tocopherol inhibits the respiratory burst in human monocytes. Attenuation of p47(phox) membrane translocation and phosphorylation.

Vitamin E (alpha-tocopherol), one of the most important natural antioxidants, is assumed to be beneficial in the prevention of cardiovascular diseases. alpha-Tocopherol exhibits acyl-peroxyl-radical scavenger properties and exerts cell-mediated actions in the hemovascular compartment, such as inhibition of superoxide anion (O-2) production by leukocytes. The aim of this study was to examine the mechanism underlying the inhibitory effect of alpha-tocopherol on O-2 production by human monocytes. In activated monocytes O-2 is produced by the NADPH-oxidase enzyme complex. The oxidase activation elicited by phorbol myristate acetate (PMA) requires membrane translocation of several cytosolic factors. We found that in human PMA-stimulated adherent monocytes, alpha-tocopherol (but not beta-tocopherol) inhibited O-2 production in intact cells but had no effect on a membrane preparation containing activated NADPH-oxidase, suggesting that alpha-tocopherol impairs the assembly process of the enzyme complex. We showed that translocation and phosphorylation of the cytosolic factor p47(phox) were reduced in monocytes preincubated with alpha-tocopherol. We verified that the tryptic phosphopeptide map of monocyte p47(phox) was similar to that of neutrophil p47(phox), indicating that several serine residues were phosphorylated. Peptides whose phosphorylation is dependent on protein kinase C (PKC) were phosphorylated to a lesser degree when p47(phox) was immunoprecipitated from alpha-tocopherol-treated monocytes. In vitro, the activity of PKC from monocytes was inhibited by alpha-tocopherol in a specific manner compared with that of beta-tocopherol or Trolox(R). Membrane translocation of PKC was not affected. These results show that alpha-tocopherol inhibits O-2 production by human adherent monocytes by impairing the assembly of the NADPH-oxidase and suggest that the inhibition of phosphorylation and translocation of the cytosolic factor p47(phox) results from a decrease in PKC activity.

Fatty acid desaturase activities and polyunsaturated fatty acid composition in human liver between the seventeenth and thirty-sixth gestational weeks.

OBJECTIVE: The aim of the study was to characterize n-3 and n-6 fatty acid delta5- and delta6-desaturase activities and their time course variations in human fetal liver between the 17th and 36th gestational week. STUDY DESIGN: Twenty-one biologic samples were obtained after legally approved medical abortion, according to French law. The desaturase activities were measured in the 21 liver samples by a radiochemical method by means of reverse-phase high-performance liquid chromatography. The fatty acid composition (percentage by weight) of liver phospholipids was assessed in 16 samples by gas-liquid chromatographic analysis. RESULTS: Both delta5- and delta6-desaturase activities were significantly expressed between the 17th and 36th gestational weeks. During the second trimester n-6 fatty acid delta5- and delta6-desaturase activities showed opposite patterns of variation; both then remained stable between the 25th and 36th weeks. Delta6-desaturation was higher in n-3 than n-6 fatty acids and peaked at the 18th gestational week. The percentages of linoleic and docosahexaenoic acids in liver microsomes were positively correlated with the gestation age (P < .01), whereas arachidonic acid remained stable. CONCLUSION: Significant n-3 and n-6 delta5- and delta6-desaturase activities are expressed in human fetal liver as early as the 17th gestational week and are stable throughout the third trimester. Their theoretic capacity evaluated from in vitro measurements appears lower than polyunsaturated fatty acid requirements and is not directly related to liver microsomal membrane fatty acid composition.

A short-term supplementation of pregnant women before delivery does not improve significantly the vitamin E status of neonates--low efficiency of the vitamin E placental transfer.

Little is known about lipid-soluble vitamin placental transfer. We supplemented ten pregnant women ranging in age from 26 to 38 years with vitamin E at a daily dose of 1 g dl-alpha-tocopherol acetate for 3 days before delivery. All pregnancies ranged from 37 to 39 weeks of gestation at the time of the study. Maternal blood was first drawn during the week preceding supplementation and then just before the delivery by hysterotomy. Neonatal blood was from cord at birth. Supplementation dramatically increased the plasma and red blood cell vitamin E of the mothers. This was true whatever the expression of the vitamin E content, i.e., plasma lipid-normalized or non-normalized vitamin E, and red blood cell vitamin E related to volume of packed cells or to membrane-phospholipid phosphorus. In contrast, the plasma vitamin E content was very low in neonates (3.51 +/- 0.38 mg/L) and did not significantly differ from that reported in a previous paper, where plasma was drawn from fetal cord blood of pregnant non-supplemented women belonging to the same geographical population (Cachia et al., Am. J. Obstet. Gynecol. 1995; 173: 42-51). This strongly suggests that the transfer of vitamin E through the placental barrier is very low. That the plasma lipid-normalized levels of mothers before supplementation and of neonates did not significantly differ also suggests that the paucity of lipids in the circulating blood of neonates is the cause of the restricted amount of plasma vitamin E. Therefore, the low level of vitamin E in neonates may result from both low maternal placental transfer and neonatal lipid transport peculiarities.

Delta6- and delta5-desaturase activities in the human fetal liver: kinetic aspects.

Delta6- and delta5-desaturase activities were studied in human fetal liver microsomes obtained after legally approved therapeutic abortion. Enzyme activities were measured by a radiochemical method using reverse-phase high performance liquid chromatography (HPLC). Free and phospholipid fatty acids were assessed in each liver sample by a combination of thin-layer chromatography (TLC) and gas-liquid chromatography (GLC) procedures. The kinetic measurements showed higher delta6-desaturase activity for the n-3 series than for the n-6 series. Apparent Km of 6.5, 3.9, and 24.5 microM and Vm of 7.5, 9.1, and 24.4 pmol x min(-1) x mg(-1) were obtained, respectively, for 18:2n-6 delta6-, 20:3n-6 delta5-, and 18:3n-3 delta6-desaturases. Beyond 30, 20, and 60 microM of 18:2n-6, 20:3n-6, and 18:3n-3 concentration, respectively, the enzyme activity deviated from Michaelis-Menten kinetics, suggesting an inhibition by excess substrate which is unlikely to occur in vivo as endogenous substrate concentration is much lower. We observed a breakdown in linearity between desaturase activity and microsomal protein concentration beyond 4-5 mg microsomal protein, whatever the enzyme or substrate. Both this phenomenon and the inhibition due to excess substrate should be taken into account in the determination of delta6- and delta5-desaturase activities. Comparison of concentrations of the respective endogenous substrates and the kinetic constants of each enzyme suggested that the higher delta6-desaturase activity observed for the n-3 series than for the n-6 series is not physiologically relevant in human fetal liver.

Monocyte superoxide production is inversely related to normal content of alpha-tocopherol in low-density lipoprotein.

Vitamin E (alpha-tocopherol) is a potent peroxyl radical scavenger. According to the oxidative theory of atherosclerosis, it prevents oxidation of low-density lipoprotein (LDL) and thereby lowers the risk of cardiovascular disease. It also mediates cell actions, and specifically decreases monocyte superoxide anion-production (O2.--production), which is involved in LDL oxidation. We investigated whether alpha-tocopherol-containing LDL decreases this production in a manner dependent on the LDL alpha-tocopherol content (the alpha-tocopherol/apoB molar ratio) in human, phorbol ester-stimulated, adherent monocytes. We found that O2.--production was inhibited by native LDL (n-LDL) in a manner highly sensitive to the increasing alpha-tocopherol content (range 4.5 8). In addition: (1) inhibition was greater when alpha-tocopherol was associated to acetylated LDL (ac-LDL), the maximal percentage of inhibition being 80% as opposed to 35% for n-LDL; (2) the alpha-tocopherol overloading of either form of LDL did not produce further inhibition; (3) the free form of alpha-tocopherol produced lower inhibition compared with the lipoprotein-associated forms; (4) inhibition was not related to the cell content of alpha-tocopherol. We propose that the cell targeting of alpha-tocopherol is crucial to the inhibition of monocyte O2.--production, and thus that the role of normal LDL-alpha-tocopherol contents (range 6-8) in the prevention of atherogenic processes needs to be reexamined.

Supplementation with wine phenolic compounds increases the antioxidant capacity of plasma and vitamin E of low-density lipoprotein without changing the lipoprotein Cu(2+)-oxidizability: possible explanation by phenolic location.

OBJECTIVES: To evaluate the effect of the red wine phenolic compound (RWPC) dietary supplementation without alcohol interference on: (1) some of the biochemical characteristics of LDL, (2) the oxidative susceptibility of LDL and (3) the antioxidant capacity of total plasma (Pl-AOC). In order to account for discrepancies between the three series of data, the in vitro stability of the association of phenolic compounds and LDL was tested. DESIGN: An intervention study with 20 volunteers. Each served as his own control. Cu(2+)-oxidizability of LDL and Pl-AOC were tested on blood samples before and after dietary supplementation. Cu(2+)-oxidizability of LDL was also tested by co-incubation in the presence of RWPC or phenolic acids with or without extensive dialysis. SETTING: The Laboratory of Lipid Biochemistry and Biology, School of Medicine, and the Laboratory of Metabolic Diseases, Lapeyronie Hospital, University of Montpellier, France. SUBJECTS: Healthy males, nonsmokers and moderate drinkers, submitted to a dietary regimen deprived of vitamin E and C for a period of 10 d before supplementation. They also abstained from alcohol, wine, fruit juices, coffee, tea and cola beverages during this period. INTERVENTION: Six 0.33 g capsules/d (namely two capsules at each meal) of a preparation of red wine phenolic compounds in a dry powder form were given to the volunteers over a period of two weeks. Blood samples were drawn in fasting conditions at day 0 and day 14 of the supplementation period. RESULTS: Supplementation led to: (1) in LDL, a significant increase in vitamin E content (n = 20, P = 0.01) or vitamin E/total fatty acid bis-allylic carbon number ratio (n = 20, P = 0.006) without modification in the other biochemical characteristics or Cu(2+)-oxidizability; (2) in plasma, a significant increase in the antioxidant capacity (n = 11, P = 0.01). In vitro studies showed that RWPC or sinapic, caffeic or ferulic acids incubated in the presence of LDL increased the protection of the lipoparticle against oxidation (caffeic > sinapic > ferulic). This effect, however, was totally lost after extensive dialysis. CONCLUSIONS: The enhancing effect of the RWPC supplementation on Pl-AOC may be due to a phenolic-compound action both in the aqueous phase of plasma and at the surface of lipoprotein particles. Surface location possibly explains the enhancing-sparing effect of supplementation on LDL vitamin E and the absence of effect on dialysed-LDL oxidizability.

Differential incorporation of fish-oil eicosapentaenoate and docosahexaenoate into lipids of lipoprotein fractions as related to their glyceryl esterification: a short-term (postprandial) and long-term study in healthy humans.

We investigated how the distribution of eicosapentaenoate (EPA, 20:5n-3) and docosahexaenoate (DHA, 22:6n-3) in the sn-2 and sn-1(3) positions of fish-oil triacylglycerols influenced their respective incorporation into triacylglycerol, cholesterol esters, and phospholipids of two lipoprotein fractions: low- and very-low-density lipoprotein (VL/LDL) and high-density lipoprotein (HDL). Nine healthy volunteers were studied over both a short-term (0-8 h) and a long-term (30 d) postprandial period of daily supplementation with 2 g EPA and 1.3 g DHA given as 11 g fish-oil triacylglycerol in which DHA was predominantly situated in the sn-2 position. Our results strongly suggest that the higher triacylglycerol incorporation of DHA and the higher metabolic availability of EPA compared with DHA for phospholipid accumulation (particularly in the short-term study) depend on their respective preferential sn-2/sn-1(3) positions in fish-oil triacylglycerol, emphasizing the important role of the triacylglycerol structure and its potential manipulation for modulating availability of either or both fatty acids.

Red blood cell vitamin E concentrations in fetuses are related to but lower than those in mothers during gestation. A possible association with maternal lipoprotein (a) plasma levels.

OBJECTIVE: The purpose was to establish which blood characteristic of vitamin E status were highly correlated between mothers and fetuses during gestation. STUDY DESIGN: Twenty-four pregnant women were selected because of suspicion of toxoplasmosis or other disease and malformation or intrauterine growth delay justifying cord blood puncture. After maternal and fetal blood was collected, analyses of plasma and red blood cell vitamin E contents were performed together with analyses of standard lipid parameters and lipoprotein (a) in maternal plasma and fatty acid compositions of maternal and fetal red blood cells. RESULTS: The maternal population was characterized by a plasma lipid-normalized vitamin E mean content higher (3.5 mmol/mol lipids) than usually found in nonpregnant adults. There was no relationship between plasma and red blood cell vitamin E contents. This was also true for fetuses. When the vitamin E status of mothers was compared with that of fetuses, we found no correlation in plasma vitamin E in the whole population and in the high lipoprotein (a) (> 300 mg/L) and low lipoprotein (a) (< 300 mg/L) groups. In contrast, statistically significant correlations appeared between maternal and fetal red blood cell contents and red blood cell relative charges in vitamin E in the whole population, whereas still higher correlations occurred in the high lipoprotein (a) group (r = 0.94 for the red blood cell content). Improved correlations were also found in the high lipoprotein (a) group for the interrelationship between vitamin E and plasma lipid contents (cholesterol and triglycerides), whereas improvement was noted in the low lipoprotein (a) group by positive correlation between age and vitamin E red blood cell content or red blood cell relative charge. CONCLUSION: Determination of red blood cell vitamin E and plasma lipoprotein (a) in mothers could be useful in antenatal blood analysis in cases of risk of prematurity at birth, to prevent peroxidative membrane damage in neonates, and > 85% of the mothers in the current population would benefit from vitamin E supplementation from the viewpoint of the fetal red blood cell vitamin E requirement in spite of the rather high maternal lipid-normalized vitamin E plasma content.