Vitamin E homologues α- and γ-tocopherol are not associated with bone turnover markers or bone mineral density in peri-menopausal and post-menopausal women.

UNLABELLED: In a large cohort of older women, we investigated the relationships that different forms of vitamin E may have with bone turnover markers and bone mineral density (BMD). We found a suggestive positive association between serum alpha-tocopherol and BMD at the femoral neck, but no other clinically relevant observations. INTRODUCTION: Vitamin E has anti-oxidant and anti-inflammatory properties hypothesized to benefit bone, but limited studies exist regarding its homologues. We examined circulating and dietary α- and γ-tocopherols with bone turnover markers (BTMs) and bone mineral density (BMD), and the role of inflammation in this relationship. METHODS: We performed two cross-sectional analyses from two visits (V2, 1997-1999, n = 3883; V3, 2007-2011, n = 2130) of the Aberdeen Prospective Osteoporosis Screening Study. Dietary and supplement intakes by food frequency questionnaire were assessed at both visits. V2 BTMs (urinary free pyridinoline and deoxypyridinoline, serum N-terminal propeptide of type 1 collagen) and V3 serum α- and γ-tocopherols, inflammatory markers (interleukin-6 [IL-6], serum amyloid A [SAA], high-sensitivity C-reactive protein [hs-CRP], E-selectin) and dual X-ray absorptiometry BMD at the femoral neck and lumbar spine were collected. Food sources of tocopherol homologues and diet-serum correlations were determined. The relationships between dietary tocopherols and BTMs (V2), and dietary and serum tocopherols with BMD (V3) were examined by multivariable regression (adjusting for age, cholesterol, inflammatory markers, carotenoids, body mass index, physical activity level, alcohol intake, smoking status and national deprivation category). RESULTS: Serum γ-tocopherol was associated with increasing concentrations of hs-CRP, SAA and E-selectin (P-trend all <0.0001), while α-tocopherol was associated with decreasing concentrations of IL-6 and hs-CRP (P-trend all <0.001). Controlling for covariates, serum α-tocopherol was positively associated with BMD at the femoral neck (ß = 0.002, P = 0.04) among those not reporting vitamin E supplementation. CONCLUSION: We did not find biologically meaningful results between dietary and tocopherol homologues with BTMs or BMD.

Human O-sulfated metabolites of (-)-epicatechin and methyl-(-)-epicatechin are poor substrates for commercial aryl-sulfatases: implications for studies concerned with quantifying epicatechin bioavailability.

Epicatechin is a widely consumed dietary flavonoid and there is substantial evidence that it contributes to the health benefits reported for flavanol-rich cocoa products including dark chocolate. Numerous reports have described the appearance of epicatechin and epicatechin phase-2 conjugates (sulfates and glucuronides of epicatechin and methylepicatechin) in blood and urine samples of subjects following ingestion of epicatechin. The most widely reported method of quantifying total epicatechin in plasma and urine samples involves hydrolysis with a mixture of ß-glucuronidase and sulfatase to convert the conjugates to epicatechin aglycone which is subsequently quantified. We observed a lack of hydrolysis of epicatechin sulfates and methylepicatechin sulfates using commercial sulfatases and investigated this further. Samples of urine or plasma from subjects who had consumed epicatechin were subjected to enzyme hydrolysis and then analysed using LC-MS/MS, or analysed without enzyme hydrolysis. Attempts to increase the extent of hydrolysis of epicatechin conjugates were made by increasing the amount of enzyme, hydrolysis pH and length of incubations, and using alternative sources of enzyme. The standard hydrolysis conditions failed to hydrolyse the majority of epicatechin sulfates and methylepicatechin sulfates. Even when the quantity of enzyme and incubation period was increased, the pH optimised, or alternative sources of sulfatases were used, epicatechin monosulfates and methylepicatechin monosulfates remained as major peaks in the chromatograms of the samples. An assessment of literature data strongly suggested that the majority of reports where enzyme hydrolysis was used had significantly underestimated epicatechin bioavailability in humans. Methods for quantifying epicatechin concentrations in blood and urine need to take account of the lack of hydrolysis of (methyl)epicatechin-sulfates, for example by quantifying these directly using LC-MS/MS.

Modulation of glutathione peroxidase activity in human vascular endothelial cells by fatty acids and the cytokine interleukin-1 beta.

Objectives of this study were (a) to assess the extent of oxidative stress elicited in human endothelial cells by n-3, n-6 and n-9 mono- and polyunsaturated fatty acids and by interleukin-1 beta and (b) to determine how such stress influenced glutathione peroxidase (GSHPx) activity. Fatty acids were co-incubated with human vascular endothelial cells (HUVEC) for 24 h. Lipid peroxidation, monitored as conjugated diene (CD) formation, increased 3-4-fold with increasing eicosapentaenoic and docosahexaenoic acids: 2-3-fold with linoleic acid; decreased by 50% with arachidonic acid and was unchanged with oleic acid. Changes in glutathione peroxidase activity mirrored conjugated diene formation in the HUVEC incubated with fatty acids. Interleukin-1 beta also increased glutathione peroxidase and conjugated diene formation; the latter increased enzyme activity dose-dependently suggesting a possible role for this oxidation product in the induction of glutathione peroxidase activity. The ability of fish oil fatty acids to induce antioxidant enzymes, particularly those of the glutathione redox system, may be an important mechanism protecting cells and tissues against oxidative and inflammatory cytokine elicited damage.

Phytochemical profile of commercially available food plant powders: their potential role in healthier food reformulations.

Reformulation of existing processed food or formulation of new foods using natural products (plant-based) will inherently confer to new products with less calories, fat, salt, phosphates and other synthetic components, and higher amounts of fibre, antioxidants, vitamins and other beneficial components. Plant ingredients, such as food plant powders, are currently being used in food manufacturing, predominantly for flavouring and colouring purposes. To expand their use as a food ingredient, freeze-dried powders representing major vegetable groups were characterised by targeted LC-MS/MS analysis of their phytochemicals. All the plant powders were found to be rich in flavonoids, phenolic acids and derivatives; total content in these compounds varied from around 130 mg kg(-1) (green pea) to around 930 mg kg(-1) (spinach). The food plant powders' phytochemical content represents valuable information for the food industry in the development of healthier novel foods and for the reformulation of existing food products in relation to antioxidants, food preservatives and alternatives to nitrite use.

Free radicals and calcium homeostasis: relevance to malignant hyperthermia?

The regulation of intracellular free calcium ions (Ca2+) in skeletal muscle at rest and during contraction depends on mechanisms such as Na(+)-Ca2+ exchangers, Ca(2+)-ATPases, and the voltage-sensitive ryanodine receptor. The susceptibility of these regulatory mechanisms to free-radical-mediated damage may be increased because of their location within the lipid membranes of sarcolemma, sarcoplasmic reticulum, and mitochondrion with resultant uncontrolled increases in myoplasmic Ca2+ concentration and cell death. The potentially fatal pharmacogenetic disorder, malignant hyperthermia (MH), is characterised by muscle rigidity, arrhythmias, lactic acidosis, and a rapid rise in body temperature. The sequence of events responsible for the MH syndrome remains uncertain, but it has been variously ascribed to faults in many of the Ca2+ regulatory mechanisms. In swine the condition is associated with a specific mutation in the ryanodine receptor, whereas in humans the syndrome is genetically heterogenous. Free-radical-mediated peroxidation of membrane lipids and proteins also results in the rapid efflux of Ca2+ from organelles, and the detection of products of free radical reactions in tissue from MH-susceptible individuals using electron spin resonance spectroscopy provides evidence for the involvement of free radicals in the MH syndrome.

Anthocyanin-rich extract decreases indices of lipid peroxidation and DNA damage in vitamin E-depleted rats.

Anthocyanins are secondary plant metabolites responsible for the blue, purple, and red color of many plant tissues. The phenolic structure of anthocyanins conveys marked antioxidant activity in model systems via donation of electrons or hydrogen atoms from hydroxyl moieties to free radicals. Dietary intakes of anthocyanins may exceed 200 mg/day, however, little is known about their antioxidant potency in vivo. Consequently, the aim of this study was to establish whether anthocyanins could act as putative antioxidant micronutrients. Rats were maintained on vitamin E-deficient diets for 12 weeks in order to enhance susceptibility to oxidative damage and then repleted with rations containing a highly purified anthocyanin-rich extract at a concentration of 1 g/kg diet. The extract consisted of the 3-glucopyranoside forms of delphinidin, cyanidin, petunidin, peonidin, and malvidin. Consumption of the anthocyanin-repleted diet significantly improved (p <.01) plasma antioxidant capacity and decreased (p <.001) the vitamin E deficiency-enhanced hydroperoxides and 8-Oxo-deoxyguanosine concentrations in liver. These compounds are indices of lipid peroxidation and DNA damage, respectively. Dietary consumption of anthocyanin-rich foods may contribute to overall antioxidant status, particularly in areas of habitually low vitamin E intake.

Vitamin E supplementation suppresses indexes of lipid peroxidation and platelet counts in blood of smokers and nonsmokers but plasma lipoprotein concentrations remain unchanged.

Smokers incur a sustained free radical load that may increase their vitamin E requirement. Erythrocytes of male smokers from a Scottish population with a habitually low vitamin E intake were more susceptible to hydrogen peroxide-stimulated peroxidation than were those from nonsmokers (P < 0.001). Plasma concentrations of lipid peroxides, thiobarbituric acid reactive substances, and conjugated dienes were also elevated in smokers compared with nonsmokers (P < 0.05). These indexes of oxidative stress were markedly decreased (P < 0.001) in the smokers and nonsmokers after consumption of 280 mg dl-alpha tocopherol acetate/d for 10 wk. Platelet numbers in serum of both smokers and nonsmokers were also decreased by vitamin E supplementation (P < 0.02). Although the clinical significance of the results is unclear, elevated indexes of lipid peroxidation are associated with the pathogenesis of atherosclerosis, and platelets are involved with fibrinolysis. Therefore, both smokers and non-smokers may benefit from increased vitamin E intakes.

Effects of smoking and vitamin E on blood antioxidant status.

Despite similar vitamin E contents, erythrocytes of smokers have an increased tendency (P less than 0.01) to peroxidize in vitro compared with those of nonsmokers. This difference is abolished by vitamin E supplementation (1000 mg alpha-tocopherol acetate/d for 14 d). The increased susceptibility to erythrocyte peroxidation in the smokers may reflect lower glucose-6-phosphate dehydrogenase (P less than 0.02) and glutathione peroxidase (P less than 0.05) activities. Smokers seem to be under a sustained oxidant stress with increased plasma-conjugated dienes (P less than 0.01) and dehydroascorbate (P less than 0.05) and decreased ascorbate (P less than 0.06) concentrations. Additionally, plasma ceruloplasmin in smokers is elevated (P less than 0.01), consistent with an acute-stress response. Plasma total cholesterol is similar in smokers and nonsmokers and is unaffected by vitamin E supplementation. Indices of sustained oxidant stress in smokers are partially ameliorated by vitamin E supplementation.

Erythrocyte vitamin E and plasma ascorbate concentrations in relation to erythrocyte peroxidation in smokers and nonsmokers: dose response to vitamin E supplementation.

Many human degenerative diseases involve free radical processes that nutritional antioxidants may ameliorate or prevent, but the optimum intake of such nutrients has yet to be established. Requirement will depend in part on the level of exposure to exogenous and endogenous reactive oxygen species. Smokers incur a sustained degree of oxidant stress from both of these sources, increasing their requirements for vitamins E and C. Male smokers (n = 50) from a Scottish population with habitually low vitamin E and vitamin C intakes consistently had lower plasma ascorbate concentrations (P < 0.02) and greater susceptibility to hydrogen peroxide-stimulated erythrocyte peroxidation in vitro (P < 0.001) than did nonsmokers (n = 50) from the same population. Erythrocyte vitamin E concentrations increased in a dose-dependent manner during 20 wk of supplementation with 70, 140, 560, and 1050 mg D-alpha-tocopherol/d. In smokers each dose was associated with a significant decrease in susceptibility of erythrocytes to peroxidation (P < 0.001). However, red cells of nonsmokers receiving the 1050-mg supplement had an increased susceptibility to peroxidation. Moreover, prolonged supplementation with D-alpha-tocopherol in nonsmokers induced a decline in plasma ascorbate concentration (P < 0.02) in association with an increasing erythrocyte vitamin E uptake (P < 0.001), and in nonsmokers receiving 1050 mg, the susceptibility to peroxidation also increased (P < 0.001). Thus, vitamin E may have prooxidant activity in nonsmokers at high and prolonged intakes.

Use of a vibrating electrode to measure changes in calcium fluxes across the cell membranes of oxidatively challenged Aplysia nerve cells.

A self-referencing and non-invasive Ca(2+)-sensitive vibrating electrode was used to assess the effects of hydrogen peroxide-induced oxidative challenges on the efflux and influx of calcium across the plasma membrane of single nerve cells cultured from abdominal ganglion of Aplysia californica. A reduced net efflux of Ca2+ from the cell soma occurred immediately after the addition of hydrogen peroxide (0.0025 mM, 0.005 mM or 0.01 mM) to the culture medium, indicating damage to the cell membrane or Ca2+ transport mechanism. There then followed a marked efflux, the extent and duration of which was related to the concentration of hydrogen peroxide used and which may reflect compensatory activity by the Ca2+ regulatory mechanisms in the plasmalemma. No morphological changes were observed in cells challenged with 0.0025 mM hydrogen peroxide and the enhanced rate of Ca2+ efflux rapidly decreased to pre-exposure values. Sustained and enhanced Ca2+ effluxes from those cells exposed to 0.005 mM or 0.01 mM hydrogen peroxide were also consistent with regulatory pumping of Ca2+ out of the cell although contraction and blebbing of neurites and swelling of the soma may indicate that a proportion of the efflux arose from release of Ca2+ from disrupted intracellular stores. The vibrating electrode is a useful additional technique for the study of the pathogenesis of neurological conditions, as ionic fluxes across single nerve cells exposed to physiologically-relevant concentrations of free radicals can be monitored non-invasively for prolonged periods.

alpha-Tocopherol binding activity of red blood cells in smokers.

Despite high plasma levels of vitamin E, red blood cell membranes contain relatively low levels of vitamin E. This suggests the existence of a selective vitamin E uptake/regeneration system in human red blood cell membranes. alpha-Tocopherol binding sites on human red blood cells are thought to be involved in the uptake of alpha-tocopherol from the plasma. To understand the role of the uptake system we have compared the alpha-tocopherol content and binding activity of red blood cells from smokers and non-smokers. The specific binding of [3H] alpha-tocopherol to pure red blood cell preparations from smokers (n = 7, 28.4 +/- 2.8 years) was 30.6 +/- 3.2 fmoles per 3 x 10(8) red blood cells and for non-smokers (n = 17, 27.9 +/- 1.3 years) was 41.7 +/- 3.7 fmoles per 3 x 10(8) red blood cells. Thus alpha-tocopherol uptake activity was significantly lower in smokers (P = 0.05). Red blood cells from smokers contained less (1.8 +/- 0.4 micrograms/gHb) alpha-tocopherol than non-smokers (2.8 +/- 0.3 micrograms/gHb), (P < 0.05), despite plasma levels of alpha-tocopherol being similar: 12.9 +/- 0.8 microM in non-smokers vs. 12.7 +/- 0.5 microM in smokers. However, adjusting plasma alpha-tocopherol for total plasma cholesterol plus triacylglycerols showed alpha-tocopherol levels were higher (P < 0.01) in non-smokers (2.84 +/- 0.10 mumol alpha-tocopherol/ mmol [cholesterol+triacylglycerol]) than in smokers (2.36 +/- 0.11 mumol alpha-tocopherol/mmol [cholesterol+triacylglycerol]). The reduced alpha-tocopherol levels in red blood cells from smokers may be due to impairment of alpha-tocopherol uptake activity. The reduced levels of alpha-tocopherol in smokers red blood cells was not associated with any changes in cell membrane fluidity. At present it is not known whether supplementation of smokers with vitamin E would normalise the alpha-tocopherol uptake activity of red blood cells.

Vitamin E supplementation increases the stability and the in vivo antioxidant capacity of refined olive oil.

Two experiments were carried out to investigate if the supplementation with vitamin E affects refined olive oil response to oxidation regarding the stability of the oil and the protection in vivo against lipid peroxidation in rats after its intake in comparison with other edible oils. In experiment 1, samples of virgin olive oil, refined olive oil, refined olive oil supplemented by us with 200 mg/kg vitamin E, and sunflower oil were collected before and after a 60 min frying process. After frying, refined olive oil supplemented with vitamin E compared with the non-supplemented refined olive oil had a higher concentration of alpha-tocopherol (240.34+/-6.07 mg/kg vs. 131.94+/-8.14 mg/kg), more resistance against oxidation (19.01+/-1.88% vs. 10.6+/-2.08%) and less polar components (4.2+/-0.06% vs. 5.45+/-0.22%). In experiment 2, 24 male Wistar rats, divided into 4 groups, were fed on diets based on the same unfried oils (8% w/w) as in experiment 1, for 4 weeks. Two days prior to the end of the experiment, the rats were intraperitoneally administered with adriamycin (10 mg/kg/ day) to provoke an oxidative stress. The rats fed on refined olive oil plus vitamin E compared to the rats fed on non-supplemented refined olive oil had lower hydroperoxides concentrations (26.8+/-2.6 nmol/mg vs. 35.6+/-2.49 nmol/mg) higher coenzyme Q levels (128.1+/-11.97 pmol/mg vs. 81.25+/-9.25 pmol/mg) and higher alpha-tocopherol values (1.23+/-0.04 mmol/mg vs. 0.93+/-0.06 mmol/mg) in microsomes of liver. In conclusion, the supplementation of refined olive oil with 200 mg/kg of vitamin E increases the stability of this oil under pro-oxidant conditions, and its intake decreases the oxidative damage generated by adriamycin in rats.

Effects of storage, iron and time of day on indices of lipid peroxidation in plasma from healthy volunteers.

The concentrations of thiobarbituric acid reactive substances and conjugated dienes in human plasma are often used as indices of lipid peroxidation. However, concentrations of thiobarbituric acid reactive substances in plasma are markedly affected by the iron content of reagents used in the analysis and by storage of samples at -70 degrees C. The assay also has a large interbatch coefficient of variation (14%). Plasma concentrations of conjugated dienes are not affected by storage and the coefficient of variation is only 4%. However, there is a marked diurnal variation in levels of conjugated dienes which is similar to the changes in concentrations of plasma triglycerides. Precise standardisation of analytical procedures is required before these assays can be reliably used in clinical medicine.

The Mediterranean diet: protective or simply non-toxic?

There is clear evidence that populations living in Mediterranean countries enjoy a longer life expectancy than Northern Europeans. Genetic or racial factors do not explain these societal differences as revealed by migrant studies. The major causes of death in affluent societies, cardiovascular disease, cancers and digestive disorders, show markedly different incidence rates in different European countries. These differences seem to depend on the varied dietary patterns in Europe but the classic lipid hypothesis alone fails to explain the differing rates of coronary heart disease. Limiting the free radical damage to cholesterol thereby reducing the induction of atherosclerosis is a plausible explanation for the finding that some countries, e.g. France as well as Mediterranean countries with their high fruit and vegetable consumption, are well protected against coronary heart disease. The Mediterranean diet is low in saturated fat content but contains either a high or low content of starch and total fat. A high fat diet reveals the genetically determined individual propensity to obesity, e.g. in Greece, but does not predispose to cardiovascular disease or mitigate against the cancer protective properties derived from the vegetable component of the Greek diet. Studies in the Mediterranean area highlight the considerable dietary diversity which is possible for achieving longevity.

Dietary intakes of polyunsaturated fatty acids and indices of oxidative stress in human volunteers.

OBJECTIVE: To assess whether nutritionally-relevant changes in polyunsaturated fatty acid (PUFA) intake alter indices of oxidative stress in human volunteers DESIGN: A split plot/change over dietary study where half the volunteers consumed a diet containing 5% PUFA (low PUFA) as food energy for 4 weeks and after a 6 week washout period consumed a 15% PUFA (high PUFA) diet for another 4 weeks. The second group of volunteers completed this protocol in reverse. Total fat, carbohydrate, protein and vitamin E contents of the diets were constant. SUBJECTS: 10 healthy, non-smoking, male volunteers aged 32.6 +/- 1.7 y RESULTS: There was a significant increase in whole blood oxidised glutathione (P < 0.05), an index of oxidative stress, after consumption of the high PUFA diet. Moreover, urinary thiobarbituric acid reactive substances (TBARS), an index of lipid peroxidation, significantly increased (P = 0.038) following consumption of the high PUFA diet and decreased (P = 0.031) after consuming the low PUFA diet. However, there was no change in non specific plasma indices of lipid peroxidation, conjugated dienes and TBARS, nor in red cell antioxidant enzymes glutathione peroxidase, glutathione reductase, and catalase. However, superoxide dismutase significantly decreased (13%, P=0.018) after consumption of the low PUFA diet. Total cholesterol increased by 13% (P=0.014) after consumption of the low PUFA diet. CONCLUSIONS: This study indicates that although increasing dietary levels of PUFA may favourably alter cholesterol profiles, the same dietary changes may adversely affect some indices of lipid peroxidation. Care should be taken when providing dietary advice on PUFA intake and an adequate intake of antioxidants to match any increased PUFA may be important for preventing oxidative stress.

An evaluation of germinating beans as a source of vitamin C in refugee foods.

OBJECTIVE: To assess whether germinating pulses and beans are a potential source of vitamin C in rations for refugee communities with poor vitamin C status. DESIGN: High pressure liquid chromatographic assessment of vitamin C content of a range of legumes following germination in light and dark and after cooking. RESULTS: Many species of pulses produced significant quantities of vitamin C up to five days following germination in both light and dark although cooking caused a marked loss of ascorbate. CONCLUSION: Germination of approximately half of the seeds of the pulse constituents of many basic rations would be likely to generate, within a 3-5 d germination period, sufficient ascorbate to provide the 10 mg needed to protect adults against the development of scurvy.

Erythrocyte membrane fatty acid composition of smokers and non-smokers: effects of vitamin E supplementation.

OBJECTIVE: Adequate dietary intakes of vitamin E and essential polyunsaturated fatty acids are important to maintain cell membrane integrity, and deficiencies have been associated with smoking related cardiovascular disease. Sufficient vitamin E is required to prevent free radical mediated peroxidation of membrane lipids. Consequently, smokers may have a greater requirement for this antioxidant. To investigated, we assessed the concurrent influences of smoking, vitamin E supplementation and red blood cell (RBC) PUFA composition on the susceptibility of the cells to lipid peroxidation in adult males. DESIGN AND SUBJECTS: Thirty male smokers and thirty male non-smokers were randomly ascribed to daily 280 mg vitamin E or placebo supplements for 10 weeks. RBC were analysed at weeks 0 and 10 for fatty acid methyl esters, vitamin E, and their susceptibility to in vitro H202 induced lipid peroxidation. RESULTS: Concentrations of essential fatty acids (EFA) in RBC were lower in smokers than in non-smokers. supplementation with vitamin E increased levels of RBC EFA in smokers and non-smokers was inversely correlated with their susceptibility to peroxidation. CONCLUSIONS: An adequate vitamin E to PUFA ratio is required to protect cell membranes from oxidative damage. The significant correlation between susceptibility to peroxidation and the PUFA content of RBC before supplementation suggests an inadequate intake of vitamin E in relation to PUFA intake. Moreover, the requirement for vitamin E appears to be greater in smokers than in non-smokers.

Vitamin E and coronary heart disease: the European paradox.

OBJECTIVE: To relate premature mortality from coronary heart disease (CHD) to national food and nutrient supplies. DESIGN: Descriptive correlational study. SETTING: Nineteen western European and five non-European countries. METHODS: Premature mortality from CHD in men below 65 years was related to recalculated Food and Agriculture Organization (FAO) food, antioxidant vitamins and other nutrient supply data in 24 developed countries for 1985-87. Longitudinal analyses of death rates from CHD and supplies between 1970 and 1987 were carried out for all the countries. Correlational analyses of supplies that preceded mortality by up to 10 years were also undertaken. RESULTS: In 17 western European countries the inter-country association of dairy product supply with CHD was of moderate strength (r = 0.5) and the principal saturated fatty acids derived from dairy products: butyric, caproic and myristic acids (C4:0, C6:0 and C14:0) were the most strongly related with CHD (r = 0.5, 0.5 and 0.4 respectively). The phenolic-antioxidant-rich foods, e.g. wine, vegetables and vegetable oils, were inversely related to CHD (r = -0.8, -0.7 and -0.6 respectively). Of the antioxidant vitamins, the alpha-tocopherol component of vitamin E was strongly related to CHD across Europe (r = -0.8). The major determinant of alpha-tocopherol supply was usually sunflowerseed oil. Vitamin C and beta-carotene gave moderate correlations (r = -0.6 and -0.5 respectively). Latency periods of 5 and 10 years between supplies and mortality rates did not markedly change the correlations. Longitudinal analyses of nutrient supplies and death rates within each country from 1970 to 1987 also showed that for the majority of countries there was an inverse association between supply of alpha-tocopherol and CHD. CONCLUSIONS: Dietary alpha-tocopherol may provide at least as good an explanation as does wine for the paradoxically low rates of CHD in several European countries which have a relatively high saturated fatty acid intake.

Selenium status of a group of Scottish adults.

OBJECTIVE: To examine dietary selenium intake and indices of selenium status (plasma and red blood cell selenium and glutathione peroxidase activities) in apparently healthy Scottish individuals. DESIGN AND SUBJECTS: One hundred subjects, aged between 40 and 60 y, completed a seven day weighed food intake and provided blood samples for selenium status analysis. SETTING: Inverurie, Aberdeenshire, Scotland. RESULTS: Average reported selenium intake was low (43 micrograms/d). A significant number of subjects had reported intakes below the RNI. Low levels of plasma selenium were also found but no subject had values below 40 micrograms/1. Red blood cell selenium was within the reference range established for a healthy UK population. Smoking status had no consistent effect on selenium status. CONCLUSIONS: The results of the present study suggest that selenium status of certain Scottish individuals may be compromised and that further studies are warranted. SPONSORSHIP: BASF, Germany; The Tobacco Products Research Trust, UK; Scottish Office Agriculture Environment and Fisheries Department.

Effects of blueberry and cranberry juice consumption on the plasma antioxidant capacity of healthy female volunteers.

OBJECTIVE: To assess whether consumption of 500 ml of blueberry juice or cranberry juice by healthy female subjects increased plasma phenolic content and antioxidant capacity. DESIGN: Latin square arrangement to eliminate ordering effects. After an overnight fast, nine volunteers consumed 500 ml of blueberry juice, cranberry juice or a sucrose solution (control); each volunteer participated on three occasions one week apart, consuming one of the beverages each time. Blood samples were obtained by venipuncture at intervals up to four hours after consumption of the juices. Urine samples were also obtained four hours after consuming the juice. RESULTS: Consumption of cranberry juice resulted in a significant increase in the ability of plasma to reduce potassium nitrosodisulphonate and Fe(III)-2,4, 6-Tri(2-pyridyl)-s-triazine, these measures of antioxidant capacity attaining a maximum after 60-120 min. This corresponded to a 30% increase in vitamin C and a small but significant increase in total phenols in plasma. Consumption of blueberry juice had no such effects. CONCLUSION: The increase in plasma antioxidant capacity following consumption of cranberry juice could mainly be accounted for by an increase in vitamin C rather than phenolics. This also accounted for the lack of an effect of the phenolic-rich but vitamin C-low blueberry juice. SPONSORSHIP: Funded by the Scottish Executive Rural Affairs Department and the Danish Government.