Selenomethionine (Semet) is the major seleno-compound in cereal grains and enriched yeast whereas Se-methylselenocysteine (SeMCYS) is the major seleno-compound in Se-accumulator plants and some plants of economic importance such as garlic and broccoli exposed to excess Se. Animals can metabolize both Semet and SeMCYS. Epidemiological studies have indicated an inverse relationship between Se intake and the incidence of certain cancers. Blood or plasma levels of Se are usually lower in patients with cancer than those without this disorder, but inconsistent results have been found with toenail-Se values and the incidence of cancer. There have been eight trials with human subjects conducted on the influence of Se on cancer incidence or biomarkers, and except for one, all have shown a positive benefit of Se on cancer reduction or biomarkers of this disorder. This is consistent with about 100 small-animal studies where Se has been shown to reduce the incidence of tumours in most of these trials. Se-enriched yeast is the major form of Se used in trials with human subjects. In the mammary-tumour model, SeMCYS has been shown to be the most effective seleno-compound identified so far in reduction of tumours. Several mechanisms have been proposed on the mechanism whereby Se reduces tumours. Even though SeMCYS was shown to be the most effective seleno-compound in the reduction of mammary tumours, it may not be the most effective seleno-compound for reduction of colon tumours.

We investigated the dietary influence of low and high levels of fish oil, supplemented with or without dietary cholesterol, on the plasma lipoprotein profile in Bio F1B hamsters, a model susceptible to diet-induced hyperlipidaemia. The MIX diet, a diet supplemented with a mixture of lard and safflower-seed oil, was used as the control diet to maintain the saturated MUFA and PUFA levels similar to the fish-oil diet. The animals were fed the specific diets for 2 weeks and fasted for 14h before killing. The plasma from the animals fed high levels of fish oil was milky and rich in chylomicron-like particles. The plasma total cholesterol, VLDL- and LDL-cholesterol and -triacylglycerol concentrations were significantly higher, whereas HDL-cholesterol was lower in hamsters fed fish oil compared with the MIX-diet-fed hamsters. Increasing the amount of fat in the diet increased plasma lipids in both the fish-oil- and the MIX-diet-fed hamsters; however, this hyperlipidaemic effect of dietary fat level was greater in the hamsters fed the fish-oil diet. The hepatic lipid concentrations were not dramatically different between the fish-oil-fed and the MIX-diet-fed hamsters. However, the hepatic LDL-receptor mRNA levels were significantly low in the fish-oil-fed hamsters compared with the MIX-diet-fed hamsters. Increasing the amount of fish oil in the diet further decreased the hepatic LDL-receptor mRNA expression. It is concluded that F1B hamsters are susceptible to fish-oil-induced hyperlipidaemia, especially at high fat levels, and this increase is partially explained by the inhibition of hepatic LDL-receptor mRNA expression.

In the present study we examined whether oral administration of bovine lactoferrin (bLF) reduces plasma or hepatic triacylglycerol and cholesterol in mice. When bLF mixed with a standard commercial diet (10g/kg) was given to mice for 4 weeks, plasma triacylglycerol and NEFA decreased, while plasma HDL-cholesterol levels increased (P<0·01). These changes in plasma lipid profiles were accompanied by significant decreases in hepatic cholesterol and triacylglycerol contents. When mice were fed a high-fat diet containing 300·0g lard, 10·0g cholesterol and 2·5g bovine bile powder/kg for 4 weeks, bovine LF did not have any significant effects on plasma or hepatic cholesterol and triacylglycerol concentrations. Furthermore, bLF had no significant effects on faecal excretion of total bile acids in mice. Interestingly, bLF showed a suppressive effect on the lymphatic triacylglycerol absorption in chronically treated rats. We conclude that bLF has a beneficial effect on plasma cholesterol levels and retards hepatic lipid accumulation in mice fed a standard diet.

Primary open-angle glaucoma (POAG) is a complex chronic neurological disease that can result in blindness. The goal of understanding the aetiology of POAG is to be able to target effective treatment to individuals who will eventually go blind without it. Epidemiological studies of POAG have not specifically addressed the possibility that nutrition may play a role in the development of POAG. A handful of papers have considered that nutrition may have an impact on POAG patients. POAG is not believed to be a ‘vitamin-deficiency disease’. The concept of ‘vitamin-deficiency diseases’ and the recommended daily allowances have not kept pace with the growing understanding of the cellular and molecular functions of vitamins and other micronutrients. The aetiology of POAG remains a mystery. Discoveries in cell physiology can be assimilated from the literature and applied to known homeostatic mechanisms of the eye. In this way the possible roles of nutritional components involved in the aetiology of POAG can be described. The mechanisms may be subject to many influences in ways that have yet to be defined. Two distinct changes in the trabecular meshwork can be identified: trabecular meshwork changes that cause intra-ocular pressure to increase and trabecular meshwork changes that are directly correlated to optic nerve atrophy. Compelling evidence suggests that collagen trabecular meshwork extracellular matrix (ECM) remodelling is correlated to increased intraocular pressure in POAG. Elastin trabecular meshwork ECM remodelling is correlated to POAG optic nerve atrophy. There appear to be two different pathways of ECM remodelling and apoptosis induction in POAG. The pathway for collagen remodelling and apoptosis induction seems to be exogenously influenced by water-soluble antioxidants, for example, glutathione. The pathway for elastin remodelling and apoptosis induction seems to be influenced by endogenous lipid-soluble antioxidants, for example, vitamin E. Roles can be defined for antioxidants in the two different pathways of ECM remodelling and apoptosis induction. This suggests that antioxidants are important in maintaining cellular homeostasis relevant to the aetiology of POAG.

Typically, poultry diets contain 1–2 mg I/kg, but higher concentrations are sometimes used to enhance the I content of eggs. In addition to an increased deposition of I in the yolk, other often adverse responses occur, especially at exceptionally high concentrations. Excess I in grower diets can prevent sexual maturation in male and female fowl, and in layer diets will progressively reduce egg production until, by about 2500 mg I/kg diet, ovulation is inhibited and egg production ceases. Most I accumulates in the thyroid gland, and it is likely that the mechanism responsible for these reproductive disorders involves a modification of thyroid hormone activity. Simultaneous with the declining rate of lay, feed intake declines, egg weight and yolk-cholesterol contents decrease and body weight increases. Whereas fertility is unaffected in female breeders, hatch of fertile eggs is reduced, hatch time extended and embryonic mortality and dead-in-shell proportions increased. In contrast, male fertility is decreased because of an increased incidence of dead spermatozoa, although hatchability of eggs from normally fed hens is unaffected. All reproductive variables, together with feed intake and body weight, are normalised within about 7 d of returning to a diet with normal I levels. Excess I suppresses growth in meat-type chickens, but does not affect feed conversion efficiency. There are transient increases in plasma I and cholesterol concentration during excess I intake in all types of bird. The evidence for varying responses to different I sources is equivocal, but the consensus is that source is probably not important.

The importance of legume proteins in cholesterol metabolism has been recognised, but the hindgut contribution is still unclear. The present work was undertaken to address the role of the caecum–colon in cholesterol metabolism in intact (I) and ileo-rectal anastomosed (IRA) pigs fed with casein or extruded soyabean (ES) diets. Four groups of six growing pigs were assigned to the treatments (casein–I, casein–IRA, ES–I, ES–IRA) for 3 weeks. Plasma total cholesterol, LDL- and HDL-cholesterol were not modified by surgery or diet. In the liver, the ES diet significantly depressed non-esterified, esterified and total cholesterol. The treatments did not affect hepatic 3-hydroxy-3-methylglutaryl CoA reductase, cholesterol 7α-hydroxylase or sterol 27-hydroxylase activities. In the gallbladder bile of ES-fed pigs, total cholesterol was depressed while total bile acid concentration was increased. IRA and the ES diet markedly decreased the biliary bile acid microbial metabolites (namely hyodeoxycholic acid) and increased the primary bile acids (mainly hyocholic acid). The concentration of bile hydrophobic acids was decreased only by the ES diet. Faecal neutral sterol output was increased in ES-fed pigs, but the bile acid and the sum of neutral and acidic steroid outputs were not. Microbial transformation of neutral and acidic steroids was markedly reduced by IRA, especially in the ES-fed pigs. Thus, surgery and ES modulated the steroid profile but the caecum–colon did not seem to play a crucial role in determining cholesterolaemia in pigs.

Serotonin (5-HT) is an important neurotransmitter involved in the brain–gut axis. It is possible to lower the 5-HT level in the body by means of a nutritional intervention using an amino acid mixture; the acute tryptophan depletion (ATD) method. We studied the effect of ATD on gastric emptying in healthy females, who received both ATD and placebo in a random order. Gastric emptying was measured using the [13C]octanoic acid breath test. The present data demonstrate significant differences in both gastric emptying and lag phase (Tlag) between the ATD and placebo experiment. Eight out of ten subjects showed a delayed gastric emptying in the ATD experiment. Both the gastric half-emptying time (T1/2) and the Tlag were significantly higher in the ATD experiment. T1/2 in the ATD experiment was 137·2 (range 76·2–634·8) min; T1/2 for the placebo experiment was 98·5 (range 63·7–168·8) min (P=0·028). Tlag in the ATD experiment was 83·7 (range 45·1–356·2) min; Tlag for the placebo experiment was 56·9 (range 23·2–101·2) min (P=0·007). We conclude that lowering the 5-HT level in the body using the ATD method leads to a significantly delayed gastric emptying of a solid meal. Nutritional manipulation of the serotonergic system in healthy volunteers may lead to alterations in gastrointestinal motility.

The aim of our present study was to compare the efficiency of conjugated linoleic acids (CLA) and fish oil in modulating atherogenic risk markers. Adult male hamsters were given a cholesterol-rich diet (0·6 g/kg) for 8 weeks; the diet was supplemented with 5 g cis-9,trans-11-CLA isomer/kg, 12 g CLA mixture (CLA-mix)/kg, 12 g fish oil/kg or 12 g fish oil + 12 g CLA-mix/kg. The plasma cholesterol status was improved only with the cis-9,trans-11-CLA (HDL-cholesterol and HDL-cholesterol:LDL-cholesterol ratio, P<0·05), but was of borderline significance for CLA-mix (HDL-cholesterol:LDL-cholesterol ratio, P=0·06), with an increase (33–40 %) in the liver lipoprotein receptors (scavenger receptor-type I and LDL ApoB/E receptor) and HDL-binding protein 2 (P<0·05). A 100 % pigment gallstones incidence and a slight insulin resistance (homeostatic model assessment index) were observed in the CLA-mix-fed hamsters (P=−0·031). In comparison, fish-oil feeding alone improved merely the scavenger receptor-type I and HDL-binding protein 2 liver status and faeces sterol output. For most of our present observations, the concomitant intake of fish oil and CLA-mix gave dominant effects that were exclusive and specific to one or the other oil. In conclusion, part of the beneficial effects of CLA in the present study can be ascribed to the cis-9,trans-11-isomer, and these did not generally overlap with those of fish oil. In addition, the CLA-mix effects are clearly affected by the marine (n-3) fatty acids.

The present study investigated the susceptibility of dietary n-3 PUFA to ruminal biohydrogenation, the stability of ingested vitamin E in the rumen and the subsequent uptake of PUFA and vitamin E into plasma. Six cannulated sheep were assigned to six diets over five 33d periods, in an incomplete 6×5 Latin square. The diets, based on dried grass, were formulated to supply 50g fatty acids/kg DM using three lipid sources: Megalac® (calcium soap of palm fatty acid distillate; Volac Ltd, Royston, Herts., UK), linseed (formaldehyde-treated; Trouw Nutrition, Northwich, Ches., UK) and linseed–fish oil (formaldehyde-treated linseed+fish oil). The diets were supplemented with 100 or 500mg α-tocopheryl acetate/kg DM. Fat source or level of vitamin E in the diet did not alter microbial activity in the rumen. Biohydrogenation of linoleic acid (18:3n-6; 85–90%), linolenic acid (18:3n-3; 88–93%), docosahexaenoic acid (22:6n-3; 91%) and EPA (20:5n-3; 92%) was extensive. Feeding formaldehyde-treated linseed elevated concentrations of 18:3n-3 in plasma, whilst 22:6n-3 and 20:5n-3 were only increased by feeding the linseed–fish oil blend. Duodenal recovery of ingested vitamin E was high (range 0·79–0·92mg/mg fed). High dietary vitamin E was associated with increased plasma α-tocopherol (2·57 v. 1·46μg/ml for 500 and 100mg α-tocopheryl acetate/kg DM respectively), although all concentrations were low. Plasma vitamin E levels, however, tended to decrease as the type and quantity of PUFA in the diet increased. The present study illustrates that nutritionally beneficial PUFA in both fish and linseed oils are highly susceptible to biohydrogenation in the rumen. Although α-tocopheryl acetate resisted degradation in the rumen, plasma vitamin E status remained deficient to borderline, suggesting either that uptake may have been impaired or metabolism post-absorption increased.

Consumption of fruits and vegetables has been associated with cancer prevention; flavonoids are widely distributed in plant foods and considered to be the active ingredients. Quercetin and kaempferol are two of the most commonly found dietary flavonols, and have been reported to prevent cancer. We have previously reported that the isoflavone genistein and the flavone baicalein exert differential actions on the oestrogen receptor (OR) α in HepG2 cells. Because of the structural resemblance to both isoflavone and flavone, we examined the effects of these dietary flavonols on ORα– and ORβ–specific transactivations and their subsequent involvement in inducing MCF-7 cell death. In the present study, both quercetin and kaempferol were able to compete for OR binding in a cell-free system and were agonistic to ORα and -β expressed in HepG2 cells, while some additive effect was observed in the oestrogen response element (ORE)-driven transcription when 17β-oestradiol was co-administered. Since the bcl-2 promoter contained two ORE, and ORE-driven transcriptional activity and Bcl-2 mRNA expression were increased by treatment with 10 μm-quercetin or kaempferol, it is possible that quercetin and kaempferol might up-regulate Bcl-2 expression through OR transactivation in MCF-7 cells. Cell death ELISA assay performed on MCF-7 cells indicated that an increase of apoptosis occurred at 25 μm-, but not 10 μm-, quercetin or kaempferol. Indirectly the results suggest that OR activation is not sufficient to induce apoptosis and that apoptosis is induced despite an increase in Bcl-2 expression.

Diabetes-prone BioBreeding (BBdp) rats often present an enteropathy that may precede the onset of autoimmune insulitis. The aim of the present study was to assess the influence of sex, the time course, the strain specificity, the distribution along the intestinal tract and the effect of diet for the changes in the activity of gut invertase, maltase and lactase found in BBdp rats, as compared with both Wistar–Furth (WF) and diabetes-resistant BioBreeding (BBc) rats. These hydrolases were measured, therefore, at day 10, 30, 45, 70, 95 and 120 in three intestinal segments of WF, BBc and BBdp rats fed, after weaning, either a protective high-casein diet, which decreases the incidence of diabetes in the BBdp rats, or one of two diabetogenic diets (National Toxicology Program; NTP or wheat-gluten-based; WG). Except for a somewhat lower lactase activity in the BBdp rats, no obvious difference in hydrolyase activity between the three strains of rats was observed at day 10. Between days 30 and 120, however, the activity of the hydrolases, especially that of invertase and lactase, was lower in the BBdp rats than in either the WF or BBc rats, at least when considering the animals fed either the NTP or WG diet. These findings support the view that BBdp rats exposed to a diabetogenic diet develop an enteropathy well before the onset of autoimmune insulitis, in a manner somehow comparable with the situation found in some type 1 diabetic patients, in whom coeliac disease may be diagnosed before diabetes onset.

Factors affecting absorption of physiological doses of vitamin C in man have not been widely studied, partly because few suitable tools exist to distinguish recently absorbed vitamin C from endogenous vitamin. Stable isotope-labelled vitamin C provides such a tool. Fifteen healthy non-smoking subjects aged 26–59 years were studied. Each received 30 mg L-[1-13C]ascorbic acid orally on two occasions, 3–4 weeks apart. The ascorbate was given alone or with Fe (100 mg as ferrous fumarate) or with red grape juice, which is rich in polyphenols. Blood was collected at frequent intervals for 1 h, and then each hour for a further 3 h. Total concentration of vitamin C was measured fluorometrically and its 13C-isotope enrichment was measured by GC–MS after conversion to volatile trimethylsilyl esters. Peak plasma enrichment occurred within 25–50 min. No kinetic variables were significantly altered by the iron fumarate supplement. Grape juice attenuated vitamin C absorption, reaching significance at the 20 min time point. There were weak correlations between isotope enrichment and body weight or endogenous ascorbate concentration. The increment in total plasma ascorbate was smaller if calculated from isotope enrichment than from vitamin C concentration increase. The dilution pool was much larger than the plasma ascorbate pool. Further studies are needed to resolve these paradoxes. Stable isotope-labelled ascorbate is potentially useful for measurement of vitamin C absorption by human subjects.

Acarbose (Glucobay®; Bayer) is an α-glucosidase inhibitor used to treat diabetes and which may have a role in the prevention of type 2 diabetes. The present study investigated the effects of acarbose treatment on the site and extent of starch digestion, large-bowel fermentation and intestinal mucosal cell proliferation. Eighteen young male Wistar rats were fed ‘Westernised’ diets containing 0, 250 and 500mg acarbose/kg (six rats/diet) for 21d. For most variables measured, both acarbose doses had similar effects. Acarbose treatment suppressed starch digestion in the small bowel but there was compensatory salvage by bacterial fermentation in the large bowel. This was accompanied by a substantial hypertrophy of small- and large-bowel tissue and a consistent increase in crypt width along the intestine. Caecal total SCFA pool size was increased more than 4-fold, with even bigger increases for butyrate. These changes in butyrate were reflected in increased molar proportions of butyrate in blood from both the portal vein and heart. There was little effect of acarbose administration on crypt-cell proliferation (significant increase for mid-small intestine only). This is strong evidence against the hypothesis that increased fermentation and increased supply of butyrate enhances intestinal mucosal cell proliferation. In conclusion, apart from the increased faecal loss of starch, there was no evidence of adverse effects of acarbose on the aspects of large-bowel function investigated.

The effect of feeding n-3 PUFA on the fatty acid composition of muscle, adipose tissue and liver of lambs was investigated. Groups of eight ram lambs per breed, Suffolk×Lleyn (24kg live weight) and Scottish Blackface (18kg live weight), were each fed one of six diets containing one of three fat sources (50g fatty acids/kg DM; Megalac® (calcium soap of palm fatty acid distillate; Volac Ltd, Royston, Herts., UK) and formaldehyde-treated whole linseed (Trouw Nutrition UK, Northwich, Ches., UK) either alone or with fish oil (1:1, w/w) and either 100 or 500mg α-tocopheryl acetate/kg DM. Feed was offered ad libitum until slaughter at approximately half breed mature live weight. The type of dietary fat had no effect on intake, growth rate or feed conversion ratio. The 3·0-fold higher concentration of 18:3n-3 in the linseed compared with the Megalac® diet approximately doubled (P<0·001) the concentration in the neutral and polar lipid fractions of musculus semimembranosus and liver, and in adipose tissue it increased 2·5-fold. Feeding protected linseed also increased (P<0·001) concentrations of 20:5n-3 and 22:5n-3 in muscle polar lipids and both lipid fractions of liver. The linseed–fish oil raised the 20:5n-3 concentrations above those for the linseed diet and also increased 22:6n-3. Scottish Blackface lambs had lower concentrations of 18:3n-3 in all lipids compared with Suffolk x Lleyn lambs, but more 20:5n-3 in the polar lipids of muscle and liver. High levels of dietary vitamin E were associated with small decreases in the concentration of monounsaturated fatty acids and increases in PUFA. Linseed raised the PUFA:saturated fatty acid ratios in liver and adipose tissue but not in muscle, and improved the n-6:n-3 fatty acid ratio, as did the linseed–fish oil. Different combinations of dietary fatty acids and better protection against rumen biohydrogenation are required to improve muscle PUFA:saturated fatty acids ratios.

The influence of a high-Na, high-protein (calciuric) diet on Ca and bone metabolism was investigated in postmenopausal women (aged 50–67 years) who were stratified by vitamin D receptor (VDR) genotype. In a crossover trial, twenty-four women were randomly assigned to a diet high in protein (90 g/d) and Na (180 mmol/d) or a diet adequate in protein (70 g/d) and low in Na (65 mmol/d) for 4 weeks, followed by crossover to the alternative dietary regimen for a further 4 weeks. Dietary Ca intake was maintained at usual intakes (about 20 mmol (800 mg)/d). Urinary Na, K, Ca, N and type I collagen cross-linked N-telopeptide (NTx; a marker of bone resorption), plasma parathyroid hormone (PTH), serum 25-hydroxycholecalciferol (25(OH)D3), 1,25-dihydroxycholecalciferol (1,25(OH)2D3), osteocalcin and bone-specific alkaline phosphatase (B-Alkphase) were measured in 24 h urine samples and fasting blood samples collected at the end of each dietary period. The calciuric diet significantly (P<0·05) increased mean urinary Na, N, K, Ca and NTx (by 19 %) compared with the basal diet, but had no effect on circulating 25(OH)D3, 1,25(OH)2D3, PTH, osteocalcin or B-Alkphase in the total group (n 24). There were no differences in serum markers or urinary minerals between the basal and calciuric diet in either VDR genotype groups. While the calciuric diet significantly increased urinary NTx (by 25·6 %, P<0·01) in the f+ VDR group (n 10; carrying one or more (f) Fok I alleles), it had no effect in the f− VDR group (n 14; not carrying any Fok I alleles). It is concluded that the Na- and protein-induced urinary Ca loss is compensated for by increased bone resorption and that this response may be influenced by VDR genotype.

Quercetin is an important dietary flavonoid with putative beneficial effects in the prevention of cancer and CVD. The in vivo bioactivity of quercetin depends on its bioavailability, which varies widely between foods. We used an in situ rat intestinal perfusion model to study whether differential small intestinal hydrolysis of the sugar moiety of five naturally occurring quercetin glycosides determines the small intestinal uptake and subsequent biliary excretion of quercetin. After 30 min perfusion, a decrease of intact quercetin glycoside in perfusate was observed for quercetin-3-O-ß-glucoside (20·9 (sem 1·4) μmol/l) and quercetin-4′-O-ß-glucoside (23·5 (sem 1·6) μmol/l), but not of quercetin-3-O-ß-galactoside, quercetin-3-O-ß-rhamnoside and quercetin-3-O-α-arabinopyranoside. Appearance of free quercetin in perfusate and conjugated quercetin metabolites (quercetin, isorhamnetin, and tamarixetin) in portal and peripheral plasma and bile were also significantly greater after treatment with quercetin-3-O-ß-glucoside or quercetin-4′-O-ß-glucoside compared with any of the other glycosides. Thus, the type of sugar moiety is a major determinant of the small intestinal absorption of quercetin glycosides, but the position (3 or 4′) of the glucose moiety does not further influence absorption. The poor bioavailability of important dietary quercetin glycosides has implications for their in vivo bioactivities.

Recent experimental data point to an interaction of dietary flavonol monoglucosides with the intestinal Na-dependent glucose transporter 1 (SGLT1). To investigate this interaction in more detail, we performed experiments with SGLT1-containing brush-border-membrane vesicles (BBMV) from pig jejunum. The flavonol quercetin-3-O-glucoside (Q3G) concentration-dependently inhibited Na-dependent uptake of radioactively labelled d-glucose into BBMV. Uptake of l-leucine was not inhibited by Q3G, indicating a specific interaction of the glucoside with SGLT1. Whereas the maximal transport rate of concentration-dependent initial glucose uptake was not altered in the presence of Q3G, the constant for half-maximal glucose uptake was increased, suggesting a competitive type of inhibition of glucose uptake by Q3G. Trans-stimulation experiments suggested the transport of Q3G via SGLT1. In addition, Q3G decreased the Na-independent diffusive uptake of glucose into BBMV. Other flavonoids were also tested for their inhibitory effect on d-glucose uptake. Among the tested quercetin glycosides, only the 4′-O-glucoside (Q4G) also inhibited Na-dependent glucose uptake into BBMV, whereas the 3-O-galactoside, the 3-O-glucorhamnoside and the aglycone quercetin itself were ineffective. Glucosides of some other flavonoid classes such as naringenin-7-O-glucoside, genistein-7-O-glucoside and cyanidin-3,5-O-diglucoside were ineffective as well. Thus, dietary quercetin monoglucosides, for example, Q3G and Q4G, have an impact on intestinal nutrient transporters such as SGLT1 and related systems.

Urinary isoflavone excretion is used to monitor compliance and examine biological effects. The present study determined if there were alterations in urinary isoflavone excretion following the ingestion of different soya foods and if age and gender potentially modified profiles. Twenty premenopausal women, seventeen post-menopausal women and twenty men received a defined single oral bolus dose (0·44mg isoflavones/kg body weight) of soya milk, textured vegetable protein (TVP) or tempeh on three separate occasions. Baseline and four consecutive complete 24h pooled urines were collected during each period. Urinary genistein recovery was influenced by gender and food matrix. For women the urinary genistein recovery was higher following soya-milk consumption compared with TVP (P<0·05). Tempeh consumption also resulted in an increased urinary genistein recovery relative to soya milk in premenopausal women (P<0·052). No differences in urinary genistein recoveries between soya foods were observed in the men. Although urinary daidzein excretion was similar across the foods studied and was not affected by age or gender, conversion to its intestinal metabolite, equol, resulted in potential matrix and chemical composition effects; urinary equol excretion was higher (P<0·01) following tempeh ingestion among equol producers. Together these data suggest that the fractional absorption of genistein is potentially different in men and women and is influenced by the food matrix and chemical composition. Furthermore, the data suggest that the metabolism of daidzein may be altered by the chemical composition of the isoflavones ingested. Further studies are required to examine the effect of higher intake and define the relative influence of these factors in elderly population groups.

Although garlic and onions have long been associated with putative cardiovascular health benefits, the effects of different commercially available onions and level of intake have not been studied. Therefore, the aim of the present study was to evaluate the potential health benefits of raw onions using the pig as a biomedical model. Twenty-five female (Large White×Landrace) pigs were used in a (2×2)+1 factorial experiment. Pigs were fed a standard grower diet supplemented with 100 g tallow/kg with the addition of Allium cepa var. cavalier or var. destiny at 0, 10 or 25 g/MJ digestible energy for 6 weeks. Overall, the consumption of onions resulted in significant reductions in plasma triacylglycerol; however, the reductions were most pronounced in pigs fed destiny onions (−26 %, P=0·042). Total plasma cholesterol and LDL:HDL ratios were not significantly different. Onion supplementation, regardless of the variety, resulted in dose-dependent reductions in erythrocyte counts and Hb levels, while the white blood cell concentrations, particularly lymphocytes, were increased in pigs that consumed onions. Furthermore, indices of blood clotting were largely unaffected by onion consumption. In conclusion, dietary supplementation with raw brown onions has moderate lipid-modulating and immunostimulatory properties. However, daily onion intake >25 g/MJ digestible energy could be detrimental to erythrocyte numbers.

Reports on the effects of carotenoids are conflicting. The present paper examines similarities and differences from contiguous studies in vitro and in vivo. Single-cell gel electrophoresis was used to measure the frequency of single-strand breaks (SSB) in the cell line MOLT-17 (as a model system) and human peripheral blood lymphocytes (PBL). MOLT-17 cells were supplemented with β-carotene, lutein or lycopene at a range of concentrations (0·00–8·00 μmol/l) using a liposome delivery method. Uptake was dose-dependent. β-Carotene concentration in the media had no effect on SSB in control cells, but incubation with lycopene or lutein (>2·00 μmol/l) increased the numbers of SSB in control cells. MOLT-17 DNA was less susceptible to oxidative damage (100 μmol H2O2/l, 5 min, 4 °C) following incubation with carotenoids between 0·50 and 1·00 μmol/l; at >1·00 μmol/l the effects were ambiguous. Apparently healthy male volunteers supplemented their habitual diets with lutein, β-carotene or lycopene (natural isolate capsules, 15 mg/d, 4 weeks) in three independent studies, raising plasma concentrations to different extents. Lycopene and lutein had no effect on SSB in control PBL or following oxidative challenge. However, increased plasma β-carotene was associated with more SSB in control cells whilst PBL DNA resistance to oxidative damage ex vivo was unaffected. These results suggest that the carotenoids are capable of exerting two overlapping but distinct effects: antioxidant protection by scavenging DNA-damaging free radicals and modulation of DNA repair mechanisms.