Intracellular vitamin C acts to protect cells against oxidative stress by intercepting reactive oxygen species (ROS) and minimising DNA damage. However, rapid increases in intracellular vitamin C may induce ROS with subsequent DNA damage priming DNA repair processes. Herein, we examine the potential of vitamin C and the derivative ascorbate-2-phosphate (2-AP) to induce a nucleotide excision repair (NER) response to DNA damage in a model of peripheral blood mononuclear cells. Exposure of cells to elevated levels of vitamin C induced ROS activity, resulting in increased levels of deoxycytidine glyoxal (gdC) and 8-oxo-2′-deoxyguanosine (8-oxodG) adducts in DNA; a stress response was also induced by 2-AP, but was delayed in comparison to vitamin C. Evidence of gdC repair was also apparent. Measurement of cyclobutane thymine–thymine dimers (T < >T) in DNA and culture supernatant were included as a positive marker for NER activity; this was evidenced by a reduction in DNA and increases in culture supernatant levels of T < >T for vitamin C-treated cells. Genomics analysis fully supported these findings confirming that 2-AP, in particular, induced genes associated with stress response, cell cycle arrest, DNA repair and apoptosis, and additionally provided evidence for the involvement of vitamin C in the mobilisation of intracellular catalytic Fe.

Anthocyanins are natural pigments abundant in various fruits and berries that are involved in the prevention of various chronic diseases. Their low concentrations in plasma and urine are explained in part by their complex chemistry and the formation of still uncharacterised metabolites. The aim of the present study was to follow the distribution of anthocyanins in the body using 14C-labelled cyanidin 3-O-glucoside (Cy3G) fed by gavage to mice. After the administration of 22·2 kBq 14C-Cy3G (0·93 mg), radioactivity was detected in most organs tested over the following 24 h with a peak observed in inner tissues at 3 h. The major fraction of the radioactivity (44·5 %) was found in the faeces collected 24 h after ingestion. At 3 h after oral administration of 141 kBq 14C-Cy3G (4·76 mg), most of the radioactivity (87·9 % of intake) was recovered in the gastrointestinal (GI) tract, especially in the small intestine (50·7 %) and the caecum (23 %). At this time, 3·3 % of the radioactivity was detected in urine. There was minimal accumulation (0·76 %) of radioactivity in tissues outside the GI tract. Distribution of radioactivity varied among organs, with liver, gallbladder and kidneys showing the highest radioactivity. Taken as a whole, these results show that Cy3G is poorly absorbed in the mouse.

Caffeine and caffeinated coffee (CC) elicit acute insulin insensitivity when ingested before a carbohydrate load. The effects of CC on glucose tolerance and insulin sensitivity when co-ingested with a high carbohydrate meal and on postprandial metabolism of a subsequent (second) carbohydrate load have not been studied. In a randomised, crossover design, ten healthy males ingested either CC (5 mg caffeine/kg body weight), decaffeinated coffee (DC) or water (W; equal volume) co-ingested with a high glycaemic index cereal followed 3 h later by a 75 g oral glucose tolerance test. After the initial meal, insulin area under the curve (AUC) and insulin sensitivity index did not differ between treatments, although glucose AUC for CC (107 (sem 18) mmol/l × 3 h) and DC (74 (sem 15) mmol/l × 3 h) was greater than W ( − 0·2 (sem 29) mmol/l × 3 h, P < 0·05). After the second carbohydrate load, insulin AUC for CC was 49 % and 57 % greater (P < 0·01) than for DC and W, respectively. Despite the greater insulin response, glucose AUC for CC (217 (sem 24) mmol/l × 2 h) was greater than both DC (126 (sem 11) mmol/l × 2 h, P = 0·01) and W (55 (sem 34) mmol/l × 2 h, P < 0·001). Insulin sensitivity index after the second meal was lower after CC (8·2 (sem 0·9)) compared with both DC (12·4 (sem 1·2), P < 0·01) and W (13·4 (sem 1·4), P < 0·001). Co-ingestion of CC with one meal resulted in insulin insensitivity during the postprandial phase of a second meal in the absence of further CC ingestion. Thus, CC may play a role in daily glycaemic management.

Selective breeding of dogs has culminated in a large number of modern breeds distinctive in terms of size, shape and behaviour. Inadvertently, a range of breed-specific genetic disorders have become fixed in some pure-bred populations. Several inherited conditions confer chronic metabolic defects that are influenced strongly by diet, but it is likely that many less obvious breed-specific differences in physiology exist. Using Labrador retrievers and miniature Schnauzers maintained in a simulated domestic setting on a controlled diet, an experimental design was validated in relation to husbandry, sampling and sample processing for metabolomics. Metabolite fingerprints were generated from ‘spot’ urine samples using flow injection electrospray MS (FIE-MS). With class based on breed, urine chemical fingerprints were modelled using Random Forest (a supervised data classification technique), and metabolite features (m/z) explanatory of breed-specific differences were putatively annotated using the ARMeC database (http://www.armec.org). GC-MS profiling to confirm FIE-MS predictions indicated major breed-specific differences centred on the metabolism of diet-related polyphenols. Metabolism of further diet components, including potentially prebiotic oligosaccharides, animal-derived fats and glycerol, appeared significantly different between the two breeds. Analysis of the urinary metabolome of young male dogs representative of a wider range of breeds from animals maintained under domestic conditions on unknown diets provided preliminary evidence that many breeds may indeed have distinctive metabolic differences, with significant differences particularly apparent in comparisons between large and smaller breeds.

Healthy human pregnancy is associated with changes in food intake, body fatness, energy expenditure and insulin resistance. However, available knowledge is limited regarding the physiological basis of these changes. Published evidence suggests that so-called adipokines (i.e. leptin, adiponectin and resistin) have significant roles when such changes are established. We explored, throughout a complete pregnancy, relationships between total body fat (TBF), energy expenditure, insulin resistance (homeostasic model of insulin resistance, HOMA-IR) and serum concentrations of leptin, adiponectin and resistin. Such concentrations were assessed before pregnancy in gestational weeks 8, 14, 20, 32 and 35, and 2 weeks postpartum in twenty-three healthy women. TBF, BMR (n 23) and HOMA-IR (n 17) were assessed before pregnancy in gestational weeks 14 and 32 and 2 weeks postpartum. TBF (%) was correlated with HOMA-IR (r 0·68–0·79, P < 0·01) and with serum leptin (r 0·85–0·88, P < 0·001) before and during pregnancy. Serum leptin was correlated with HOMA-IR (r 0·53–0·70, P < 0·05) before and during pregnancy. Serum adiponectin was inversely correlated with HOMA-IR in gestational week 32 (r − 0·52, P < 0·05). When HOMA-IR was regressed on TBF (%), the slope of the regression line was 0·046 before pregnancy, which was significantly (P < 0·05) different from the corresponding value, 0·111, in gestational week 32. The results indicate that pregnancy has an enhancing effect on the relationship between body fatness and insulin resistance. This effect, possibly mediated by leptin, may represent a mechanism by which offspring size is regulated in response to the nutritional situation of the mother.

Numerous studies indicate that polyphenol-rich chocolate reduces fasting blood glucose, blood pressure (BP) and total cholesterol in healthy individuals and hypertensives with or without glucose intolerance. The aim of the present study was to investigate the effect of two doses of polyphenol-rich dark chocolate (DC) on fasting capillary whole blood glucose, total cholesterol and BP and to examine whether improvements in these parameters are associated with changes in adrenocorticoid excretion in overweight and obese individuals. The study used a randomised, single-blind, cross-over design where fourteen overweight and obese subjects were randomised to either take 20 g DC with 500 mg polyphenols then 20 g DC with 1000 mg polyphenols or vice-versa. Participants followed each diet for 2 weeks separated by a 1-week washout period. It was observed that the 500 mg polyphenol dose was equally effective in reducing fasting blood glucose levels, systolic BP (SBP) and diastolic BP (DBP) as the 1000 mg polyphenol dose suggesting that a saturation effect might occur with increasing dose of polyphenols. There was also a trend towards a reduction in urinary free cortisone levels with both groups although it did not reach statistical significance. No changes in anthropometrical measurements were seen. We suggest that more research is required to investigate the mechanism(s) by which polyphenol-rich foods influence health.

Maternal protein restriction in rat pregnancy is associated with altered feeding behaviour in later life. When allowed to self-select their diet, rats subject to prenatal undernutrition show an increased preference for fatty foods. The main aim of the present study was to evaluate the contribution of folic acid in the maternal diet to programming of appetite, since disturbances of the folate and methionine–homocysteine cycles have been suggested to impact upon epigenetic regulation of gene expression and hence programme long-term physiology and metabolism. Pregnant rats were fed diets containing either 9 or 18 % casein by weight, with folate provided at either 1 or 5 mg/kg diet. Adult male animals exposed to low protein (LP) in fetal life exhibited increased preference for high-fat food. Providing the higher level of folate in the maternal diet prevented this effect of LP, but offspring of rats fed 18 % casein diet with additional folate behaved in a similar manner to LP-exposed animals. Among day 20 gestation fetuses, it was apparent that both protein restriction and maternal folate supplementation could have adverse effects upon placental growth. Examination of methionine–homocysteine and folate cycle intermediates, tissue glutathione concentrations and expression of mRNA for methionine synthase, DNA methyltransferase 1 and methyltetrahydrofolate reductase revealed no gross disturbances of folate and one-carbon metabolism in either maternal or fetal tissue. The present findings indicated that any role for DNA methylation in programming of physiology is not related to major perturbations of folate metabolism, and is likely to be gene-specific rather than genome-wide.

The cytoplasmic serine/threonine ribosomal protein S6 kinase (S6K1) plays a critical role in controlling protein translation. There is evidence that amino acids regulate S6K1 and protein synthesis in avian species, but the effect of dietary protein level on the activation of S6K1 in neonatal chicks is unknown. Therefore, the aim of the present experiment was to investigate the effect of different protein levels, supplied during the first 5 d post-hatch, on body growth, breast muscle development and on the activation of S6K1 and its downstream target, the S6, in neonatal chicks. Chicks were fed a pre-starter diet during the first 5 d post-hatch containing low (19·6 % crude protein (CP); LP), medium (23·1 % CP; MP) or high (26·7 % CP) levels (HP) of protein. Weight gain of chicks fed the HP diet was higher (P < 0·05) compared with those fed the LP diet during day (d)3–d5 and the numerical advantage of this group was maintained from d2 to d7. On d2 and d3, greater levels of S6K1 and S6 phosphorylation and/or activity were observed in chicks receiving the HP diet compared with LP and MP diets, without differences between results of the latter two dietary treatments. In conclusion, the present results suggest that early protein nutrition impacts the development of broiler chicks.

The present study quantifies the relationships between diet fatty acid profile and fatty acid composition of rat skeletal muscle phospholipids. Young adult male Sprague–Dawley rats were fed, for 8 weeks, on one of twelve moderate-fat diets (25 % of total energy) differing only in fatty acid profile. SFA content ranged from 8–88 % of total fatty acids, MUFA 6–65 %, total PUFA 4–81 %, n-6 PUFA 3–70 % and n-3 PUFA 1–70 %. Diet PUFA included only essential fatty acids 18 : 2n-6 and 18 : 3n-3. The balance between n-3 and n-6 PUFA (PUFA balance) in the diet ranged from 1 : 99 to 86 : 14 % n-3 PUFA:n-6 PUFA. The slope of muscle phospholipid composition plotted against diet composition quantifies the response of muscle membrane composition to dietary fat (0, no response; 1, complete conformity with diet). The resulting slopes were 0·02 (SFA), 0·10 (PUFA), 0·11 (MUFA), 0·14 (n-3 PUFA) and 0·23 (n-6 PUFA). The response to PUFA balance was biphasic with a slope of 0·98 below 10 % diet PUFA balance and 0·16 above 10 %. Thus, low diet PUFA balance has greater influence on muscle composition than 18-carbon n-3 or n-6 PUFA individually. Equations provided may allow prediction of muscle composition for other diet studies. Diet PUFA balance dramatically affects muscle 20 : 4n-6 and 22 : 6n-3. This may have significant implications for some disease states in human subjects.

The study was based on correlating a dataset of in vivo mean starch digestibility coefficients obtained in the immediate post-weaning phase of piglets with a range of dietary in vitro variables. The paper presents a model that predicts (R2 0·71) in vivo average starch digestibility coefficients in the 0·5 small-intestinal region of newly weaned piglets fed cereal-based diets using seven in vitro variables describing starch properties that are fundamentally associated with the quality of feed materials, i.e. hydration, structure and amylolytic digestion. The variables were: Rapid Visco Analyser (RVA; measures the viscosity of materials when sheared under defined hydration and temperature regimens); RVA end viscosity; RVA (gelatinisation) peak viscosity; ΔH (gelatinisation enthalpy that provides an estimate of helical order or degree of crystallinity in starch); water solubility index (WSI; that denotes the amount of soluble polysaccharides released from starch granules to the aqueous phase); grain endogenous amylase (concentration of endogenous α-amylase in cereals, assessed by pasting cereal flours in 25 g of AgNO3, an amylase inhibitor v. water using RVA).

Leafy vegetables are important sources of provitamin A carotenoids. Information on their ability to provide vitamin A is often misleading because of the methodology used to assess bioefficacy. Mongolian gerbils were used to evaluate the bioefficacy of provitamin A carotenoids in tropical leafy vegetables (i.e. Solanum nigrum, Moringa oleifera, Vernonia calvoana and Hibiscus cannabinus) that are indigenous to Africa. Gerbils (n 67) were vitamin A-depleted for 5 weeks. After a baseline kill (n 7), the gerbils were weight-matched and assigned to six treatment groups (n 10; four vegetable groups; negative and positive controls). For 4 weeks, the treatments included 35 nmol vitamin A (theoretical concentrations based on 100 % bioefficacy) in the form of vegetables or retinyl acetate. In addition to their diets, the control and vegetable groups received daily doses of oil, while the vitamin A group received retinyl acetate in oil matched to prior day intake. Serum and livers were analysed for vitamin A using HPLC. Serum retinol concentrations did not differ among groups, but total liver vitamin A of the vitamin A and vegetable groups were higher than that of the negative control group (P < 0·0001). Liver β-carotene 15,15′-monooxygenase-1 expression levels were determined for two vegetable groups and were similar to the positive and negative controls. Conversion factors for the different leafy vegetables were between 1·9 and 2·3 μg β-carotene equivalents to 1 μg retinol. Small quantities of these vegetables maintained vitamin A status in gerbils through efficient bioconversion of β-carotene to retinol.

Personal food preferences can either enhance or suppress the development of obesity and the selection and proportion of macronutrients in the diet seem to have a heritable component. In the present study, we therefore focused on dietary composition as a specific trait related to obesity and we determined whether genetic variations in leptin (LEP), LEP receptor (LEPR), adiponectin (ADIPOQ), IL-6 and pro-opiomelanocortin (POMC) underlie specific native food preferences and obesity-related anthropometric parameters. The total of 409 individuals of Czech Caucasian origin were enrolled into the present study and 7 d food records were obtained from the study subjects along with selected anthropometric measurements. In a subset of study subjects, plasma levels of ADIPOQ, LEP and soluble LEPR were measured. Independently of the BMI of the individuals, common variations in LEP and LEPR genes were associated with specific eating patterns, mainly with respect to timing of eating. The LEP+19A/G polymorphism served as an independent predictor for BMI, percentage of body fat and skinfold thickness and significantly affected the time structure of the daily energy intake. The POMC RsaI polymorphism was associated with percentage of body fat. The ADIPOQ 45 T/G polymorphism was associated with the thickness of the subscapular skinfold. The LEPR Gln223Arg polymorphism was associated with multiple parameters, including diastolic blood pressure, meal sizes during the day and plasma ADIPOQ levels. In a separate analysis, soluble leptin receptor (sObR) plasma levels and LEP:sObR ratio were significantly correlated with systolic blood pressure (β = − 0·66, P = 0·002; β = − 1·23, P = 0·02) and sObR plasma levels also served as an independent predictor for diastolic blood pressure (β = − 0·50; P = 0·04). To conclude, we report common allelic variants associated with specific feeding behaviour and obesity-related anthropometric traits. Moreover, we identified allelic variants that significantly influence the time structure of food intake during the day.

The present study focused on the hypothesis that dietary supplementation with medium-chain TAG (MCT) will improve cognitive function in aged dogs by providing the brain with energy in the form of ketones. Aged Beagle dogs were subjected to a baseline battery of cognitive tests, which were used to establish cognitively equivalent control or treatment groups. The dogs in the treatment group were maintained on a diet supplemented with 5·5 % MCT. After an initial wash-in period, all the dogs were tested with a battery of cognitive test protocols, which assessed sequentially landmark discrimination learning ability, egocentric visuospatial function and attention. The groups were maintained on the diets for 8 months. The MCT-supplemented group showed significantly better performance in most of the test protocols than the control group. The group differences also varied as a function of task difficulty, with the more difficult task showing greater supplementation effects than the easier tasks. The group given the MCT supplement showed significantly elevated levels of β-hydroxybutyrate, a ketone body. These results indicate, first, that long-term supplementation with MCT can have cognition-improving effects, and second, that MCT supplementation increases circulating levels of ketones. The results support the hypothesis that brain function of aged dogs can be improved by MCT supplementation, which provides the brain with an alternative energy source.

Using a nutrigenomics approach we studied the response of second-generation chickens at a transcriptional level to organically grown feed ingredients compared with conventionally grown feed ingredients. Both diets consisted of the same amounts of ingredients, the only difference was the production method. Gene expression was analysed in jejuni using whole genome chicken cDNA arrays. After analysis, forty-nine genes were found to be differentially regulated between chickens fed on the different diets, independent of their genetic background. Of these forty-nine genes, seven genes were involved in cholesterol biosynthesis. Genes involved in cholesterol biosynthesis were higher expressed in jejuni from organically fed birds. Other genes found to be regulated were involved in immunological processes, such as B-G protein (part of chicken major histocompatibility complex), chemokine ah221, and the immunoglobulin heavy chain. Using quantitative PCR the effect of genetic background on the differential expression of genes was studied. Differences in gene expression existed between animals fed different diets as well as between different chicken lines. This indicated that diet and genetic background influence the transcriptional response of the jejunum. This is the first time that significant differences in gene expression were shown between animals on diets with organically or conventionally produced ingredients.

African catfish (Clarias gariepinus) were fed four isonitrogenous diets (34 % crude protein), each containing one of two lipid (100 or 180 g/kg) and two l-carnitine (15 or 1000 mg/kg) levels. After 81 d of feeding, thirty-two fish (body weight 32 g) from each dietary group were randomly selected, sixteen fish were induced to a 3-h swim (speed of 1·5 body length (BL)/s), while the other sixteen fish were kept under resting condition. Fish fed 1000 mg l-carnitine accumulated 3·5 and 5 times more l-carnitine in plasma and muscle, respectively, than fish fed the 15 mg l-carnitine. Muscle l-carnitine content was significantly lower in exercised fish than in rested fish. High dietary lipid level (fish oil) led to an increase in muscle n-3 PUFA content and a decrease in SFA and MUFA content. In liver, the increase in dietary lipid level resulted in an increased levels of both n-6 and n-3 PUFA. l-carnitine supplementation significantly decreased n-3 PUFA content. Exercise decreased n-3 PUFA in both muscle and liver. Plasma lactate and lactate dehydrogenase, normally associated with increased glycolytic processes, were positively correlated with exercise and inversely correlated with dietary l-carnitine level. l-carnitine supplementation reduced significantly the RQ from 0·72 to 0·63, and an interaction between dietary l-carnitine and lipid was observed (P < 0·03). Our results indicate that an increase in fatty acids (FA) intake may promote FA oxidation, and both carnitine and exercise might influence the regulation of FA oxidation selectivity.

The aim of these studies was to evaluate the potential of some nutritional approaches to prevent or reduce the body load of organochlorines (OC) in humans. Study 1 compared plasma OC concentrations between vegans and omnivores while study 2 verified if the dietary fat substitute olestra could prevent the increase in OC concentrations that is generally observed in response to a weight-reducing programme. In study 1, nine vegans and fifteen omnivores were recruited and the concentrations of twenty-six OC (β-hexachlorocyclohexane (β-HCH), p, p′-dichlorodiphenyldichloroethane (p, p′-DDE), p, p′-dichlorodiphenyltrichloroethane (p, p′-DDT), hexachlorobenzene, mirex, aldrin, α-chlordane, γ-chlordane, oxychlordane, cis-nonachlor, trans-nonachlor, polychlorinated biphenyl (PCB) nos. 28, 52, 99, 101, 105, 118, 128, 138, 153, 156, 170, 180, 183 and 187, and aroclor 1260) were determined. In study 2, the concentrations of these twenty-six OC were measured before and after weight loss over 3 months in thirty-seven obese men assigned to one of the following treatments: standard group (33 % fat diet; n 13), fat-reduced group (25 % fat diet; n 14) or fat-substituted group (1/3 of dietary lipids substituted by olestra; n 10). In study 1, plasma concentrations of five OC compounds (aroclor 1260 and PCB 99, PCB 138, PCB 153 and PCB 180) were significantly lower in vegans compared with omnivores. In study 2, β-HCH was the only OC which decreased in the fat-substituted group while increasing in the other two groups (P = 0·045). In conclusion, there was a trend toward lesser contamination in vegans than in omnivores, and olestra had a favourable influence on β-HCH but did not prevent plasma hyperconcentration of the other OC during ongoing weight loss.

Data on N utilisation by sheep-fed diets containing foliages were analysed to develop prediction equations for N excretion in faeces (FN) and urine (UN), and to determine endogenous N excretion. Overall, 218 dietary treatments from forty-four publications were compiled in the database. This database was split into three subsets: without foliage in the diets (FL-0); foliage levels (FL) in between 0 and 310 g/kg (FL-L); FL in between 310 and 800 g/kg diets (FL-H) to study the effects of foliages on metabolic faecal N (MFN) and endogenous urinary N (EUN). Nitrogen intake (NI) as single independent factor was the best predictor of FN (R2 0·75), UN (R2 0·81) and total N excretion (R2 0·86). Addition of dietary N concentration and FL for FN (R2 0·82), dietary N concentration and foliage NI for UN (R2 0·85), and FL and foliage NI for total N excretion (R2 0·92) as supporting predictors to this relationship slightly increased R2 values. The monomolecular and exponential models slightly improved the prediction of N excretion with NI as a predictor compared with the linear model. The excretion of MFN was greater for FL-H compared with FL-0, but was similar between FL-0 and FL-L, and FL-L and FL-H. However, EUN decreased in FL-H compared with FL-0 and FL-L, but was similar between FL-0 and FL-L. In conclusion, using NI as the primary predictor produced an accurate prediction of N excretion. Inclusion of foliages in the diets may shift N excretion from urine to faeces and increase the excretion of MFN and EUN.

Four goats (20 (SD 2·5) kg) fitted with ruminal, duodenal and ileal cannulae were used in a 4 × 4 Latin square design to estimate the effects of a dietary starch source on the duodenal and ileal flows of endogenous N (EN) and endogenous amino acids (EAA) in growing goats. Goats were fed total mixed rations containing four starch sources (mainly from maize (MR), wheat (WR), paddy (PR) and sorghum (SR) treatments). There were no significant (P>0·05) effects of the dietary starch source on the intestinal flows of EN and EAA. The duodenal flows of EN were 2·40, 2·39, 2·18 and 1·56 g/d for the MR, WR, PR and SR treatments, respectively, as determined by the difference method, and the duodenal flows of EAA were 10·76, 11·29, 10·95 and 10·96 g/d by estimation with the amino acid profile method. The flows of EN and EAA at the ileum were 1·17, 1·12, 1·01, 0·70 and 4·87, 4·95, 4·94, 4·99 g/d, respectively, as estimated by the water-soluble method. The average intestinal reabsorption of EN and EAA was 57·5 %, and the endogenous Leu by the MR treatment was significantly (P < 0·05) lower than that of the other three treatments. The present results indicate that losses of endogenous protein in the intestine were not affected by the dietary starch source.

A study was conducted to assess the effect of substituting high levels of dietary fish oil (FO) and fishmeal (FM) for vegetable oil (VO) and plant protein (PP) on the intestinal arachidonic acid (AA) cascade in the carnivorous fish species Atlantic salmon. Four diets were fed to salmon over a period of 12 months, including a control FMFO diet, with varying replacements of plant-derived ingredients: 80 % PP and 35 % VO; 40 % PP and 70 % VO; 80 % PP and 70 %VO. Subsequently, fish were examined pre- (0 h) and post- (1 h) acute stress for blood parameters and intestinal bioactive lipidic mediators of inflammation (prostaglandins). Plasma cortisol responses were greatest in the FMFO group, while 80 % PP and 70 % VO fish exhibited increased plasma chloride concentrations. The n-3:n-6 PUFA ratio in intestinal glycerophospholipids from 70 % VO groups significantly decreased in both proximal and distal regions due to elevated levels of 18 : 2n-6 and the elongation/desaturation products 20 : 2n-6 and 20 : 3n-6. Increases in n-6 PUFA were not concomitant with increased AA, although the AA:EPA ratio did vary significantly. The 40 % PP and 70 % VO diet produced the highest intestinal AA:EPA ratio proximally, which coincided with a trend in elevated levels of PGF2α, PGE2 and 6-keto-PGF1α in response to stress. PGE2 predominated over PGF2α and 6-keto-PGF1α (stable metabolite of PGI2) with comparable concentrations in both intestinal regions. Cyclo-oxygenase-2 (COX-2) mRNA expression was an order of magnitude higher in distal intestine, compared with proximal, and was significantly up-regulated following stress. Furthermore, the 80 % PP and 70 % VO diet significantly amplified proximal COX-2 induction post-stress. Results demonstrate that high replacements with plant-derived dietary ingredients can enhance COX-2 induction and synthesis of pro-inflammatory eicosanoids in the intestine of salmon in response to acute physiological stress.

The health benefits of seafood are well documented and based on the unique supply of n-3 highly unsaturated fatty acids (HUFA). Aquaculture now contributes about 50 % of food-grade seafood globally and Atlantic salmon (Salmo salar) is a rich source of n-3 HUFA. However, salmon and other oily fish can accumulate lipophilic persistent organic pollutants (POP), including dioxins (PCDD/F), polychlorinated biphenyls (PCB) and polybrominated diphenyl ethers (PBDE), derived largely from feed. In the present study, triplicate groups of salmon, of initial weight 0·78 kg, were fed one of three experimental diets for 11 weeks. The diets were coated with either a northern fish oil (FO) with a high POP content (cNFO), the same oil that had been decontaminated (deNFO) or a blend of southern fish oil, rapeseed and soyabean oils (SFO/RO/SO). Dietary PCDD/F+dioxin-like PCB (DL-PCB) concentrations were 17·36, 0·45 and 0·53 ng toxic equivalents (TEQ)/kg, respectively. After 11 weeks, the flesh concentrations in fish fed the cNFO, deNFO and SFO/RO/SO diets were 6·42, 0·34 and 0·41 ng TEQ/kg, respectively. There were no differences in flesh EPA and DHA between fish fed the cNFO or deNFO diets although EPA and DHA were reduced by 50 and 30 %, respectively, in fish fed the SFO/RO/SO diet. Thus, decontaminated FO can be used to produce salmon high in n-3 HUFA and low in POP. Salmon produced using deNFO would be of high nutritional value and very low in POP and would utilise valuable fish oils that would otherwise be destroyed due to their high pollutant concentrations.