The present review attempts to provide an update of the scientific knowledge on the renal toxicity which occurs in human subjects as a result of chronic ingestion of low-level dietary Cd. It highlights important features of Cd toxicology and sources of uncertainty in the assessment of health risk due to dietary Cd. It also discusses potential mechanisms for increased susceptibility to Cd toxicity in individuals with diabetes. Exposure assessment on the basis of Cd levels in foodstuffs reveals that vegetables and cereals are the main sources of dietary Cd, although Cd is also found in meat, albeit to a lesser extent. Cd accumulates particularly in the kidney and liver, and hence offal contains relatively high amounts. Fish contains only small quantities of Cd, while crustaceans and molluscs may accumulate larger amounts from the aquatic environment. Data on Cd accumulation in human kidney and liver obtained from autopsy studies are presented, along with results of epidemiological studies showing the relationship between renal tubular dysfunction and kidney Cd burden. These findings suggest that a kidney Cd level of 50 μg/g wet weight is a maximum tolerable level in order to avoid abnormal kidney function. This renal Cd burden corresponds to a urinary Cd excretion of 2 μg/d. Accordingly, safe daily levels of Cd intake should be kept below 30 μg per person. Individual variations in Cd absorption and sensitivity to toxicity predicts that a dietary Cd intake of 30 μg/d may result in a slight renal dysfunction in about 1 % of the adult population. The previous guideline for a maximum recommended Cd intake of 1 μg/kg body weight per d is thus shown to be too high to ensure that renal dysfunction does not occur as a result of dietary Cd intake.

The term essential fatty acid no longer clearly identifies the fatty acids it was originally used to describe. It would be more informative if the concept of essentiality shifted away from the symptoms arising from the lack of de novo synthesis of linoleate or α-linolenate and towards the adequacy of the capacity for synthesis and conservation of both the parent and the derived long-chain polyunsaturates. For instance, despite the existence of the pathway for synthesis of docosahexaenoate from α-linolenate, the former would be more correctly classified as ‘conditionally indispensable’ because the capacity of the pathway appears insufficient during early development, although it may be sufficient later in life in healthy individuals. Similarly, despite the inability to synthesize linoleate de novo, abundant linoleate stores and its relatively slow turnover in healthy adults probably makes linoleate ‘conditionally dispensable’ for long periods. There are two other anomalies with the terms essential and non-essential fatty acids: (1) under several different experimental circumstances, the C-skeleton of essential fatty acids is avidly used in the synthesis of non-essential fatty acids; (2) to function normally, the brain is required to endogenously synthesize several non-essential fatty acids. As with essential amino acids, which have been reclassified as indispensable or conditionally indispensable, such a change in terminology should lead to an improved understanding of the function and metabolism of polyunsaturates in particular, and long-chain fatty acids in general.

Colonic fermentation of organic matter to short-chain fatty acids has been implicated in the improvement in insulin sensitivity achieved by feeding diets rich in complex carbohydrates. The present study assessed the potential role of the colon in determining postprandial glucose kinetics. Metabolic responses to a complex-carbohydrate test meal were determined in conjunction with a primed continuous infusion of D-[6,6-2H]glucose in a group of ileostomists and sex-matched controls. Glucose disposal (GD) was computed using non-steady-state kinetics on a single compartment model. Insulin sensitivity was derived using cumulative GD as the dependent variable, and time and the integrated insulin concentration as independent variables. The ileostomist group had a significantly higher postprandial plasma insulin concentration (P=0·034) compared with the control group, but no difference in the plasma glucose concentration. Total GD was similar in each group, although the insulin-dependent GD was substantially lower in the ileostomists (0·46 v. 0·13 mg glucose/min per pmol, P=0·015). The ileostomist group also showed a 50 % lower rate of glucose oxidation in the postprandial period (P=0·005), although the rate of non-oxidative GD was not significantly affected. The present study indicates that loss of the colon is associated with several characteristics of the insulin resistance syndrome, and favours a view that the colon has a role in the control of postprandial glucose.

We investigated whether short-term underfeeding could induce adaptative mechanisms in portal-drained viscera (PDV) that would allow nutrients to be spared for vital functions in adult ewes. Six ewes (three of them fitted with catheters in the mesenteric artery and portal and mesenteric veins) were fed, in a double 3×3 Latin square design (2 weeks per experimental period), a regrowth of natural grassland hay at 143 (high; H), 88 (medium; M) and 51 (low; L) % of their energy maintenance requirements. The digestibility of the diet was measured in all six ewes and the net portal fluxes of nutrients in the three catheterized ewes. The organic matter content and N digestibility of the diet were not affected by underfeeding. Urinary and faecal N losses and N balance were linearly related to feed intake. Arterial concentration of acetate was linearly related to feed intake. Arterial concentrations of the other volatile fatty acids, 3-hydroxybutyrate, lactate, glucose, NH3, urea and total amino acids were not affected by underfeeding. Arterial concentration of non-esterified fatty acids (NEFA) increased with underfeeding. The portal net release of all volatile fatty acids, 3-hydroxybutyrate and NH3 were linearly related to intake. The portal net flux of both essential and non-essential amino acids, and thus total amino acids, remained unchanged between levels H and M, and decreased between levels M and L. A significant net uptake for glycine and total non-essential amino acids occurred at level L. The portal net uptake of glucose, urea, glutamate and glutamine, and the portal net release of lactate and NEFA were not affected by underfeeding. Summation of portal energy fluxes indicated that 51 % of the metabolizable energy intake was recovered in the portal blood with the three levels of intake. In conclusion, no quantitative adaptation to spare energy, in terms of percentage of intake, occurred in PDV of short-term underfed ruminants, but the pattern of absorption of energetic nutrients was modified.

The purpose of this study was to determine the effect of altering substrate availability on metabolism and performance during intense cycling. Seven highly trained men ingested a random order of three isoenergetic meals 90 min before cycling at 80 % maximal oxygen uptake (VO2max) for 20 min (about 310 W), followed by a 600 kJ time trial lasting about 30 min. Meals consisted of either 1·2 g saturated fat/kg body mass (BM) with 3500 U heparin intravenously (HIFAT) to elevate circulating plasma free fatty acid (FA) concentration, 2·5 g carbohydrate/kg BM (CHO) to elevate plasma glucose and insulin concentrations or 2·5 g carbohydrate+20 mg nicotinic acid/kg BM (NA) to suppress lipolysis and reduce free FA concentration. HIFAT elevated free FA concentration (HIFAT 1·3 (SEM 0·2), CHO 0·2 (sem 0·1), NA 0·1 (sem 0·1) mm; P<0·001), lowered the RER (HIFAT 0·94 (sem 0·01), CHO 0·97 (sem 0·01), NA 0·98 (sem 0·01); P<0·01) and increased the rate of fat oxidation (HIFAT 24 (sem 3), CHO 12 (sem 2), NA 8 (sem 3) μmol/kg per min; P<0·01) during the 20 min ride. Marked differences in fat availability and fuel utilisation, however, had little effect on performance in the subsequent time trial (HIFAT 320 (sem 16), CHO 324 (sem 15), NA 315 (sem 13) W). We conclude: (1) increased fat availability during intense cycling increases the rate of fat oxidation; but (2) the reduction in the rate of carbohydrate oxidation in the presence of high circulating plasma free FA is unlikely to enhance intense exercise performance lasting about 1 h; (3) substrate selection during intense (about 80 % VO2max) exercise is dominated by carbohydrate oxidation.

Rye is an important source of plant lignans in Finland. In the present crossover trial we wanted to study the effect of rye bread as part of the usual diet on serum and urine enterolactone (ENL) concentrations in healthy volunteers. Eighteen men aged 43 (SEM 2·0) YEARS AND TWENTY-ONE WOMEN AGED 43 (sem 1·6) years consumed wholemeal rye bread and white wheat bread in random order for 4 weeks. The bread periods were separated by a 4 week wash-out period. The breads provided at least 20 % of the daily energy intake. The mean intakes of rye bread were 219 (sem 14·6) and 162 (sem 5·3) g/d and those of wheat bread were 200 (sem 9·6) and 153 (sem 5·8) g/d for men and women respectively. Blood samples were collected from all subjects and three 24 h urine samples were collected from ten men and twelve women at the end of both bread periods for the determination of serum concentration and urinary excretion of ENL. The mean serum ENL concentrations in both men and women at the beginning of baseline period and at the end of the rye-bread period remained constant and were significantly higher than those at the end of the wheat-bread period. Correspondingly, daily urinary ENL excretion increased significantly during the rye-bread period compared with the wheat-bread period and was 5- and 10-fold higher in men and women respectively in comparison with the amount of plant lignan precursors measured in the rye bread. These data indicate the presence of other precursors for ENL in rye which are not detected by the current method of measuring plant lignans in food. The possible role of fibre in enhancement of the formation of mammalian lignans from their plant precursors in the gut also remains to be determined.

Bioavailability of iron (Fe) from a low-Fe infant formula was determined by erythrocyte incorporation of 58Fe 14 d after administration in ten healthy, non-Fe-deficient infants. Two feeding protocols were compared, with each infant acting as his/her own control. At 140 and 154 d of age, infants were fed 1000 g of 58Fe-labelled formula (1·44 mg total Fe/1000 g) as six feeds over 24 h (Protocol A) or as two feeds/day on three consecutive days (Protocol B). A water solution with 57Fe and ascorbic acid was given separately as a reference dose in both study protocols. Erythrocyte incorporation of 58Fe and 57Fe was determined by thermal ionisation mass spectrometry. Geometric mean 58Fe incorporation was 7·6 % (range 3·3–13·5 %) with Protocol A as compared to 10·6 % (range 6·7–18·6 %) with Protocol B (P=0·05); paired t test. Inter-individual variability of 58Fe was not reduced by correcting for the incorporation of 57Fe from the reference dose, or by correcting for plasma ferritin concentration. Fractional erythrocyte incorporation of Fe from low-Fe infant formula was in the same range as our earlier published data on erythrocyte incorporation of Fe from human milk extrinsically labelled with 58Fe (). The methodological evaluations included in this study clearly indicate the importance of using standardised study protocols when evaluating Fe bioavailability in infants. Corrections of erythrocyte incorporation data based on plasma ferritin or erythrocyte incorporation of Fe from a reference dose were not found to be useful.

This study was performed to examine the postprandial effects of meals containing dietary fats, with their natural fatty acid composition and tocopherol content, on the plasma triacylglycerols (TG) and tocopherols and on the resistance of VLDL and LDL to oxidation. On six separate days eighteen healthy male subjects were given low-fat meals (LF) or the LF meals enriched with sunflower oil (SO), rapeseed oil (RO), olive oil (OO), palm oil (PO), or butter (B) in a crossover design. The fat-rich meals all resulted in similar postprandial TG responses while the LF test meal did not increase plasma TG level. The postprandial plasma fatty acid profile changed to resemble the fatty acid composition of the ingested test fat. The α-tocopherol:γ-tocopherol ratios in postprandial plasma and VLDL samples were greater than in the test fats. We found that the resistance of VLDL particles to oxidation in the postprandial state as assessed from lag time was increased after the PO-rich meal as compared with the SO-rich meal (P=0·018), and the propagation rate was greater after the SO- and RO-rich meals compared with the others (P<0·001). The resistance of LDL particles to oxidation was unaffected by the meals. In postprandial VLDL samples, the content of α-tocopherol was greater after the OO- and SO-rich meals compared with the meal rich in PO (P=0·034 and 0·042 respectively). The γ-tocopherol content of VLDL was highest after RO-meal as compared with all other test meals (P=0·0019), and higher after SO as compared with B (P=0·0148). Large individual differences were noted. In conclusion, meals enriched with different fats lead to the formation of VLDL particles with varying resistance to oxidation.

Urine volume is the greatest risk factor for nephrolithiasis. High fluid intake is the first general advice given to stone-forming patients for the prevention of their recurrence. The aim of the present study was to evaluate the influence of bicarbonate-rich mineral water (1715 mg bicarbonate/l) on urinary-stone risk factors in comparison with sodium potassium citrate, a well-established treatment for urinary stones. The mineral water and sodium potassium citrate were administered in equimolar concentrations, with respect to the alkali load. All investigations were carried out in healthy male subjects aged 23–38 years. The study followed a cross-over design. All subjects received a standardized diet during the cross-over phase, which was formulated according to the dietary recommendations of the German Society of Nutrition (). On the loading day of the cross-over phase, fruit tea was substituted for either mineral water or sodium potassium citrate dissolved in fruit tea. The treatment offered during the second part of the cross-over phase was continued for a 4-week follow-up under normal dietary conditions. During the cross-over phase, there was a significant increase in urinary pH (P<0·001). There was also a significant increase in the excretion of citric acid (P<0·01), a decrease in the excretion of oxalic acid, and therefore a decrease in the relative supersaturations for calcium oxalate and uric acid. In the follow-up phase also, the relative supersaturations decreased and there were beneficial effects on the other urinary variables. The effect of the bicarbonate-rich mineral water was similar to that of the sodium potassium citrate, which suggests that it could be useful in the prevention of the recurrence of calcium oxalate and uric acid stones.

A model to predict voluntary water intake (WI) of a pig fed a known diet in a known environment is described. The daily retentions of protein, lipid, water and ash were estimated over time using a published pig growth model. Food intakes were estimated using published methods. WI was estimated by adding the amounts required for digestion (WD), faecal excretion (Wfec), growth (WG), evaporation (WE), urinary excretion (WU) and by then subtracting the water arising from feed (WF), from nutrient oxidation (WO) and synthesis of body constituents (WS). WD was predicted assuming an absorption of water of 0·10, 0·16 and 0·07 kg/kg digestible carbohydrate, crude protein and lipid respectively. Wfec was estimated taking into account the water associated with the undigested protein (0·86 kg/kg), diethyl ether extract (-12·11 kg/kg), crude fibre (1·86 kg/kg), ash (-0·42 kg/kg) and N-free extract (4·4 kg/kg). The basal level of WE was estimated from the heat production of the pig fed ad libitum (MJ/d) as: 0·25×(metabolizable energy-energy retained as protein and lipid)×0·4, where 0·25 is the assumed proportion of the insensible heat loss at the comfort temperature and 0·4 is the water lost per MJ dissipated heat. WE in a hot environment was predicted by assuming that evaporation increased up to three times the basal level to offset the decreased sensible heat loss. To predict WU a water requirement for renal excretion of 2·05 and 3·40 kg/osmol excreted N as urea and minerals respectively was assumed. The urinary load of N and minerals was predicted from the intake of digestible nutrients and their retention. From the oxidation of 1 kg carbohydrate, protein, and fat it was assumed that 0·6, 0·42 and 1·07 kg water (WO) were released respectively. WS was predicted by assuming a release of 0·16, 0·07 and 0·57 kg water per kg retained protein, retained lipid coming from digestible lipid, and retained lipid coming from digestible carbohydrate respectively. The model is strongly rooted in a theoretical structure. When its predictions were compared with data from suitable experiments, the results were not significantly different. Both the pattern and the magnitude of responses of the model to changes in body weight, feed intake and environmental temperature are sensible and it allows a fuller prediction of voluntary water intake than the methods currently available.

Apolipoprotein E (ApoE) genotype influence on the relationship between dietary risk factors for cardiovascular disease and blood serum lipid levels was investigated in 132 free-living individuals participating in the European Prospective Investigation of Cancer (EPIC) study. All subjects (age 40–69) were clinically healthy and provided information on their usual diet. ApoE genotype and serum lipid concentrations were determined in all subjects. Relationships of intake of dietary constituents with serum lipid levels were compared in different genotype groups. There was a significant correlation between total serum cholesterol and intake of energy derived from total fat (r 0·195; P 0·025) and saturated fat (r 0·174; P 0·046) in the cohort as a whole. However, individuals with the ApoE ε3/ε4 genotype displayed a much stronger positive correlation between LDL cholesterol level and the percentage of energy derived from intake of saturated fat (r 0·436; P 0·043). There were no significant associations in the groups with ε3/ε3 or ε2/ε2 & ε2/ε3 genotype. A significant positive correlation between alcohol consumption and HDL cholesterol level was present in individuals bearing ApoE ε2 allele. These findings support current public health recommendations that saturated fat consumption should be reduced in order to reduce coronary heart disease risk. Total cholesterol concentrations were positively related to saturated fat intake in the cohort as a whole, but elevated LDL cholesterol levels associated with high saturated fat intake can be expected particularly in those individuals who combine a ‘risky’ dietary behaviour with the presence of the ε4 variant of ApoE.

The 677cytosine (c)→thymine(T) mutation identified in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene has been frequently associated with an elevated plasma homocysteine concentration. The aim of the present study was to determine the impact of this MTHFR common mutation on plasma and erythrocyte folate (RCF) and plasma total homocysteine (tHcy) concentrations in healthy French adults. A cohort of 291 subjects living in the Paris area and participating in the Supplementation en Vitamines et Mineraux Antioxydants (SU.VI.MAX) study were analysed to assess the impact of MTHFR polymorphism 677C→T on folate status and plasma tHcy concentration. The frequency of the mutant homozygote for 677C→T polymorphism (677TT genotype) in the present cohort was 16·8%. There were significant differences in plasma tHcy between 677CC, 677CT and 677TT genotype groups. The RCF concentrations were significantly different between each genotype, the lowest levels being associated with the 677TT genotype. When segregated by gender, no differences in tHcy between homozygous 677TT, heterozygous 677CT and wild-type 677CC genotype groups in women were observed. The fasting tHcy in women was unrelated to the 677C→T mutation. However, tHcy was significantly increased in men with the homozygous 677TT genotype. We also analysed the possible implication of a second new MTHFR polymorphism (1298A→C) in subjects with mild hyperhomocysteinaemia (4th quartile of homocysteinaemia; tHcy >11·1 μmol/l). The polymorphism 1298A→C did not have a notable effect on tHcy or on the RCF levels. Our observations confirm a relatively high frequency of the 677TT genotype in the French population. Women with this genotype did not show the same increase in tHcy observed in men. In the present study dietary folate intake was not measured. Thus, the interaction of dietary folate with the MTHFR genotype in the French population needs further study.

In Australia, the process by which food energy factors are derived for food labelling purposes is under review. One of the questions of international relevance is whether energy factors should be derived using a definition of metabolisable energy (ME) or a definition of net (metabolisable) energy (NME), or some mixture of the two. ME describes the food energy available for heat production and body gains. NME deducts obligatory thermogenesis from ME in an attempt to reflect the food energy that can be converted to ATP energy within the body. Some countries use NME to derive energy factors for novel food ingredients such as sugar alcohols and polydextrose, but continue to use ME for protein, fat, carbohydrate, and alcohol. The present paper puts a case for using a consistent system (ME at the present time) for all food components. Reasons for this include: consistent application to all food components allows valid comparisons between products; food energy values and estimates of energy expenditure (food energy requirements) should be directly comparable; NME does not account for all sources of thermogenesis; differences between ME and NME for sugar alcohols and polydextrose are small in the context of the whole diet; and the ME system does not preclude information about metabolic efficiency being provided as additional information. Any major change to the way in which energy values are expressed (e.g. global adoption of the NME system) merits wide discussion among the human nutrition community. One aim of this present paper is to stimulate this discussion.

Fe absorption was measured in adult human subjects consuming different cereal foods fortified with radiolabelled FeSO4, ferrous fumarate or NaFeEDTA, or with radiolabelled FeSO4 or ferric pyrophosphate in combination with different concentrations of Na2EDTA. Mean Fe absorption from wheat, wheat–soyabean and quinoa (Chenopodium quinoa) infant cereals fortified with FeSO4 or ferrous fumarate ranged from 0·6 to 2·2 %. For each infant cereal, mean Fe absorption from ferrous fumarate was similar to that from FeSO4 (absorption ratio 0·91–1·28). Mean Fe absorption from FeSO4-fortified bread rolls was 1·0 % when made from high-extraction wheat flour and 5·7 % when made from low-extraction wheat flour. Fe absorption from infant cereals and bread rolls fortified with NaFeEDTA was 1·9–3·9 times greater than when the same product was fortified with FeSO4. Both high phytate content and consumption of tea decreased Fe absorption from the NaFeEDTA-fortified rolls. When Na2EDTA up to a 1:1 molar ratio (EDTA:Fe) was added to FeSO4-fortified wheat cereal and wheat–soyabean cereal mean Fe absorption from the wheat cereal increased from 1·0 % to a maximum of 5·7 % at a molar ratio of 0·67:1, and from the wheat–soyabean cereal from 0·7 % to a maximum of 2·9 % at a molar ratio of 1:1. Adding Na2EDTA to ferric pyrophosphate-fortified wheat cereal did not significantly increase absorption (P>0·05). We conclude that Fe absorption is higher from cereal foods fortified with NaFeEDTA than when fortified with FeSO4 or ferrous fumarate, and that Na2EDTA can be added to cereal foods to enhance absorption of soluble Fe-fortification compounds such as FeSO4.

The aim of this present study was to investigate the effect of amount and degree of oxidation of dietary oil on type 2 T-helper cell (TH)-related immune responses. Four groups of BALB/c mice were fed either 50 g soyabean oil/kg (50-S), 50 g oxidized oil/kg (50-O), 150 g soyabean oil/kg (150-S) or 150 g oxidized oil/kg (150-O). After 14 weeks consuming the experimental diets, the mice were immunized with ovalbumin (OVA) plus Al and antigen-specific immunoglobulin (Ig)E, IgG1 and IgG2a, inflammatory mediators such as prostaglandin (PG) E2 and leukotriene (LT)B4 were determined. Higher hepatic microsomal cytochrome P450 was noted in mice fed 150 g oxidized oil/kg compared with those of other groups. OVA-specific IgG1 and IgE were higher in mice fed 150 g oxidized oil/kg compared with those of the other groups. The data suggested the interleukin (IL)-4: interferon (IFN)-γ ratio was higher in mice fed 50 g dietary oxidized oil/kg compared with that of the 50-S group. The IL-5:IFN-γ ratios were higher in the 150-S and 150-O groups than in the 50-S and 50-O groups. PGE2 and LTB4 produced by macrophages stimulated by lipopolysaccharide were highest in mice in the 150 g oxidized oil/kg group. The data suggested that an increased intake of oxidized oil might exert an unfavourable effect on the TH2 response involved in allergic disease.

The effect of dietary intake of flavonols (predominantly quercetin) on oxidative DNA damage was studied in thirty-six healthy human subjects (sixteen men, twenty women). The study was a randomised crossover study, comprising two 14 d treatments of either a low-flavonol (LF) or high-flavonol (HF) diet with a 14 d wash-out period between treatments. Subjects were asked to avoid foods containing flavonols, flavones and flavanols during the LF dietary treatment period and to consume one 150 g onion (Allium cepa) cake (containing 89·7 mg quercetin) and one 300 ml cup of black tea (containing 1·4 mg quercetin) daily during the HF dietary treatment. A 7 d food diary was kept during each dietary period and blood samples were taken after each dietary treatment. Products of oxidative damage to DNA bases were measured in DNA from leucocytes. The study had more than 95 % power to detect a change of 20 % in DNA damage products Plasma vitamin C and plasma quercetin concentrations were also measured. No significant differences in intake of macronutrients or assessed micronutrients, measured DNA base damage products, or plasma vitamin C were found between the HF and LF dietary treatments. The plasma quercetin concentration was significantly higher after the HF dietary treatment period (228·5 (SEM 34·7) nmol/l) than after the LF dietary treatment period (less than the limit of detection, i.e. <66·2 nmol/l). These findings do not support the hypothesis that dietary quercetin intake substantially affects oxidative DNA damage in leucocytes.

The aim of this study was to investigate comparative effects of vitamin A deficiency on respiratory activity and structural integrity in liver and heart mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochondria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the activities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a significant increase in the endogenous coenzyme Q content in liver and heart mitochondria when compared with control values. Vitamin A deficiency induced a decrease in the activity of complex I (NADH–CoQ reductase) and complex II (succinate–CoQ reductase) and in the levels of complex I and cytochrome c in heart mitochondria. However, NADH and succinate oxidation rates were maintained at the control levels due to an increase in the CoQ content in accordance with the kinetic behaviour of CoQ as an homogeneous pool. On the contrary, the high CoQ content did not affect the electron-transfer rate in liver mitochondria, whose integrity was preserved from the deleterious effects of the vitamin A deficiency. Ultrastuctural assessment of liver and heart showed that vitamin A deficiency did not induce appreciable alterations in the morphology of their mitochondria. After refeeding the control diet, serum retinol, liver and heart CoQ content and the activity of complex I and complex II in heart mitochondria returned to normality. However, the activities of both whole electron transfer chain and complex I in liver were increased over the control values. The interrelationships between physiological antioxidants in biological membranes and the beneficial effects of their administration in mitochondrial diseases are discussed.

The present study was designed to study the mechanisms by which dietary conjugated linoleic acids (CLA) decrease serum cholesterol. Hamsters were fed a semi-synthetic diet containing 1 g cholesterol/kg diet with or without supplementation with 20 g linoleic acid (LA) and 20 g CLA/kg diet. After 8 weeks, serum fasting total cholesterol (TC) and triacylglycerol (TG) were significantly lower in the LA-supplemented and CLA-supplemented groups compared with those of the control (CTL) hamsters. In contrast to LA, CLA significantly lowered hepatic cholesterol but it increased the level of adipose tissue cholesterol, suggesting that the hypocholesterolaemic mechanism of CLA is different from that of LA. CLA decreased the activity of intestinal acyl CoA:cholesterol acyltransferase (ACAT) whereas LA had no effect on this enzyme. Consequently, CLA supplementation increased the faecal excretion of total neutral sterols, but it had no or little effect on the faecal acidic sterols. If the ACAT is associated with cholesterol absorption, the part of mechanisms by which CLA decreases serum cholesterol may involve down-regulation of intestinal ACAT activity.