Six sedentary to moderately active men with biochemical signs of riboflavin deficiency were studied under metabolic ward conditions to examine the effects of physical activity on riboflavin status. All participants were subjected to additional exercise (EXER) for an 18 d period between two maintenance (Ml and M2) periods (16 and 13 d respectively) of habitual physical activity. Energy balance and riboflavin intake were maintained throughout the study. Riboflavin status, as judged by a significant reduction in erythrocyte glutathione reductase (EC 1.6.4.2) activation coefficient (EGR-AC), improved on changing from home (1.53 (SD 0.14)) to period M1 (1.36 (SD 0.21)) diets. The exercise period, however, resulted in a significant deterioration in riboflavin status (1.57 (SD 0.31)) which persisted in the subsequent period M2 (1.54 (SD 0.15)). There was a concomitant fall in the urinary excretion of riboflavin only in the EXER period, when results were expressed as a percentage of the dietary intake of riboflavin. These results suggest an increased demand for the vitamin for selective biochemical functions during exercise. However, the energy cost of walking (treadmill 4 km/h), 50 W and 100 W work-loads (bicycle ergometer) as well as delta mechanical efficiency (DME) did not change during the three metabolic periods. The urinary excretion of riboflavin was inversely related to DME (r — 0.49; P < 0.05) and directly correlated with haemoglobin levels (r 0.63; P < 0.005). The present study suggests that riboflavin status further deteriorates during a short period of increased physical activity in individuals whose riboflavin status is marginal.

The effect of riboflavin deficiency on gastrointestinal Fe distribution and loss was studied in weanling rats. Riboflavin deficiency was associated with a significant increase in crypt depth in the upper and mid small intestine and a twofold increase in the rate of crypt cell production compared with weight-matched and ad lih.-fed control rats. The rate of loss of endogenous Fe, measured as faecal 59Fe after intraperitoneally administered 59Fe, was twice that from riboflavin-deficient rats compared with weightmatched controls. We suggest that while there may be a contribution from turnover of enterocytes with an enhanced Fe content, enhanced Fe loss associated with riboflavin deficiency is due predominantly to an accelerated rate of small-intestinal epithelial turnover.

The relationship between vitamin C intake and status was investigated in a group of adolescents (13–14 years old). Dietary intakes were assessed using a 7 d weighed dietary record method, coupled with the collection of duplicate diets. Vitamin C intakes calculated using food composition tables were compared with values obtained by direct analysis of duplicate diets. Vitamin C status was judged via measurement of plasma ascorbic acid (AA) concentration in blood samples taken after a 12–15 h fast. The relationship between calculated and analysed vitamin C intake and plasma AA concentration was examined. Average daily calculated vitamin C intakes, for the group (n 54) as a whole over a 7 d period, gave a good estimate of intake, as judged by prompt analysis of duplicate diets. However, analysed v. calculated intakes were significantly different for approximately one-third of subjects when data were examined on an individual basis. Large discrepancies between analysed and calculated values could not be accounted for on a food group basis. In all but two individuals, calculated vitamin C intake was in excess of the new reference nutrient intake (RNI, part of the new daily reference values (Department of Health and Social Security, 1991)) of 40 mg and all plasma AA concentrations were well above those used to indicate even a moderate risk of deficiency. A relationship between vitamin C intake and plasma AA was observed for both males (n 19) and females (n 35). However, the relationship was much stronger for males who showed a wider range of both intake and plasma AA values.

Thirty-three New Zealand women aged 18–23 years received daily for 32 weeks, 200 μg Se as Seenriched yeast (selenomethionine), or brewer's yeast mixed with selenate, or no added Se (placebo) in a double-blind trial. Se supplementation raised (P = 0.001), platelet glutathione peroxidase (EC 1.11.1.9; GSHPx) activity, and also Se and GSHPx in whole blood, erythrocytes and plasma. Selenomethionine was more effective in raising blood Se concentrations than selenate, but both were equally effective in raising GSHPx activities in whole blood, erythrocytes and plasma, indicating a similar bioavailability for the two forms. These observations and those of gel filtration studies of erythrocytes and plasma proteins reported elsewhere (Butler et al. 1991) are consistent with the incorporation of Se from selenomethionine into a general tissue protein pool while selenate is directly available for GSHPx synthesis, and explain the poorer correlation between Se and GSHPx in individuals with higher Se status. However, selenate raised platelet GSHPx activities to a greater extent than did selenomethionine suggesting some other effect of selenate on platelets which needs further investigation. A response of GSHPx activity in these New Zealand subjects indicates that their dietary Se intake is insufficient to meet recommended intakes based on the criterion of saturation of GSHPx activity, and could reflect a marginal Se status. The level of blood Se necessary for saturation of GSHPx of about 100 ng Se/ml whole blood confirms observations in earlier studies.

In ad lib.-fed rats the epithelium of the small intestine, like the liver, contains large quantities of glutathione, 17.0 and 32.4 nmol/mg protein respectively. Following 24 h food restriction the glutathione content in both tissues fell 53 and 69% respectively. Unlike the liver, however, the glutathione content of the intestinal mucosa is not regulated to a diurnal rhythm, suggesting that the liver may provide glutathione or glutathione precursors to maintain intestinal glutathione levels. Intestinal epithelial cell preparations obtained from 24 h food-deprived rats had depleted glutathione stores (50%) and as a consequence were more susceptible to the oxidizing effects of cumene hydroperoxide. These results suggest that if glutathione plays a major role in the defence of the intestinal mucosa from ingested toxins then depletion of this defence during periods of food restriction could significantly increase the susceptibility of the individual to toxins present in the diet.

Experiments in rodent models of insulin-dependent diabetes mellitus (IDDM) suggest that destruction of pancreatic p cells can be both initiated and inhibited by certain environmental factors such as dietary constituents. We studied nutritional impact of certain protein sources of natural-ingredient, non-purified (NP) rodent diet on diabetes incidence and insulitis severity in the spontaneous diabetic, non-obese diabetic (NOD) mouse. Long-term ad lib. feeding of diets containing wheat flour (800 g/kg), and to a lesser extent soya-bean meal (400 g/kg), were associated with relatively high diabetes incidence (65 and 45% respectively), whereas a diet based on hydrolysed casein (HC; 200 g/kg) as the only source of protein significantly (compared with the wheat-flour diet) inhibited expression of diabetes (22 YO). Feeding a hypo-allergenic soya-bean-protein hydrolysate resulted in diabetes incidence and insulitis severity similar to that of the soya-bean-meal-fed group. This may indicate that protein hydrolysis per se may not be necessary for dietary modification of diabetes in the NOD mouse. The window of vulnerability to diabetogenic diets was found to be between weaning and about 70 d of age. In the diabetic mice insulitis was less frequent in the HC-fed group when compared with those fed NP (P = 0.04), soya- bean meal (P = 0.03), soya-bean-protein hydrolysate (P = 0.012) or wheat flour (P = 0.0002). In the non-diabetic mice the wheat-flour diet was associated with a high insulitis severity in comparison with the HC group (P = 0.004). Early avoidance of NP diet was associated with lower degree of insulitis in both diabetic (P = 0.00003) and non-diabetic mice (P =0.001) when compared with the mice fed on the HC diet later in life. These findings are contributing to further clarification of diabetes-promoting dietary constituents, which may have some nutritional implications for IDDM-susceptible children.