The aim of the present study was to investigate whether oral potassium supplementation during food deprivation could stimulate rumen electrolyte absorption and maintain plasma electrolyte concentration. Eight goats were subjected to food deprivation in combination with intrarumen loads of potassium chloride or, as a control, mannitol in a change-over design. In addition, four KCI- and four mannitol-treated goats were given an extra KCI load towards the end of the experiment. Food-deprived goats which were given KCI maintained their plasma concentration of Na and CI, while plasma K concentration increased from 3.6 mM to 4.4 m.M. In control goats receiving mannitol during food deprivation, the plasma concentration (mM) decreased from 144 to 140 for Na, 105 to 100 for CI and from 3.8 to 3.6 for K, but concentrations were restored when these goats were given a load of KCI. The plasma renin activity was suppressed in food-deprived goats receiving KCI, while those given mannitol showed increased activity. It is suggested that the hyponatraemia which occurs in food-deprived ruminants is mainly caused by diminished K intake.

Estimates of iron status in a random sample (218 men, 283 women) of the Northern Ireland population (aged 18–64 years) were obtained from blood measurements. Multiple criteria were used to determine Fe deficiency and body Fe stores were calculated as an index of Fe sufficiency. Three distinct groups with respect to Fe stores were identified on the basis of sex and menstrual status. Estimates of body Fe stores, mean (and SD), were 13.4 (SD 5.97), 5.3 (SD 6.09) and 8.5 (SD 6.72) mM for men, women aged 18–44 years and women aged 45–64 years respectively. The prevalence of Fe-deficincy was low. ranging from 0.5% in men to 6.6% and 4.6% in the younger and older women respectively. The prevalence of Fe deficiency was low in men (1.4%) and older women (5.7%) rising to 11.0% in the younger group of women. The disproportionately elevated serum ferritin relative to transferrimn saturation supported the suggestion that chronic inflammation might have influenced Fe status measurements in men and older women.

Inositol compounds with three to five phosphate groups (IP3–IP5) were produced by hydrolysis of phytate (inositol hexaphosphate, IP6) and their binding affinities for calcium and zinc investigated at neutral pH with relative concentrations that had been found in a range of students' meals. Zn solubility was negligible at many of these concentrations, with less Zn bound to precipitates of Ca-IP6 than Ca-IP5. The capacity to precipitate Zn at these ratios fell between IP5 and IP3. Zn was partially desorbed by soluble chelators (histidine and picolinate), especially when it had been adsorbed to preformed Ca-IP precipitates. A lower proportion of Zn was accessible to soluble chelators from Ca-IP4 than the other compounds. IP3-IP4 were hydrolysed. by phytase more readily than IP5–IP6.

Two studies were conducted to investigate the possibility that pteroylmonoglutamic acid supplementation would alleviate teratogenesis in zinc-deficient rats. Pregnant rats of the Wistar strain were fed on Zn-deficient (< 0.5 mg Zn/kg) or Zn-supplemented (75 or 95 mg Zn/kg) diets from mating until day 18.5 of gestation. The basal level of pteroylmonoglutamic acid added to all diets (0.56 mg/kg) was supplemented with 30–200 mg/kg in selected diets. Dietary Zn deprivation resulted in fetal resorption, fetal growth retardation and reduced concentrations of Zn in fetuses and maternal plasma and tibia. Low maternal body-weight at conception emerged as an important determinant of risk of resorption in Zn-deficient rats. Dietary Zn deficiency resulted in reduced maternal plasma folate concentrations and these values were inversely correlated with litter size or weight in Zn-deficient rats. Pteroylmonoglutamic acid supplementation increased maternal plasma folate concentrations, but did not reduce the high incidence of teratogenesis which occurred in Zn-deficient rats. Supplementation of Zn-deficient rats with pteroylmonoglutamic acid significantly increased the incidence of clubbed foot and tended to increase the incidence of brain or meningeal abnormalities, or both, and cleft palate, but did not reduce maternal or fetal Zn status. Pteroylmonoglutamic acid supplementation also increased the weights of Zn-supplemented control fetuses.

Damage to skeletal muscles may be mediated via free radicals or intracellular calcium overload. To look for inter-relationships between these pathways we have examined the effect of intracellular Ca overload on muscles from rats fed on either a vitamin E-deficient or vitamin E-sufficient diet and assessed the non-enzymic lipid peroxidation in these muscles by examining the production of thiobarbituric acid reactive substances by homogenates. Vitamin E-deficient muscles were more susceptible to Ca-induced intracellular enzyme efflux and this was acutely corrected by supplementation of the external medium with 230 μmol α-tocopherol/l. Vitamin E-deficient muscles showed increased levels of basal lipid peroxides and were more susceptible to iron-catalysed lipid peroxidation. Addition of the Ca ionophore A23187 increased lipid peroxidation in vitamin E-deficient muscle homogenates, but had the opposite effect in vitamin E-sufficient muscles. These results demonstrate that vitamin E-deficient muscle has an increased susceptibility to intracellular Ca overload, but that this effect cannot be explained by a direct stimulatory effect of the ionophore on non-enzymic lipid peroxidation.

Measurement of peroxyl-radical trapping capacity (TRAP) were made in plasma from patients with malaria from a rural and an urban Thai community. The results were compared with those from control subjects living in the same areas and chosen to match the patients closely. Measurements were also made of various antioxidants including nutritional indices vitamin C and α-tocopherol and the non-nutritional indices urate and protein-sulphydryl. Parasite counts, temperature on examination and the duration of illness were recorded together with measurements of plasma caeruloplasmin (EC 1.16.3.1), retinol and malondialdehyde (MDA). In general, most measurements made in the villagers were lower than those in the comparable urban groups. The exceptions were caeruloplasmin and MDA when the latter was expressed as MDA: cholesterol ratio. TRAP values were extremely low in 50% of the villagers and 25% of the urban patients with malaria and these results correlated with retinol and vitamin C and inversely with malonaldehyde. The results suggested that low TRAP values are associated with lipid peroxidation and that vitamin C and possibly retinol may be destroyed by the oxidative conditions present in the plasma in this disease.

Eighteen different infants' drinks from five manufacturers were examined for their carbohydrate, calcium, phosphorus and acid contents, and their attack on tooth mineral. Seven of the drinks were compared with nine varieties of adults' soft drinks, and demineralization was studied with and without the presence of a cariogenic oral streptococcus. The influence of the acids already in the drinks in dissolving Ca and P outstripped that of any acid generated in these studies in vitro by microbial fermentation of the sugars they contained, giving an indication of their relative erosiveness rather than their cariogenic action. Various other features of the drinks relevant to dental health were identified. Titratable acid was a better guide than pH to their dental properties. Although there were considerable differences between the various infants' drinks taken as a group, their acidity levels and demineralizing powers were generally lower than those of the adults' drinks.

The site where osmotically active substances act to depress food intake was determined in sheep. After 5 × 5 h of food deprivation, solutions of sodium chloride or polyethylene glycol-200 (PEG-200) were added to either the reticulo-rumen or the abomasum. The sheep were then immediately offered pelleted lucerne (Medicago sativa). Water was withheld during the first 60 min of feeding but was available from 60 to 90 min. There was a linear inhibition in food intake in the first 10 min after loading 2.37, 6.25, 12.5, 25.0 or 50.0g NaCI into the rumen according to a 5.5 Latin square design (P = 0.0001). The intake reduction was 3.49 g food/g NaCI. An osmotic load of PEG-200 equivalent to 50 g NaCI also significantly inhibited food intake in the first 10 min of the meal compared with a control treatment. The inhibition of food intake after loading 55 g NaCI into the rumen was not affected by injecting lidocaine hydrochloride into the reticulum immediately before NaCI loading. NaCI injected into the abomasum did not significantly affect food intake in the first 10 min of feeding even though the tonicity of abomasal digesta was increased to unphysiological levels. There was no consistent relationship between food intake and the change in the tonicity of jugular plasma following solute loading and drinking. The sensing site of hypertonicity was localized to the wall of the reticulo-rumen where neuronal receptors appear to be capable of detecting osmotic pressure within the physiological range to depress food intake. These receptors should be identified and characterized because of their possible significance in limiting food intake by ruminants.