Young chicks were fed a vitamin K-deficient soybean concentrate basal diet containing graded levels of menadione from menadione nicotinamide bisulfite (MNB) or menadione dimethyl-pyrimidinol bisulfite (MPB) to assess prothrombin time as a function of menadione intake. Prothrombin time decreased linearly as menadione dose increased from 0 to 400 micrograms/kg. Multiple linear regression slope-ratio calculations indicated that both sources of menadione were of equal potency. To assess niacin bioactivity of MNB, graded doses of nicotinamide (0 to 5 mg/kg) from MNB or nicotinamide were added to a niacin-deficient diet based upon corn, corn gluten meal and vitamin-free casein. Weight gain increased linearly as a function of nicotinamide dose, and multiple linear regression analysis of weight gain as a function of supplemental nicotinamide intake revealed no significant differences in slope between the two sources of nicotinamide. Using excess doses, MNB was compared with MPB in acute (single crop intubation) or chronic (fed in the diet for 14 d) toxicity trials. With a single menadione dose of 1600 mg/kg body wt, weight gain in the subsequent 14-d period was reduced by MNB but not by MPB. Mortality rates of 25 and 17% occurred for MPB and MNB, respectively, at this dose level. Doses lower than 1600 mg/kg body wt caused neither morbidity nor mortality. When provided in the diet for a 14-d feeding period, menadione doses of 3000 mg/kg diet from MNB reduced gain, feed intake, gain:feed ratio and blood hemoglobin concentration. Menadione doses of 6000 mg/kg diet were required to produce morbidity of this type when MPB was fed.(ABSTRACT TRUNCATED AT 250 WORDS)

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A niacin-deficient purified amino acid diet that contained adequate (40 mg/kg) or deficient (10 or 15 mg/kg) iron was used to assess the growth promoting efficacy of tryptophan as a niacin precursor. Basal diets contained 1400 mg/kg tryptophan, a level that was established as meeting the requirement for tryptophan per se in diets containing excess nicotinic acid. Chicks fed the iron-deficient diets had markedly lower hemoglobin concentrations than those fed the iron-adequate diets. Regardless of iron level, chicks exhibited linear growth responses to either nicotinic acid or tryptophan supplementation. Using multiple-linear regression of weight gain on supplemental tryptophan or nicotinic acid intake, the efficiency (wt:wt) of tryptophan conversion to niacin activity (i.e., tryptophan slope divided by nicotinic acid slope) was a mean of 1.77% (56:1) for chicks fed the iron-deficient diet. This was significantly (P < 0.05) lower than the 2.39% (42:1) efficiency calculated for chicks fed the iron-adequate diet. Thus, iron deficiency reduced tryptophan utilization (for NAD synthesis) but had no effect on nicotinic acid utilization. The results suggest that pellagra in populations having endemic anemia and protein-energy malnutrition may be due not only to inadequate intakes of bioavailable niacin but also to inadequate intakes of bioavailable iron.

Based on zinc uptake in chick tibia, Zn bioavailability in cooked ground beef was equal to that of Zn in an inorganic standard (ZnSO4), whether Zn supplements were added to a soy-concentrate diet containing phytate or to a phytate-free egg-white diet. With both diet types, total tibia Zn was a linear (P < .01) function of supplemental Zn intake from ZnSO4, but the slope of the linear regression line was twice as great for the egg-white diet as for the soy-concentrate diet that contained phytate. At 10 mg/kg of supplemental Zn, freeze-dried ground beef produced the same tibia Zn concentration (and total Zn content) as that obtained with ZnSO4. The results suggest that the relative bioavailability of Zn in cooked ground beef is as great as that in ZnSO4, whether consumed in diets with or in those without phytate.

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