F. H. Kratzer

Phytic acid-metal complexes.

Summary Sodium phytate corresponding to a formula of C6H6O24P6Na12 · 3H2O (formula weight 977.8) was titrated against metal ions and in each case an inflection in the titration curve was obtained when 5 moles of a divalent metal ion had been added per mole sodium phytate. At a pH of 7.4, sodium phytate formed complexes with metals in the following decreasing order: Cu++, Zn++, Ni++, Co++, Mn++ Fe+++, and Ca++.

Inherited myopathy in the chicken.

Inherited muscular dystrophy in the chicken is a simple autosomal recessive to normal (Asmundson & Julian, 1956). The comparative pathology of muscular dystrophy of the chicken has been summarized recently (Julian & Asmundson, 1963). Although there appears to be no single muscular dystrophic entity of man which is directly comparable to muscular dystrophy of the chicken, the condition in the chicken does have a variety of characteristics which in themselves are directly comparable to characteristics of the various myopathies of man as described by Adams et al., 1954. The test used to identify the dystrophic bird is to lay it on its back on a flat surface and record the number of times it can rise from the supine position. Those that could rise 5 times were assigned a score of 6 and considered normal. To determine age at onset the birds were tested once a week from day hatched until 12 weeks old. Age at onset was assigned to the first day with a score of less than 6 after which the birds uniformly failed to rise 5 times. Age, from a behavioral standpoint, has an effect on the number of times a bird will rise from the supine position since day-old chicks may make no attempt to rise. By three or four weeks of age, all birds will attempt to rise. The bird with inherited myopathy sooner or later reaches a stage at which it cannot rise because of inability to move its wings except within a very limited range or because of weak muscles in some older birds with less restricted wing movements. If the tendon of birds with immobolized wings is cut, the bird is able to rise again until the tendons grow together. Variation in age at onset indicated that this is a high-heritability polygenic trait. Selection for early and late onset on the basis of individual performance shows that to be the case. TABLE 1 shows the effect of selection and of sex. This was the first example observed of a high degree of genetic plasticity in the muscular dystrophy syndrome in this species. Frequency of testing, i.e. exercise, and to some extent temperature, also influence age at onset. When birds of line 304 were exercised (tested), daily onset was delayed as compared with birds exercised once a week (TABLE 2) in agreement with the results of Dowben ( 1 963) with patients whose response differed according to the syndrome. Since selection was proving to be an effective method of obtaining birds characterized by late onset these experiments were not continued. Exhaustion scores were determined in 1959 for a large number of birds with inherited muscular dystrophy as well as F1, FP and backcross progeny of crosses with normal line 200 New Hampshire chickens. Birds with inherited muscular dystrophy were able to rise on the average from 1 or 2 times for line 304 to 8 to 10 times for line 305, at 5 to 6 weeks of age, with line 301 birds intermediate. By 8 weeks the average for 305 had dropped to 4. On the other hand, normal birds, whether heterozygous or homozygous, were able to rise on the average 13 to 27 times at ages 5 to 8 weeks. While there were also some differences between lines of normal birds, these were small and less consistent than the difference between the normal and muscular-dystrophic. Our results agree with

Aflatoxin effects in poultry.

Summary A systematic study was made of the effect of graded levels of dietary aflatoxin on the performance of broilers under simulated practical conditions. No adverse effects were detected when a ration containing 400 ppb aflatoxin was fed to Arbor-Acres broiler chicks from 1 day to 8 weeks of age. At higher levels (800 and 1600 ppb) adverse liver effects were detected, based on biochemical and histological studies. By chemical analysis, no evidence of aflatoxin was found in the meat, liver or blood of broilers fed 1600 ppb for 60 days prior to slaughter, nor in the eggs, meat, liver, or blood of White Leghorn hens fed a ration containing 2700 ppb aflatoxin for a period of 48 days.

Furazolidone residues in chicken and swine tissues after feeding trials

Broiler chickens and swine fed furazolidone in their diet were sacrificed, and samples of liver, kidney, skin/fat and muscle were harvested and analyzed for furazolidone residue. Chickens fed 200 g of furazolidone/ton of feed were withdrawn from treatment 21, 14, 7, 5, 3, or 0 days before slaughter. Birds withdrawn from medication more than 5 days prior to slaughter had no residues in any of the tissues sampled. One of the 12 birds in each of the 5 day and 3 day withdrawal groups had detectable residues in the skin/fat. Seven of the 12 birds in the 0 day withdrawal group had residues of less than 2 ppb in skin/fat samples. Chickens fed 400 g furazolidone/ton of feed were withdrawn from treatment 0 days before slaughter. Residues of 0.7 to 3.5 ppb were found in the skin of these birds; residues were not found in other tissues. Swine were fed 300 g furazolidone/ton of feed for 2 weeks or 150 g/ton for 5 weeks. They were withdrawn from treatment 10, 7, 5, 3, or 0 days before slaughter. Tissue samples taken from these swine did not contain detectable furazolidone residues.

Intestinal Absorption of Zinc or Calcium-Ethylenediaminetetraacetic Acid Complexes in Chickens

Summary Carbon-14 and zinc-65 or cal-cium-45 appeared in the blood perfusing an isolated segment of the small intestines of chickens following placement of EDTA-2-C14 complexed with Zn65 and Ca45 in the lumen. The lumen tended to adsorb the zinc from its complex but not calcium. An efflux of 2.7 μM/hr cm was observed for calcium-45. The values for zinc-65 varied from 0.2-0.6 μM/hr cm.

Electrolytes in Normal and Dystrophic Chickens as Influenced by Dietary Potassium

Summary Normal and genetically dys-trophic chickens showed different responses in electrolyte balance when fed two different levels of potassium. Dystrophic chickens had significantly higher levels of sodium, potassium, and calcium in their pectoral muscle, significantly higher sodium and lower magnesium levels in their gastrocnemius muscle, and no significant differences in the electrolyte levels of their cardiac muscle compared with normal chicks. Electrolyte composition was greatly affected in the pectoral muscle, less affected in the gastrocnemius muscle, and unaffected in the cardiac muscle in the normal chicks when potassium was increased from 0.5 to 1%. In dystrophic chicks, however, only the gastrocnemius muscle was affected by an increase in dietary potassium.

Quantitative relation of EDTA to availability of zinc for turkey poults.

Summary Various levels of EDTA and zinc were added to the poult diet containing isolated soybean protein. One hundred mg of EDTA/kg were equivalent to approximately 8 mg/kg zinc in supplementing the basal diet. When 7 or 10 mg of zinc/kg were added to the diet, 100 mg of EDTA/kg were equivalent to approximately 19 mg of zinc/kg. The data indicate that EDTA improves the effectiveness of added zinc as well as increasing the utilization of zinc already present in the basal diet. Perosis increased as the zinc level of the diet increased to approximately 30 mg/kg and decreased as zinc was added above this level.

Fat Deposition in Musculature of the Genetically Dystrophic Chicken.

Summary Genetically dystrophic chickens contain significantly more crude fat in the superficial pectoral muscle (% of wet sample) than do normal chickens. An increased fat deposition is noted as early as 15 weeks of age and is associated with physical manifestation of dystrophy resembling certain muscular dystrophies in man. Females deposit more crude fat than males.

Study of the reaction of formaldehyde with vitamin B12

Abstract Formaldehyde-C 14 reacts with vitamin B 12 in vitro to form complexes that cannot be separated from vitamin B 12 by crystallization, paper chromatography, or paper electrophoresis at several pH values. No differences were noted in the absorption spectra in the visible, ultra-violet, and infrared regions between vitamin B 12 reacted with formaldehyde and unreacted vitamin B 12 . Four samples prepared by slightly different methods contained 0.5, 1, 2, and 3 moles of formaldehyde-C 14 combined with each mole of vitamin B 12 .

Biotin-related Abnormal Fat Metabolism in Chickens and Its Consequences

The “fatty liver kidney syndrome” that caused high mortality in young chicks in the United Kingdom and Australia was found to be biotin responsive by Payne et al.‘ and Whitehead et a1.* Another condition, the “sudden death syndrome” (SDS), has been a problem in the United States and Canada’ and is characterized by the sudden death of predominately male chickens that are above average weight. They are found lying on their backs with feet and neck extended. Our studies were related to determining whether biotin might be involved in this problem and by what mechanism. Several studies were carried out with broiler-type chickens fed a biotin-deficient purified diet based upon corn starch, isolated soybean protein, and dried egg albumin to reduce the available biotin content. In the first study, graded levels of biotin were used and the biotin content of the liver determined at the end of a 28-day feeding period by the isotope dilution method of Hood.4 The biotin level in the liver varied with the dietary biotin content. The biotin content in the livers of chicks that died of SDS under field conditions was significantly lower (FIG. 1) than in our experimental chicks that received an equivalent level of biotin as well as chicks from the field that had died of causes other than SDS. In a second experiment, chicks were fed marginal, barely adequate, and adequate levels of biotin in diets containing an antibiotic, or no supplement with and without an oral Lactobacillus acidophillus ino~ulat ion.~ The Lactobacillus inoculation of chicks fed the marginally deficient diet caused reduced growth, lowered liver biotin and changes in liver fatty acids characteristic of a biotin deficiency. It appears that the lactobacilli competed with the chicken for biotin and produced a deficiency when the diet was marginal. No significant changes were noted with the antibiotic feeding. In a third study, the egg yolk and plasma biotin levels of laying hens that were fed various levels of biotin showed a linear response to the dietary biotin content and reached equilibrium in from 7 to 14 days. These levels were used to determine the amount of biotin that was available from a given feedstuff. By comparing this value with the determined total biotin, it was possible to develop a relatively rapid assay for biotin availability. This method confirmed the results of others that biotin in wheat and sorghum is relatively unavailable while that in corn is highly available. Biotin in the feed of the chicks showing SDS in the field was relatively available. Recently we have investigated the fatty acid composition in selected tissues from chicks fed various levels of biotin and measured prostaglandins in plasma and freeze-clamped heart tissue by radioimmunoassay. Liver tissue from fasted, biotindeficient chicks showed a decrease in 20:4n6 and 20:3n6, but an increase in 18:2n6. A significant decrease in 20:4n6 was found in heart tissue of fasted chicks compared to their fed counterparts. Plasma levels of PGEl and PGF,, were elevated in fasted, biotin-deficient chicks, but heart PGE2 levels were depressed. Prostaglandin fatty acid precursors (20:3n6 and 20:4n6) may be indirectly reduced via elevated 18:3n3 and