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Twenty-four weanling Yorkshire pigs were used in a 2 × 2 × 2 factorial arrangement of treatments to determine their response to high levels of dietary lead (Pb) (1,000 ppm) and zinc (Zn) (4,000 ppm) (as lead acetate and zinc oxide), to investigate the influence of high dietary calcium (Ca) (1.1%) on the biochemical and morphological manifestations of Pb and Zn toxicity, and to determine the effect of excess Zn on Pb toxicity. Clinical signs of Pb toxicity included behavioral changes, lameness, and anorexia. Pb content of blood, soft tissues, and bone was increased markedly by 1,000 ppm Pb in the diet during the 13-week experiment. Zn and Pb fed together, as compared with Pb alone, tended to increase Pb levels in blood, soft tissues, and bone and to enhance the toxic effects of Pb as shown by reduced weight gains, severe clinical signs, and pathological changes. High Ca reduced blood and bone Zn and Pb concentrations. The results indicate that high dietary Ca has a protective effect against the adverse effects of diet Pb and Zn, and that Zn aggravates Pb toxicity in growing pigs.

Two levels each of Cu, Fe and ascorbic acid (AA) were used in a factorial arrangement in diets fed to 3-week-old pigs in an attempt to determine the influence of high levels of dietary Fe and AA on the deleterious effects of 250 ppm dietary Cu, to ascertain the mode of action of high Cu in inducing anemia and to delineate the effects of high dietary AA on Fe and Cu metabolism. Pigs fed high Cu had decreased plasma and liver Fe concentrations, increased latent and total Fe binding capacity, decreased saturation of transferrin, increased rate of removal of intravenously administered 59Fe from the plasma and increased utilization of 59Fe by RBC, all manifestations of Fe deficiency. The rapid uptake of 59Fe by RBC, low levels of tissue Fe and low degree of transferrin saturation indicate no block in Fe release from the reticuloendothelial system. Liver Cu concentration of pigs fed high Cu was greatly reduced by addition of 0.5% AA to the diet. AA had no effect on altering the level of Fe retained in the liver or intestine, but did increase the plasma Fe level, the degree of saturation of plasma transferrin, and the rate of removal from plasma and uptake by RBC of 59Fe. It is concluded that the Fe deficiency induced by high dietary Cu is due to impairment in Fe absorption from the gastrointestinal tract and that this impairment is ameliorated by AA.

Cestrum diurnum(day-blooming jessamine) has been proposed to cause calcinosis in horses and cattle in Florida. The present studies investigated some physiological properties of the plant, using the chick as the experimental animal. The inclusion of dried leaf powder in a rechitogenic diet restored intestinal calcium-binding protein synthesis (CaBP) and increased calcium absorption in the cholecalciferol-deficient chick. The estimated level of cholecalciferol-equivalents in the dried leaf was about 30,000 to 35,000 IU/kg. Most of the activity was extractable with methanol:chloroform (2:1), indicating that the major cholecalciferol-like component in C. diurnumwas different from the water soluble factor(s) in Solanum malacoxylon. The time course of effect of C. diurnumextract in rachitic chicks was similar to that of 1,25-dihydroxycholecalciferol but the former had a longer lag time. The strontium fed chick, in which the kidney 25-hydroxycholecalciferol-1α-hydroxylase is inhibited, responded to C. diurnumextract, confirming the 1α, 25-dihydroxycholecalciferol-like character of the Cestrumfactor. The extract also appeared to interact with the intestinal 1α,25-dihydroxycholecalciferol cytosol receptor although this observation is preliminary. These findings indicate that the 1α,25-dihydroxycholecalciferol-like principle in C. diurnummay cause excessive calcium and phosphate absorption leading to calcinosis.

Yorkshire pigs weaned at 3 to 5 weeks of age, weighing an average of 7.2 kg initially in experiment 1 and 4.9 kg in experiment 2, were pair-fed 3% protein purified diets containing 5 or 25% corn oil. The daily feed intake of the member of each pair fed the low fat diet was equalized with the ad libitum consumption of its mate fed the high fat diet. The total calorie consumption per pig was approximately 29% greater in the high fat group than in the low fat group. A similar diet containing 24% protein was fed as a positive control diet at a level of 4.5% of body weight daily in experiment 1 and 4.0% in experiment 2. Total serum protein level and percentage of albumin decreased significantly (P< 0.01) after feeding the low protein diets for 8 weeks. Pigs fed the low protein-high fat diet showed a more severe depression in serum proteins than those fed the low protein-low fat diet even though protein intake was equal for the 2 groups. Liver lipid concentration was 34.1% in the pigs fed low protein-high fat as compared with 9.7% in those fed low protein-low fat and 12.3% in positive control pigs. Pigs in the former group developed typical kwashiorkor-like symptoms, including severe edema in the umbilical and genital regions and general feebleness and apathy. In contrast, pair-fed mates fed the low protein-low fat diet failed to develop these symptoms and remained thin in appearance and active, indicating 2 different manifestations of protein deficiency, one resembling kwashiorkor, the other marasmus. Gross energy concentration of whole empty bodies of pigs fed the 2 low protein diets was similar (6.5 vs. 6.2 kcal/g of dry sample) but that of positive control pigs was significantly lower (P< 0.01) (5.6 kcal/g). This similarity in energy storage in the 2 low protein groups, despite the 29% difference in calorie intake, indicates not only an increased specific dynamic effect with low protein diets, but an additional increase when greater calorie intake accompanies protein deficiency.

The effects of feeding diets containing no fat, 3% hydrogenated coconut oil (HCO) or graded levels (0.1, 0.5, 1.0 or 3%) of safflower oil (SO) on serum cholesterol, lipids and protein level; on total heart and liver cholesterol and lipid level and on growth rate and skin condition were studied in weanling Yorkshire and Yorkshire × Hampshire pigs. Pigs fed the fat-free diet for 21 weeks developed severe skin lesions not observed in pigs fed HCO diets. Highly significant elevation of serum, liver and heart lipid and liver cholesterol, and a highly significant depression of total serum protein were observed with the feeding of HCO or fat-free diets. Serum cholestrol was significantly increased by HCO as compared with the fat-free diet or diets containing SO during the repletion period. Total heart cholesterol, growth rate and erythrocyte fragility were unaffected by diets. It is concluded that growth rate is not adversely affected in the pig by fat-free diets and that HCO does not produce skin lesions in the pig characteristic of fatty acid deficiency. Of all the correlation coefficients analyzed, only the serum cholesterol and total serum lipids were consistently highly significantly correlated, while serum protein was significantly inversely related to the total liver lipid.

Ten female and 230 male kits were used to study the need for pantothenic acid by growing mink. Three trials were conducted using purified diets with ad libitum and equalized paired-feeding techniques. The minimal pantothenic requirement for growth was found to be 5 mg of calcium pantothenate/kg of diet, whereas 8 mg/kg of diet were required for optimal performance. Anorexia and reduced serum cholesterol were early responses to hypovitaminosis. The gross pathological findings were diarrhea, cachexia, and dehydration with hemorrhagic gastric ulcers and specific starvation lesions.

Poor growth, mortality and myopathies of the heart and gizzard have been produced experimentally in young poults fed a practical-type diet containing all nutrients previously shown to be required by the poult except for supplemental vitamin E and methionine. The corn and soybean meal used in this diet were obtained from geographical areas where the soil is known to be low in selenium. Addition of vitamin E and methionine to the diet improved growth but gizzard myopathy was not prevented and maximal growth was not achieved until the diet also was supplemented with at least 0.1 ppm of selenium as sodium selenite. Under the conditions of these experiments, therefore, the selenium requirement in a practical-type diet depended to some extent upon the amount of vitamin E or methionine supplementation; it ranged from approximately 0.18 ppm in the presence of vitamin E to approximately 0.28 ppm of selenium in the absence of added vitamin E. Although myopathy of the skeletal (pectoral) muscle was not observed grossly, necropsy studies revealed histological changes in skeletal muscle typical of Zenker's degeneration. The order of prominence of the “selenium-responsive” diseases of the young poult appear to be: myopathy, first of the smooth muscle (gizzard); second, of the myocardium; and third, of the skeletal muscle. Selenium appears to be the primary nutritional factor required. Vitamin E is of less importance and sulfur amino acids are completely ineffective in prevention of these myopathies in poults.

A combined protein-vitamin E deficiency syndrome causing severe liver damage in the pig was studied by manipulating dietary levels of methionine, choline and selenium. Yorkshire pigs weaned at 3 weeks of age, weighing an average of 5 kg, were used in 4 experiments. During the 8-week experimental period the animals were fed a basal diet containing 3% isolated soy protein and 25% corn oil; it was marginal in vitamin E and selenium but adequate in all other nutrients. Consumption of this diet resulted in the development of liver necrosis which was most obvious histologically at weeks 2 and 4; at week 8 severe postnecrotic scarring of the liver predominated with little evidence of acute necrosis. The liver damage was completely preventable by supplementation with α-tocopherol, or selenium, or both. Choline supplementation aggravated the liver damage; however, methionine supplementation provided considerable, and in some cases, complete protection against necrosis and scarring but did not prevent the appearance of hyaline bodies in the hepatocytes. The methionine effect was not related to contamination of the supplemental methionine with selenium.

Young pigs (approximately three weeks old, average weight 6.3 kg) were used to study the effect of caloric density and protein quality of the diet on the biochemical and anatomical manifestations of protein deficiency. Purified diets containing 5% of protein from casein or wheat gluten and either 3 or 23% fat (corn oil) were fed ad libitum for 14 weeks. A stock diet containing 18% of protein served as the positive control.

Thirty-four weanling Yorkshire pigs were used in two experiments to determine the effect of dietary Fe and Cu levels on growth, hemoglobin, hematocrit, red blood cell count (RBC), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), plasma ceruloplasmin and plasma and liver Cu, Fe and Zn. A level of 10 ppm Cu in a semipurified diet containing dried skim milk, glucose, cornstarch, corn oil, cellulose powder and vitamins and minerals produced faster growth and greater feed consumption than levels of 2 or 250 ppm Cu. Pigs fed a diet containing 250 ppm Cu developed severe microcytic hypochromic anemia (6 g hemoglobin/100 ml blood) by week 5, while hemoglobin of pigs fed 2 ppm or 10 ppm Cu remained relatively constant throughout the 9-week experiment (9 to 10 g/100 ml). Plasma ceruloplasmin was not affected by 250 ppm Cu, but was significantly reduced beginning at week 4 by 2 ppm Cu in the diet. RBC was significantly depressed by either 2 or 250 ppm Cu when compared to RBC for pigs fed 10 ppm Cu. MCV, MCH and MCHC were not affected by the diet containing 2 ppm Cu but MCV and MCH were significantly reduced in pigs fed 250 ppm Cu. Plasma and liver Cu were significantly decreased by 2 ppm Cu and significantly increased by 250 ppm Cu when compared to values in plasma and liver of pigs fed 10 ppm Cu. Plasma and liver Fe were reduced at 2 ppm Cu and at 250 ppm Cu in the diet. Plasma and liver Zn were not significantly affected by dietary Cu level. In a factorially arranged experiment with 20 or 100 ppm of dietary Fe and 10 or 250 ppm dietary Cu, body weight gain, hemoglobin, hematocrit, RBC, MCV, MCH, MCHC were significantly reduced by 250 ppm Cu. The mean for all parameters above (except RBC) was lower in the 20 ppm Fe-250 ppm Cu group than in all other groups, suggesting a protective effect of high Fe on the anemia induced by added Cu. No gross or histopathological changes were observed, aside from the anemia. It is concluded that the microcytic hypochromic anemia observed in pigs fed 250 ppm Cu is the result of changes in Fe utilization.