Nutrient requirements of poultry

Publisher Summary This chapter discusses that the knowledge of phytic acid had its beginning in the discovery by Hartig, who isolated small particles or grains (which were not starch grains) from the seeds of various plants. Phytic acid has been generally regarded as the primary storage form of both phosphate and inositol in almost all seeds. The amount of phytic acid varies from 0.50% to 1.89% in cereals (except polished rice), from 0.40% to 2.06% in legumes, from 2.00% to 5.20% in oil seeds except soybeans and peanuts (grouped under legumes), and from 0.40% to 7.50% in protein products. Many foods and seeds contain myo-inositol hexaphosphate as an important source of phosphorus, and accurate methods for its determination are needed. Phytase (meso-inositol hexaphosphate phosphohydrolase, EC 3.1.3.8) is widely distributed in plants, animals, and fungi. In mature cereal grains, legumes, and oil seeds, the major portion of the total phosphorus is present in the form of phytic acid (phytate). Experiments with animals have suggested that phytic acid in plant foods complexes with dietary essential minerals such as calcium, zinc, iron, and magnesium and makes them biologically unavailable for absorption. The correlation of phytate with the cooking quality of peas was first suggested by Mattson. Phytic acid, myo-inositol 1,2,3,4,5,6-hexakis dihydrogen phosphate serves as the main phosphorus store in mature seeds and grains. In cereals and legumes, phytic acid content ranges from 0.14% to 2.05%, which accounts for 18 to 88% of the total phosphorus.

Phytates in Legumes and Cereals

This public health statement tells you about manganese and the effects of exposure to it.The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in the nation. These sites are then placed on the National Priorities List (NPL) and are targeted for long-term federal clean-up activities. Manganese has been found in at least 869 of the 1,699 current or former NPL sites. Although the total number of NPL sites evaluated for this substance is not known, the possibility exists that the number of sites at which manganese is found may increase in the future as more sites are evaluated. This information is important because these sites may be sources of exposure and exposure to this substance may harm you.When a substance is released either from a large area, such as an industrial plant, or from a container, such as a drum or bottle, it enters the environment. Such a release does not always lead to exposure. You can be exposed to a substance only when you come in contact with it. You may be exposed by breathing, eating, or drinking the substance, or by skin contact.If you are exposed to manganese, many factors will determine whether you will be harmed. These factors include the dose (how much), the duration (how long), and how you come in contact with it. You must also consider any other chemicals you are exposed to and your age, sex, diet, family traits, lifestyle, and state of health.

Toxicological Profile for Manganese

Chicks were used to determine whether the addition of a mold phytase to a diet containing natural phytate phosphorus causA§dthe phosphorus in the phytate to be hydrolyzed in vivo to a form which could be utilized by the chick. Phytase, produced by Aspergillus ficuum NRRL 3135, was fed as an ace tone-dried preparation. The diets contained from 0.18 to 0.24% natural phytate phosphorus supplied primarily by corn and soybean meal. Phytase supplement was added at levels ranging from 1 to 8 g/kg of diet. One gram of the supple ment hydrolyzed 950 mg of inorganic phosphate from calcium phytate in vitro in 1 hour under standard conditions. For comparative purposes, graded levels of either monobasic sodium orthophosphate, or beta-tricalcium phosphate were added at levels to supply from 0.04 to 0.21% phosphorus. The percentage of bone ash was used to evaluate in vivo phytase activity. The addition of phytase to the diet produced an increase in percentage bone ash indicating hydrolysis of phytate by the enzyme. Total hydrolysis of phytate occurred when 3 g phytase supplement was used per kilogram diet. Chicks utilized the hydrolyzed phytate phosphorus as well as supplemental inorganic phosphorus. Phytase activity oc curred in the alimentary tract of the chick and not in the feed prior to ingestion. J. Nutr. 101: 1289-1294, 1971. The ability of poultry to utilize phytate phosphorus is a controversial subject (1, 2). The probability that the differences re ported for the availability of phytate phos phorus to the chick are caused by dietary variables was discussed in a recent review (3). The presence of phytase, an enzyme which hydrolyzes phytate to phosphoric acid and inosinic acid (4-6) in some feed ingredients (7, 8) may have enhanced the utilization of phytate phosphorus. Phytase of plant origin appears to retain its activity when added to animal diets (7-10). The reaction conditions of in vitro studies with some phytases suggest that the enzyme is active in the digestive tract of animals (11, 12) since the in vitro conditions are similar to those found in the chick's ali mentary tract. A purified extract of phytase from wheat bran was inactive in the rat (13). Phytase obtained from Escherichia coli was active when fed to chicks (14). The present report describes quantitative studies of the effect of a mold phytase on J. NUTRITION, 101: 1289-1294. the utilization of phytate phosphorus by chicks. EXPERIMENTAL PROCEDURE The breed, sex and number of chicks used are listed in the design of each ex periment. The replication of treatments varied and was dependent on the amount of phytase preparation available. Day-old chicks were allotted to the treatments and were housed in electrically heated brooders with raised wire mesh floors. Feed and water were supplied ad libitum. Body weights and feed consumption were re corded weekly. At the end of week 3 the Received for publication February 9, 1971. 1Presented in part at the 51st annual meeting of the Federation of American Societies for Experimental Biology, Chicago, Illinois, 1967. Federation Proc. 26: 416 (abstr.). 2Present address: Department of Animal Sciences, University of Arkansas, Fayetteville, Arkansas 72701. 3Reprint requests should be addressed to this au thor. 4Present address: Department of Biological Sci ences, Florida Technological University, Orlando, Flor ida 32816. 5Present address: 2921 Glenwood Lane, Billings, Montana 59102.

Effect of supplemental phytase on the utilization of phytate phosphorus by chicks.

1. Forms of Selenium.- 1.1 Low Molecular-Weight Compounds.- 1.1.1 Selenocysteine.- 1.1.2 Selenocystine.- 1.1.3 Selenohomocystine.- 1.1.4 Se-methylselenocysteine.- 1.1.5 Selenocystathionine.- 1.1.6 Selenomethionine.- 1.1.7 Se-methylselenomethionine.- 1.1.8 Dimethyl Selenide.- 1.1.9 Dimethyl Diselenide.- 1.1.10 Trimethyl Selenonium.- 1.1.11 Elemental Selenium.- 1.1.12 Selenotaurine.- 1.1.13 Selenocoenzyme A.- 1.1.14 Other Compounds.- 1.2 Macromolecular Forms of Selenium.- 1.2.1 Formate Dehydrogenase.- 1.2.2 Glycine Reductase.- 1.2.3 Nicotinic Acid Hydroxylase.- 1.2.4 Xanthine Hydrogenase.- 1.2.5 Thiolase.- 1.2.6 Glutathione Peroxidase.- 1.2.7 Miscellaneous Selenoproteins.- 1.2.8 Seleno-tRNA's.- 11.11 References.- 2. Selenium Deficiency Diseases in Animals.- 2.1 Introduction.- 2.2 Dietary Liver Necrosis and Factor 3.- 2.2.1 Discovery.- 2.2.2 Pathology.- 2.2.3 Biochemical Defect.- 2.2.4 Hepatosis Dietetica.- 2.3 Nutritional Muscular Dystrophy.- 2.3.1 Pathology.- 2.3.2 Prevention of NMD.- 2.4 Exudative Diathesis.- 2.5 Pancreatic Degeneration.- 2.6 Mulberry Heart Disease.- 2.7 Reproductive Problems.- 2.8 Myopathy of the Gizzard.- 2.9 Growth.- 2.10 Selenium-Responsive Unthriftiness of Sheep and Cattle.- 2.11 Periodontal Disease of Ewes.- 2.12 Encephalomalacia.- 11.11 References.- 3. Metabolism of Selenium.- 3.1 Absorption.- 3.2 Placental Transfer.- 3.3 Mechanism of the Antioxidant Action of Selenium.- 3.4 Effect of Paraquat.- 3.5 Effect on Cytochrome P-450.- 3.6 Selenium and Hepatic Heme Metabolism.- 11.11 References.- 4. Comparative Metabolism and Biochemistry of Selenium and Sulphur.- 4.1 Introduction.- 4.2 Comparative Metabolism of Selenium and Sulphur.- 4.2.1 Microorganisms.- 4.2.2 Plants.- 4.2.3 Animals.- 4.3 Comparative Biochemistry of Selenium and Sulphur.- 4.3.1 Selenopersulfide as an Electron Transfer Catalyst.- 4.3.2 Iron-Sulphur Proteins.- 4.3.3 Sulphur Salts and Selenium Toxicity in Animals.- 4.3.4 Other Selenium-Sulphur Interactions.- 11.11 References.- 5. Biological Interactions of Selenium with Other Substances.- 5.1 Cadmium.- 5.1.1 Pathological Effects.- 5.1.2 Cadmium-Zinc Interactions.- 5.1.3 Cadmium-Selenium Interactions.- 5.1.4 Effect on Drug Response.- 5.2 Arsenic.- 5.3 Copper.- 5.4 Silver.- 5.5 Cobalt.- 5.6 Manganese.- 5.7 Lead.- 5.8 Mercury.- 5.8.1 Inorganic and Organic Mercury.- 5.8.2 Tissue Distribution.- 5.8.3 Properties of the Mercury-Selenium Complex.- 5.8.4 Teratogenicity.- 5.9 Thallium.- 5.10 Tellurium.- 5.11 Vanadium.- 5.12 Bismuth.- 5.13 Other Substances.- 11.11 References.- 6. Environmental Occurrence of Selenium.- 6.1 Geochemistry of Selenium.- 6.2 Soil Selenium.- 6.3 Uptake and Concentration of Trace Elements in the Roots, Stems, and Leaves of Plants.- 6.4 Forage Selenium.- 6.5 Selenium in Water.- 6.6 Selenium in Food.- 6.7 Intakes and Recommended Daily Allowance in Humans.- 6.8 Regulations in Regard to Animal Diets.- 11.11 References.- 7. Toxicity of Selenium.- 7.1 Introduction.- 7.1.1 Acute Toxicity.- 7.1.2 Blind Staggers.- 7.1.3 Alkalai Disease.- 7.1.4 Toxicity in Rabbits.- 7.1.5 Toxicity in Hamsters.- 7.1.6 Toxicity in Sheep.- 7.1.7 Toxicity in Rats.- 7.1.8 Effect of Diet on Toxicity.- 7.1.9 Biochemical Lesions.- 7.1.10 LD50 of Various Selenium Compounds.- 7.2 Industrial Medical Aspects.- 7.2.1 Occupational Hazards.- 7.2.2 Permissible Limits for Selenium Exposure.- 7.2.3 Toxicity in Humans.- 11.11 References.- 8. Selenium in Health and Disease.- 8.1 Selenium and Cancer.- 8.1.1 Skin Cancer.- 8.1.2 Liver Cancer.- 8.1.3 Colon Cancer.- 8.1.4 Breast Cancer.- 8.1.5 Tracheal Cancer.- 8.1.6 Chemotherapeutic Effect of Selenium.- 8.1.7 Epidemiological Relationship.- 8.1.8 Selenium Blood Levels in Cancer Patients.- 8.1.9 Selenium as a Carcinogen.- 8.2 Selenium and Mutagenesis.- 8.2.1 Antimutagenicity.- 8.2.2 Mutagenicity.- 8.3 Selenium and Immunity.- 8.3.1 Effect of Selenium on Humoral Immunity.- 8.3.2 Cell-Mediated Immunity.- 8.3.3 Nonspecific Immune Effects of Selenium.- 8.4 Selenium and Dental Caries.- 8.5 The Anti-Inflammatory Properties of Selenium.- 8.6 Selenium and Heart Disease.- 8.6.1 Animals.- 8.6.2 Humans.- 8.7 Selenium and Aging.- 8.8 Cystic Fibrosis.- 8.9 Multiple Sclerosis.- 8.10 Cataracts.- 8.11 Other Diseases.- 8.12 Radioselenium as a Diagnostic Agent.- 11.11 References.- 9. Synthetic Forms of Selenium and Their Chemotherapeutic Uses.- 9.1 Anti-Infective Agents.- 9.1.1 Antibacterial.- 9.1.2 Antiviral.- 9.2 Antifungal Agents.- 9.3 Antiparasitic Agents.- 9.4 Compounds Affecting the Central Nervous System.- 9.4.1 Hypnotics.- 9.4.2 Analgesics and Local Anesthetics.- 9.4.3 Tranquilizing Drugs.- 9.5 Compounds that Affect the Autonomic Nervous System.- 9.6 Compounds that Affect the Circulatory System.- 9.7 Anti-Inflammatory Compounds.- 9.8 Antihistamines.- 9.9 Anticancer Agents.- 9.10 Antiradiation Agents.- 9.11 Steroids.- 9.12 Selenocoenzyme A.- 9.13 Selenium-Containing Carbohydrates.- 9.14 Seleno-Amino Acids.- 11.11 References.- 10. Analytical Methods of Selenium Determination.- 10.1 Introduction.- 10.2 Sample Preparation and Storage.- 10.3 Destructive Analysis.- 10.3.1 Ashing.- 10.3.2 Closed-System Combustion.- 10.3.3 Wet Digestion.- 10.3.4 Measurement of Selenium.- 10.4 Nondestructive Analysis.- 10.4.1 Neutron Activation Analysis.- 10.4.2 X-Ray Fluorescence Analysis.- 10.4.3 Proton-Induced X-Ray Emission.- References.

/pdf/biochemistry-of-selenium-gu73q1uo0t.pdf

Biochemistry of selenium.

http://science.sciencemag.org/content/sci/84/2176/252.2.full.pdf

L. C. Norris

Papers

The rôle of certain inorganic elements in the cause and prevention of perosis

Studies on the biological value of inorganic phosphates.

Studies on vitamin E in poultry nutrition.

The Role of Manganese and Certain Other Trace Elements in the Prevention of Perosis

The utilization by the chick of phosphorus from different sources.