Diet and Resistance to Disease PDF
Preview Diet and Resistance to Disease
DIET AND RESISTANCE TO DISEASE ADV ANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY Editorial Board: NATHAN BACK, State University of New York at Buffalo N. R. DI LUZIO, Tulane University School of Medicine EPHRAIM KATCHALSKI-KATZIR, The Weizmann Institute of Science DAVID KRITCHEVSKY, Wistar Institute ABEL LAJTHA, New York State Re.earch Inltitute for Neurochemiltry and Drug Addiction RODOLFO PAOLETTI, University of Milan Recent Volumes in this Series Volume 129 AGING PHENOMENA: Relationships among Different Levels of Organization Edited by Kunio Oota, Takashi Makinodan, Masami lriki, and Lynn S. Baker Volume 130 THE RENIN-ANGIOTENSIN SYSTEM Edited by J. Alan Johnson and Ralph R. Anderson Volume 131 THE CEREBRAL MICROVASCULATURE: Investigation of the Blood-Brain Barrier Edited by Howard M. Eisenberg and Robert L. Suddith Volume 132 ALCOHOL AND ALDEHYDE METABOLIZING SYSTEMS-IV Edited by Ronald G. Thurman Volume 133 SEROTONIN: Current Aspects of Neurochemistry and Function Edited by Bernard Haber, Sabit Gabay, M. R. Issidorides, and S. G. A. Alivisatos Volume 134 HAMSTER IMMUNE RESPONSES IN INFECTIOUS AND ONCOLOGIC DISEASES Edited by J. Wayne Streilein, David A. Hart, Joan Stein-Streilein, William R. Duncan, and Rupert E. Billingham Volume 135 DIET AND RESIST ANCE TO DISEASE Edited by Marshall Phillips and Albert Baetz DIET AND RESISTANCE TO DISEASE Edited by Marshall Phillips and Albert Baetz u.s. Department of Agriculture Science and Education Administration-Agricultural Research National Animal Disease Center Ames, Iowa PLENUM PRESS • NEW YORK AND LONDON Library of Congress Cataloging in Publication Data Symposium on Diet and Resistance to Disease, Houston, Tex., 1980. Diet and resistance to disease. (Advances in experimental medicine and biology; v. 135) "Proceedings of the Symposium on Diet and Resistance to Disease held at the American Chemical Society Agricultural and Food Division meeting, held March 26, 1980 in Houston, Texas." Includes index. 1. Natural immunity-Congresses. 2. Diseases-Causes and theories of causation Congresses. 3. Diet in disease-Congresses. I. Phillips, Marshall. II. Baetz, Albert. III. Title. IV. Series. [DNLM: 1. Allergy and immunology-Congresses. 2. Diet-Con gresses. 3. Nutrition-Congresses. WI AD559 v. 135/QW 504 D565 1980] QRI85.2.S96 1980 613.2 80-29542 ISBN-13: 978-1-4615-9202-0 e-ISBN-13: 978-1-4615-9200-6 DOI: 10.1007/ 978-1-4615-9200-6 Proceedings of the symposium on Diet and Resistance to Disease held at the American Chemical Society Agricultural and Food Division Meeting, held March 26, 1980, in Houston, Texas © 1981 Plenum Press, New York Softcover reprint of the hardcover 1st edition 1981 A Division of Plenum Publishing Corporation 227 West 17th Street, New York, N.Y. 10011 All rights reserved No part of this book may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, microfilming, recording, or otherwise, without written permission from the pttblisher PREFACE Intuitively, we realize that animals that are well fed and well cared for are healthier than animals that are not well fed or well cared for. Although nutritionists have long been concerned with minimum nutrient requirements for maximal growth rate and maintenance, it has been only recently that investiagators have begun to look at the nutritional requirements that provide optimal health. The increasingly sophisticated methods of immunology have allowed investigators to define indicators of resistance to disease such as cell mediated immunity, lymphocyte functions, and macrophage functions. When these immunological tools are combined with the classical methods of nutrition research it is possible to determine how dietary constituents affect each of these cellular immune systems, and to gain an overall understanding of how these systems affect resistance to disease. This symposium was organized to bring together people working on various nutritional problems that have an interrelationship to resistance to disease, so that this rapidly expanding area of nutritional immunology could be reviewed. We felt that the Agricultural and Food Division of the American Chemical Society was an ideal forum to present this material. In relating nutrition and infection, two areas of importan~e must be considered: (1) public health, i.e., the prevention and treatment of human disease and metabolic disorders; and (2) live stock and poultry production. The production of meat, fibre, and animal materials continues to be a more intensive operation in the agricultural system of this country and the world. The number of high density systems or "confinement operations" will continue to increase. With the expansion of these operations, new and more severe problems of disease control have appeared. The nutritionists that develop diets for these confinement operations are responsible not only for providing the basic nutrient requirements, but are also called upon to optimize the health of the animals through diet to reduce the impact of infection and other stresses. We hope the information presented here will be a step in that direction. v PREFACE The Agricultural and Food Division wish to thank the u.s. Department of Agriculture, Science and Education Administration, National Animal Disease Center; Hoffmann-LaRoche Incorporated; and Syntex Corporation for financial assistance in arranging this symposium, and Plenum Publishing Corporation for publishing this compendium of the presentation. Marshall Phillips Albert Baetz National Animal Disease Center Ames, Iowa 50010 CONTENTS Ascorbic Acid and the Immune Response......................... 1 B. Leibovitz and B. V. Siegel Vitamin E, Immunity and Disease Resistance ••.••••..•••.•••.•. 27 R. P. Tengerdy, M. M. Mathias, and C. F. Nockels Anti-Inflammatory, Immunologic and Carcinostatic Attributes of Selenium in Experimental Animals ..•••••... 43 J. E. Spallholz Effects of Dietary Folate, Vitamin Bl2 and Methionine/Choline Deficiency on Immune Function ....•... 63 K. M. Nauss and P. M. Newberne Role of the B Vitamins in the Immune Response .•••..•.•..•.•... 93 A. E. Axelrod Effect of Dietary Zinc Deficiency on Lymphocyte Function in the Mouse •.•.•..•...•..•.•.•..••••.•.•...... 107 P. J. Fraker and R. W. Leucke The Role of Copper in Metabolic Disorders ••.••.•••••••.•••...• 121 G. W. Evans Antimicrobial Properties of Iron Binding Proteins ••••..•.....• 139 A. Bezkorovainy A Possible Role of Iron Deficiency in Gastric Cancer in Colombia .••. , •....•.••••...•••••••••.•....•... 155 S. A. Broitman, H. Velez, and J. J. Vitale Host Defense Mechanisms in Protein Energy Malnutrition •••••... 183 G, T. Keusch Lis t of Contributors.......................................... 211 Subject Index •••••••••.••..••...•..•.••...•.•••.••....•..•..• , 213 vii ASCORBIC ACID AND THE IMMUNE RESPONSE Brian Leibovitz and Benjamin V. Siegel Department of Pathology University of Oregon Health Sciences Center Portland, Oregon 97201 INTRODUCTION Since the introduction of ascorbic acid as an antiviral and antibacterial agent (Klenner, 1951; McCormick, 1952; Klenner, 1974) interest has focused on the possible immunologic mechanisms involved in its protective effect. The role of ascorbic acid in the immune response is reviewed here with regard to cellular and humoral functions, and experiments pertaining to the role of ascorbic acid in autoimmunity and anaphylaxis are discussed. The structure of ascorbic acid is shown in Figure 1. The reduced form (ascorbic acid) is a hexose sugar with an ene-diol moiety; loss of one electron results in oxidation to the ascorbate free radical, while loss of two electrons results in the formation of dehydroascorbic acid. In both processes, the released electrons may be utilized to quench various free radicals. Thus, during the oxidation of ascorbic acid to dehydroascorbic acid, two molecules of free radicals may be quenched, which underscores the importance of ascorbic acid with regard to its antioxidant properties. In fact, ascorbic acid is only slightly less effective in quenching superoxide anion radical than is the enzyme superoxide dismutase, when considered at physiological concentrations (Leibovitz and Siegel, 1980). Further, both the ascorbate free radical and dehydroascorbic acid may be reduced to ascorbic acid by the enzymes NADH:semidehydroascorbate reductase and dehydroascorbate reductase, respectively (Figure 1), which provides an effective recycling mechanism. We have recently reviewed the role of ascorbic acid as a free radical quencher in biological systems (Leibovitz and Siegel, 1980). B. LEIBOVITZ AND B. V. SIEGEL 2 H~ H L' ~ LH > H-OH ascorbic H20H ~ acid NADH: semI y roascorbate ascorbate free reductase radical GSSG L L· dehydro 2GSH ascorbate reductase LH oAH-DH ~H20H dehydroascorbic acid FIGURE 1. Structure of Ascorbic Acid and Its Oxidation Products. ASCORBIC ACID AND T-LYMPHOCYTE FUNCTION The activity of T-lymphocytes is well known to be affected by ascorbic acid. Mueller et al. (1962) noted that vitamin C depriva tion afforded protection against the induction of experimental allergic encephalomyelitis, a T-cell-mediated disease. Moreover, the degree of protection was directly proportional to the duration of vitamin C deficiency. In the scorbutic guinea pig a marked suppression of the tuberculin reaction has also been observed (Mueller and Kies, 1962; Zweiman et al., 1966). Interestingly, the anergy of the scorbutic guinea pig to tuberculin reactions may be at the efferent level: passive transfer of peritoneal exudate cells from scorbutic guinea pigs was noted to transfer tuberculin sensitivity to normal recipients, while transfer of cells from tuberculin-sensitive donors to scorbutic guinea pigs did not induce tuberculin sensitivity (Zweiman et al., 1966). These results may indicate anergy to tuberculin reactions at the level of the inflammatory response, as is discussed in detail below. ASCORBIC ACID AND THE IMMUNE RESPONSE 3 We have examined the effect of supplementary ascorbic acid on mitogen-induced T-1ymphocyte blast transformation in the mouse, and have noted a significant enhancement in Con A-induced blast trans formation of splenic lymphoid cells in BALB/c mice given high doses of dietary ascorbic acid (250 mg% in the drinking water) (Siegel and Morton, 1977). Mice, unlike humans and guinea pigs, produce their own ascorbic acid, and our results described above therefore indicate a pharmacological effect rather than a physiological effect of ascorbic acid. These results have been confirmed in various laboratories. Thurman and Goldstein (1979) have reported a marked depression in T-1ymphocyte blast transforamtion in guinea pigs given a scorbutic diet, while Yonemoto et a1. (1976) observed a significant enhancement in PHA-induced T-1ymphocyte blast trans formation in humans given 5 g ascorbic acid per day for 3 days. More recently, Anderson et a1. (1980) have reported a significant enhancement of PHA- and Con A-induced blast transformation in lymphocytes from humans given 1-3 g of ascorbic acid per day. In vitro, however, ascorbic acid has been noted to cause a dose-dependent inhibition of PHA-induced blast transformation in human lymphocytes (Ramirez et a1., 1979), suggesting an in vitro cytotoxic effect of ascorbic acid. Vitamin C deficiency~a~o been noted to diminish other T-1ymphocyte-mediated activities, including allograft survival (Ka1den and Guthy, 1972) and cell-mediated cytotoxicity (Anthony et a1., 1979). ASCORBIC ACID AND ANTIBODY PRODUCTION Ascorbic acid may playa role in antibody production; however, conflicting reports make analysis of this phenomenon difficult. With regard to the plaque-forming cell (PFC) capacity of the spleen, we have observed that supplementary ascorbic acid (250 mg% in the drinking water) did not affect the PFC response to LPS and sheep erythrocytes (SRBC) in BALB/c mice (Siegel and Morton, 1977). Thurman and Goldstein (1979), however, have noted a diminished PFC response to SRBC in scorbutic guinea pigs, an effect which could be reversed by vitamin C supplementation. Long (1950) observed that the primary antibody response of guinea pigs to alum-precipi tated diphtheria toxoid was unaffected by vitamin C deficiency; however, secondary responses were reduced in the deficient animals. Kumar and Axelrod (1969) have repeated the study by Long, and have reported no detrimental effect of severe vitamin C deficiency on either primary or secondary antibody responses to diphtheria toxoid. More recently, Anthony et ale (1979), using guinea pigs immunized with chicken erythrocytes, observed no difference in antibody titers among vitamin C-deficient, pair-fed, or ad libitum-fed controls. In contrast, supplementation of normal humans with 1 g/day ascorbic acid has been noted to increase serum levels on non-specific IgG and IgM (Prinz et al., 1977; Vallance, 1977).
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