Diet and Resistance to Disease

221 Pages·1981·22.4 MB·English

by  Marshall Phillips, Albert Baetz

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
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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).
M. Phillips et al. (eds.), Diet and Resistance to Disease
© Plenum Press, New York 1981
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).