Male fertility and lipid metabolism

273 Pages·2003·9.363 MB·English

by  Stephanie R De Vriese, Armand B Christophe

Male Fertility
and Lipid Metabolism
Editors
Stephanie R. De Vriese
Scientific Institute of Public Health
Brussels, Belgium
Armand B. Christophe
Ghent University Hospital
Ghent, Belgium
Champaign, Illinois
Copyright ©2003 by AOCS Press
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To be the global forum for professionals interested in lipids and related materials through
the exchange of ideas, information, science, and technology..
AOCS Books and Special Publications Committee
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R. Adlof, USDA, ARS, NCAUR, Peoria, Illinois
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T. Foglia, USDA, ARS, ERRC, Wyndmoor, Pennsylvania
L. Johnson, Iowa State University, Ames, Iowa
H. Knapp, Deaconess Billings Clinic, Billings, Montana
M. Mossoba, U.S. Food and Drug Administration, Washington, D.C.
A. Sinclair, RMITUniversity, Melbourne, Victoria, Australia
P. White, Iowa State University, Ames, Iowa
R. Wilson, USDA, REE, ARS, NPS, CPPVS, Beltsville, Maryland
Copyright ©2003 by AOCS Press. All rights reserved. No part of this book may be repro-
duced or transmitted in any form or by any means without written permission of the pub-
lisher.
The paper used in this book is acid-free and falls within the guidelines established to ensure
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Library of Congress Cataloging-in-Publication Data
Male fertility and lipid metabolism / editors, Stephanie R. De Vriese,
Armand B. Christophe.
p. cm.
ISBN 1-893997-39-1
1. Spermatozoa. 2. Fertility. 3. Unsaturated fatty
acids—Metabolism. 4. Lipids—Metabolism. I. Vriese, Stephanie R. De.
II. Christophe, Armand B.
QP255.M2123 2003
612.6'1--dc21
2003006193
Printed in the United States of America with vegetable oil-based inks.
5 4 3 2 1
Copyright ©2003 by AOCS Press
Preface
The interest in lipid metabolism and, more specifically, in polyunsaturated fatty acids
in relation to sperm production has increased during the last decade. The motivation for
the research described in this book originates from the discovery that sperm lipids con-
tain extremely high proportions of long-chain polyunsaturated fatty acids, thus estab-
lishing a link between lipid biochemistry and male fertility. Moreover, the fact that
polyunsaturated fatty acids must, in some form, be supplied in the diet suggests a rela-
tionship between fertility and nutrition and raises the possibility of improving male fer-
tility by dietary means.
Reactive oxygen species play a pivotal role in male fertility. Increased generation
of reactive oxygen species has been documented in subfertile men with varicocele,
immunological infertility, and idiopathic oligozoospermia. Excessive reactive oxygen
species can cause oxidative damage to the sperm DNAand the sperm membrane. The
long-chain polyunsaturated fatty acids in the sperm membrane are highly susceptible to
peroxidation. However, the high content of these long-chain polyunsaturated fatty acids
is necessary for the optimal membrane fluidity required for the acrosome reaction and
membrane fusion. Furthermore, sperm motility plays an important role in male fertili-
ty, as spermatozoa with decreased motility have reduced fertilizing capacity. It has been
suggested that the fluidity of the membranes of the spermatozoa, which among others
depends on the fatty acid composition of the phospholipids in the membrane, is relat-
ed to sperm motility.
These new insights have contributed to the development of supplementation ther-
apies with fatty acid mixtures and antioxidants.
This book intends to give the reader an up-to-date view of several aspects of male
fertility in relation to lipid and fatty acid metabolism.
An overview of the different factors related to male fertility is given in chapter 1.
Chapter 2 discusses the synthesis of long-chain polyunsaturated fatty acids by Sertoli
cells in the testis. Chapters 3 to 5 deal with the phospholipid and fatty acid composition
of human testicular cells and human sperm. The effect of supplementation of docosa-
hexaenoic acid on male fertility is also described. Chapter 6 discusses the manipulation
of the lipid composition of boar spermatozoa and its effect on reproductive efficiency
in pigs. Chapters 7 and 8 address the lipid and fatty acid composition of avian semen.
The regulation of mammalian and avian sperm production by dietary fatty acids is sum-
marized in chapter 9. The role of sterols in the epididymis is discussed in chapter 10,
whereas the physiological and biophysical properties of sulfogalactosylglycerolipid in
male germ cells are handled in chapter 11. Chapter 12 discusses the regulation of oxy-
tocinase activity in the testis by dietary lipids. Finally, chapters 13 to 16 deal with
oxidative stress and oxidative damage of polyunsaturated fatty acids in spermatozoa
and antioxidant protection of sperm.
Copyright ©2003 by AOCS Press
The book should be useful for: researchers in the domain of male fertility, fatty
acid metabolism, and antioxidants; medical personnel involved in the treatment of male
infertility; fat technologists; students in nutrition, dietetics, biochemistry, pharmacy,
and medicine; and everybody interested in the field.
Finally, we would like to express our thanks to all of the authors for their valuable
discussions, suggestions, and contributions. The assistance provided by the AOCS
Press staff in Champaign is gratefully acknowledged.
February 2003
Stephanie R. De Vriese
Armand B. Christophe
Editors
Copyright ©2003 by AOCS Press
Contents
Chapter 1 Factors Affecting Male Fertility
F. Comhaire, A. Mahmoud, A. Zalata, and W. Dhooge
Chapter 2 Metabolism of Long-Chain Polyunsaturated Fatty Acids
in TesticularCells
Thien N. Tran, Kjetil Retterstøl, and Bjørn O. Christophersen
Chapter 3 Fatty Acid Remodeling during Sperm Maturation: Variation
of Docosahexaenoic Acid Content
Mario Ollero and Juan G. Alvarez
Chapter 4 Docosahexaenoic Acid Supplementation and Male Fertility
Julie A. Conquer and Francis Tekpetey
Chapter 5 Phospholipid Composition of Human Sperm and Seminal Plasma
in Relation to Sperm Fertility
N.M. Gulaya
Chapter 6 Docosahexaenoic Acid-Rich Marine Oils and Improved
Reproductive Efficiency in Pigs
A. Maldjian, P.C. Penny, and R.C. Noble
Chapter 7 Specificity of Fatty Acids in Domestic Bird Spermatozoa
E. Blesbois and D. Hermier
Chapter 8 Lipid Composition of Chicken Semen and Fertility
SilviaCerolini
Chapter 9 Regulation of Avian and Mammalian Sperm Production
by Dietary Fatty Acids
Brian K. Speake, Peter F. Surai, and John A. Rooke
Chapter 10 Neutral Sterols in the Epididymis: High Concentrations
of Dehydrocholesterols
G. Haidl, B. Lindenthal, and K. von Bergmann
Chapter 11 Physiological and Biophysical Properties of Male Germ
Cell Sulfogalactosylglycerolipid
Nongnuj Tanphaichitr, Maroun Bou Khalil, Wattana
Weerachatyanukul, Morris Kates, Hongbin Xu, Euridice
Carmona, Mayssa Attar, and Danielle Carrier
Copyright ©2003 by AOCS Press
Chapter 12 Regulation of Oxytocinase Activity in the Testis by Dietary Lipids
M.J. Ramírez-Expósito, M.J. García-López, M.D. Mayas,
M.P. Carrera, and J.M. Martínez-Martos
Chapter 13 Significance of Oxidative Stress and Sperm Chromatin Damage
in Male Infertility
Ashok Agarwal
Chapter 14 ScavengerSystems and Related Therapies Against
Lipoperoxidation Damage of Polyunsaturated Fatty Acids
in Spermatozoa
Andrea Lenzia, Loredana Gandini, Federica Tramer,
Vittoria Maresca, Francesco Lombardo, Gabriella Sandri,
Mauro Picardo, Enrico Panfili
Chapter 15 Comparative Aspects of Lipid Peroxidation and Antioxidant
Protection in Avian Semen
Peter F. Surai, Brian K. Speake, and Nick H.C. Sparks
Chapter 16 The Effect of Antioxidants on Nicotine and Caffeine Induced
Changes in Human Sperm—An in VitroStudy
Mehran Arabi, Sankar Nath Sanyal, Usha Kanwar,
Ravinder Jit Kaur Anand
Copyright ©2003 by AOCS Press
Chapter 1
Factors Affecting Male Fertility
F. Comhairea, A. Mahmouda, A. Zalatab, and W. Dhoogea
aGhent University Hospital, Department of Internal Medicine, Center for Medical and Urological
Andrology, 6K12 IE, De Pintelaan 185, B-9000, Ghent, Belgium
bBiochemistry Department, Faculty of Medicine, Mansoura University, Egypt
Abstract
Male infertility is a multifactorial disease resulting from the interaction between
genetic, lifestyle, and environmental factors and urogenital pathologies. In particular,
endogenous and exogenous estrogenic substances and oxidative overload have been
implicated in synergistic damage to male fertility. The deleterious effects are mediat-
ed through changes in the phospholipid composition of the sperm membrane, oxida-
tive changes to DNA, and the suppression of the neuroendocrine regulation of sper-
matogenesis. The treatment of specific pathologies, e.g.,varicocele or accessory gland
infection, even though it has significantly increased the effective rate of conception
resulting in live birth of healthy children, has limited effectiveness. Complementary
treatment with a pure antiestrogen and with antioxidants appears to enhance the rever-
sal of pathogenic processes, resulting in improvement of the fertility status of infertile
men.
Introduction
Spermatogenesis takes place in the seminiferous tubules of the testes. Male fertility
requires adequate testicular stimulation (Fig. 1.1) and optimal function of the accesso-
ry sex glands. In developed countries, between 8 and 10% of all men are infertile and
unable to attain conception in their partner within a time period of 12 months (1). The
mechanisms through which impairment of male fertility occur are progressively being
unravelled, and an efficient approach to the standardized investigation and diagnosis,
as well as the clinical management, of the infertile male has been developed (1).
Regulation of Spermatogenesis
Pulsatile secretion of luteinizing hormone releasing hormone (LHRH) by the hypo-
thalamus induces pulsatile release of luteinizing hormone (LH) by the pituitary, which
causes pulsatile secretion of testosterone by the cells of Leydig in the interstitial space
of the testes. Testosterone is released into the interstitial fluid surrounding the semi-
niferous tubules, which are themselves exposed to extremely high concentrations of
Copyright ©2003 by AOCS Press
Fig. 1.1.Hormonal regulation of spermatogenesis.
this steroid (2). It is not known whether constant exposure of the seminiferous tubules
to a high testosterone concentration has the same effect as pulsatile exposure, which
may pace the tightly timed sequence of spermatogenesis. On the other hand, stimula-
tion of the intratubular nutritive cells of Sertoli by follicle stimulating hormone (FSH)
is required for optimal spermatogenesis, though some degree of sperm production can
be maintained by the effect of testosterone alone (3).
The stimulatory system is controlled by neurotransmitters affecting the LHRH
pulse generator and by feedback regulation (Fig. 1.1). The hypothalamo-pituitary unit
is inhibited by testosterone that is aromatized to estradiol by the neuroendocrine cells
of the hypothalamus and to 5-alfa-dihydrotestosterone in the pituitary. FSH secretion
by the pituitary is under the feedback control of Inhibin B, a secretory product of the
cells of Sertoli (4). There is some evidence that Inhibin B also exerts a direct inhibito-
ry effect on spermatogenesis (5,6).
Male Infertility: A Multifactorial Disease
Four groups of factors act in synergy to reduce male fertility (Fig. 1.2). Genetic causes
include, among others, translocations of autosomal chromosomes, numeric and struc-
tural abnormalities of the sex chromosomes (such as Klinefelter’s syndrome), muta-
tions of the cystic fibrosis gene, and microdeletions of the long arm of the Y chromo-
Copyright ©2003 by AOCS Press
Fig. 1.2.Sub/infertility: A multifactorial disease.
some (Yq11.23). Life style factors include the excessive use of tobacco, alcohol, or
recreational drugs; certain nutritional habits and obesity; regular exposure to high tem-
peratures, such as during hot baths; tight clothing; and perhaps stress. There is strong
evidence that exposure to professional and environmental toxic agents exerts major
deleterious influence on sperm quality. In particular, substances with a hormone dis-
rupting effect have been blamed because of their pseudo-estrogenic and/or antiandro-
genic effects (7). Hormone disrupters include pesticides such as DDT and DDE,
alkyl-phenols, polychlorinated biphenyls, dioxines, and also pharmaceutical products
such as ethinylestradiol and, possibly, testosterone itself. The fourth group of factors
refers to the more specific andrological diseases of the urogenital tract including
varicocele, male accessory gland infection, immunological causes from anti-sperm-
antibodies, and hormonal diseases such as hypogonadotropic hypogonadism. It has
become increasingly evident that factors in different groups act in synergy. For
instance, men with varicocele that do not smoke have a better sperm quality than
those who smoke (8), and the number of white blood cells required to cause deteriora-
tion of sperm quality and production is lower in cases with than without coincidental
genital pathology (Fig. 1.3a and b, A.M. Mahmoud et al., unpublished data). The
presence of certain gene mutations in men with varicocele might render them more
susceptible to sperm DNA oxidative damage (9). Also, patients with varicocele are
more susceptible to the known toxic effects of cadmium on spermatogenesis due to
selective accumulation of this element in their testes (10).
Mechanisms of Sperm Deterioration
Whereas some infertile men present a single causal factor amendable to treatment
(e.g., hypogonadotropic hypogonadism), many others present a combination of fac-
Copyright ©2003 by AOCS Press
Fig. 1.3. A. Sperm production index: Total number of spermatozoa in the ejaculate (in
million) divided by the total testicular volume in mL, normal value > 4.9 million/mL
testis. B. White blood cells (WBC) (Receiver Operating Characteristic (ROC) curve) dif-
ferentiate between varicocele patients with abnormal (n= 75) or normal (n= 10) sperm
production index. Criterion = criterion value; AURC = area under ROC curve
tors. In the latter cases common mechanisms may be involved in disrupting spermato-
genesis. We suggest that reactive oxygen species and hormonal imbalance are instru-
mental in this process (Fig. 1.4). Hormonal imbalance results from increased exposure
of both the testes and the hypothalamo-pituitary unit to endogenous and/or exogenous
estrogens. These decrease the mass of LHRH secreted during the pulses, reducing the
secretion of LH and of testosterone. Also, the physiological increase of FSH fails to
occur in response to low sperm concentration (oligozoospermia). In fact, estrogens
have been documented to increase the Inhibin B secretion by cells of Sertoli cultured
Copyright ©2003 by AOCS Press