1.1                                               INTRODUCTION

Infertility is the inability of a person, animal, or plant to reproduce by natural means. It is usually not the natural state of a healthy adults organism, expect notably among certain eusocial species (mostly haplodiploid insects). (Dunson et al., 2012).

Male infertility refers to a male’s inability to cause pregnancy in a fertile female. In humans, it affects approximately 7% of all men (Brugh and Lipshultz, 2014). Male infertility is commonly due to deficiencies in the semen and semen quality is used as a surrogate measure of male fecundity. (Lotti and Maggi, 2014)

Age is a time of life usually defined in years or how long something has existed. (word wed dictionary, 2014). Some research suggests that increased male age is associated with a decline in semen volume, sperm motility and sperm morphology. In studies that controlled for female age, comparisons between men under 30 and men over 50 found relative decreases in pregnancy rates between 23% and 38% .(Kidd et al., 2012). It suggests that sperm count declines with age, with men aged 50-80 years producing sperm at an average rate of 75% compared with men aged 20-50 years. However, an even large difference is seen in how many of the seminiferous tubules in the testes contain mature sperm:

  1. In male’s 20-39years old, 90% of the seminiferous tubules contain mature sperm.
  2. In male 40-69 years old, 50% of the seminiferous tubules contain mature sperm
  3. In males 80 years old and older, 10% of the seminiferous tubules contain mature sperm. (Campagne and Daniel, 2013).

Decline in male fertility is influenced by many factors, including lifestyle, environmental and psychological factors. It has been proposed that foreplay might have a role increasing fertility rates and sperm quality in men (Campagne and Daniel, 2013).

Oxidative stress  on the other hand is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants.

A free radical is an oxygen containing molecule that has one or more unpaired electrons, making it highly reactive with other molecules while antioxidants are molecules present in cells that prevent these reaction by donating an electron to the free radicals without becoming destabilized themselves. An imbalance between oxidants and antioxidants is the underlying basis of oxidative stress (Mandel, 2014)

Oxidative stress (Os) has been identified as one of the many mediators of male infertility by causing sperm dysfunction. It is a state related to increased cellular damage triggered by oxygen and oxygen-derived free radicals known as reactive oxygen species (ROS).During this process, augmented production of ROS overwhelms the body’s antioxidant defenses while small amount of ROS are required for normal sperm functioning, disproportionate levels can negatively impact the quality of spermatozoa and impair their overall fertilizing capacity. Oxidative stress has been identified as an area of great attention because reactive oxygen species and their metabolites can attack DNA, lipids and proteins; alter enzymatic systems; producing irreparable alterations; cause cell death and ultimately, lead to a decline in the semen parameters associated with male infertility.( Benedetti et al., 2012)

Statistics from the United States indicate that oxidative stress is one of the major   causes of male infertility, that’s 30% to 40% infertile men have elevated levels of reactive oxygen species in their semen and plasma Spermatozoa were the first cell type reported to show potential susceptibility of oxidative stress. In some situations, the damage induced by oxidative stress because they lack the necessary cytoplasmic enzyme repair systems. This is one of the factors that make spermatozoa unique in their susceptibility to oxidative insult. This is predominantly due to the fact that their cell membranes are rich in polyunsaturated fatty acids (PUFAs) rendering them highly susceptible to oxygen-induced damage and hence, lipid pre-oxidation (LPO).

Subsequently, a rapid loss of intracellular adenosine triphosphate (ATP) form LPO causes axonemal damage, decreased sperm viability and increased mid-piece sperm viability morphological defects, all of which contribute to decreased sperm motility (Ashbok et al., 2014).

Sex steroids, also known as gonadal steroids are steroid hormones that interact with vertebrate androgen or estrogen receptors (Guerriero, 2009). Their effects are mediated by the slow genomic mechanism through nuclear receptors as well as by fast non-genomic mechanism through membrane-associated receptors and signaling cascades. The term sex hormone is nearly always synonymous with sex steroid. The non-steroid hormones, luteinizing hormone, follicle-stimulating hormone and gonadotropin-realeasing hormone are usually not regarded as sex hormones, although they play major sex-related roles (Thakur et al.,2009)


Natural sex steroids are made by the gonads (Ovaries or testes) by      adrenal glands or by conversion from other sex steroids in other tissue such as Liver or Fat (Catherine, 2011).

In many contexts, the two main classes of sex steroids are androgen and estrogen, of which the most important human derivatives are testosterone and estrodol respectively. Other contexts will include progesterons as a third class of sex steroids, distinct from androgens and estrogens. Progesterone is the most important and only naturally-occuring human progestogen. In general, androgens are considered “male sex hormones”, since they have masculinizing effects, while estrogens and progestogens are considered “female sex hormones” although all types are present in each sex, different levels (El Attar et al.,2003).


To evaluate the effects of Age on some sex steroids, and markers of oxidative stress in some infertile male subjects in Owerri Metropolis.


1) To determine the changes in some sex steroids, Testosterone and FSH in infertile male subjects.

2) To establish the effect of age on the levels of these sex steroids.

3) To determine the status of some markers of oxidative stress namely MDA and vitamin E in some infertile and fertile male subjects in Owerri metropolis

4) To determine the effect of age on changes in markers of oxidative stress in infertile and fertile male subjects.

5) To compare the levels of some sex steroids and markers of oxidative  stress in different age groups in infertile and fertile male subjects.


There is a general believe among our people that women are the causes of 95% infertility in couples. This may be supportive if the research is demonstrated if male subjects sustain fertility till above 60years. (kidd et al., 2012)

It has been recorded by some researchers that men at the age of 60 to 70 were able to produce 50% mature sperm cells. (Campagne and Daniel, 2013).

Some recent studies now have it that 50% of infertility cases are caused by males that are within the reproductive age and this is worse with the people of this part of the world. (Johnson et al., 2003)

This becomes worrisome and tend to ask some questions like;

  • Are males losing their long lasting reproduction capacities which is initially prolonged and why?
  • Is andropause here with our people at earlier age? (Dunson et al., 2012).  Not much has been done in this area of study in this part of the globe though.

This study hence becomes needful and timely to evaluate the levels of mallonde aldehyde (MDA) which is a potent marker of oxidative stress , Follicle Stimulating Hormone(FHS), Vitamin E (antioxidant) and Testosterone(a male reproductive steroid ) in male subjects of different age groups in Owerri Metropolis, to address the increasing number of infertility cases in our society, especially with a great percentage of their female counterparts being reproductively healthy by medical assessments.

With the lack of information regarding this area of research in this part of the world, this work is justified.