Running head: MALE REPRODUCTIVE SYSTEM AND FERTILIZATION 1

Male Reproductive System and Fertilization

(Author’s name)

(Institutional Affiliation)
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Introduction

The male reproductive system consists of both internal and external organs, in which the

testes in the scrotum produce the male gamete ejaculates seminal fluid by the help of the penis to

donate sperm for fertilization of the female ovum. Fertilization occurs with the insertion of the

penis via the vulva and into the vagina as the seminal fluid rich in sperms ejaculates towards the

cervix. The sperm that succeeds in getting through the cervix at that moment has the chance to

inseminate an ovum. In some cases, fertilization does not occur because of a dysfunctional

reproductive system in either male or female. Infertility affects approximately 8 million couples

in the United States of America with the main part associated with the male “factor.” It affects

around 15% of couples, while genetic abnormalities make up 15% to 30% of male factor

infertility (Bellenir, 2006). Genetics instigates infertility by manipulating a range of

physiological processes such as sperm quality, hormonal homeostasis and spermatogenesis. For

that reason, an understanding of the chromosomal basis of generative failure is essential to

manage an infertile couple. Well-thought-out as one of the most confusing conditions in

reproductive health, male factor infertility is widespread, and its occurrence rises while its

etiology remains elusive.

This paper discusses male factor infertility and its genetic causes today as it explains the

requirement for an improved understanding of the ailment, to illustrate a broad outline of these

genetic components, and to evaluate the techniques utilized to come up with new perceptions in

fertility research. The background of this research acknowledges the complexity of male factor

infertility, as it affects a huge sector of the population; and yet, several etiologies of its kind are

still unknown. By expounding on the causal genetic source of infertile phenotypes, it may

perhaps be possible to find out the causes of infertility and conclude effective cures for patients.
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Immunologic Infertility

Immunogenic infertility, sometimes also referred to autoimmune infertility is an

inappropriate cellular or humoral bodily immune response against sperm antigens that creates the

basis of sperm functional dysfunction. This process eventually results into male infertility. In

general, immunologic infertility accounts for approximately 4.5% of the overall male fertility

problem. However, in a deeper perspective, this approximation may increase to almost 40%

among men with Unexplained Male Infertility (UMI), (Bellenir, 2006). The Testis is an

immunologically restricted site to safeguard the freshly evolving haploid spermatozoa after

immune recognition. The integrity of the blood-testis barrier helps in the achievement of this

protection by. In addition, the epithelial barriers integrity amplified by confined cellular

immunosuppressive barriers structure the segregation of the sperm in the supplementary areas of

the male genital tract. Remarkably, there are three hypothesized theories that elucidate the

foundation of loss of immune lenience to the sperm as well as the developing of immune

responses against sperm as alien cells. The first theory postulates that newly mounting haploid

sperm partake diverse chromosomal composition from somatic cells. The second theory asserts

that sperms are absent in the course of the embryonic life when immune tolerance transpires to

self-antigens. However, the third theory, referred to as the immunosuppressive theory,

hypothesizes that T-suppressor lymphocytes, which are in charge of prevention of the immune

response against sperm, may possibly be down regulated by constant leakage of antigens from

spermatozoa originating from the genital area. The two arms responsible for immune reaction:

humoral and cellular, may perhaps feature in the etiology of UMI (Carrell, 2007).
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Humoral Immune Infertility

Humoral Immune Infertility depend on antisperm antibodies (ASA) to execute this function. By

directing these antibodies to a number of sperm antigens followed by its implication, sperm

dysfunction takes place. Approximately 10% of men with infertility have ASA as opposed to 2%

of ordinary fertile men. On the other hand, Carrell (2007) observed that the occurrence of ASA is

considerably greater (42.5%) among patients with unsolved and insistent infertility. The

interruption of epithelial barriers or blood-testis barrier is a genital tract insults or an

immunosuppression defect, which represent the crucial mechanisms accountable for leakage of

sperm antigens and development of ASA. Conversely, it is still unidentified whether the

formation of ASA takes place within the genital tract or simply transuded from the serum.

Explicitly, there are three locations in the serum, in which ASA exist: seminal plasma, serum and

sperm-bound. Sperm-bound are the most clinically appropriate among all of the above.

Furthermore, the immunoglobulin (Ig) sections of ASA, specifically IgG (both locally formed

and transuded from serum), as well as IgA, (always known as only locally formed) are the most

frequently involved in the pathogenesis of humoral immune infertility. To make this explanation

further confusing, infertile women, approximately 7% to 17%, can also form antisperm

antibodies in their cervical fluids (Sabanegh, 2011).

ASA inhibit a number of sperm functions, for example the premature introduction of

acrosome and apoptosis reaction. ASA may also hamper fertilization occurrence by interfering

with cervical mucus diffusion, spermatocyte fusion and zona pellucida binding. In addition, ASA

may modify some functions of macromolecules and sub-cells by changing protein folding,

chaperon function, as well as disulphide bonds. The result is that pregnancy rates significantly

reduces due to the involvement of ASA.

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Cellular Immune Infertility

Indication of cellular immune infertility arises from diversity of human and animal

research on rotation, which had the ability to identify the swelling of cell infiltrate in the

contralateral testis. This only takes place in the face of nonexistence of ASA. In addition, cell

facilitated immunoreactivity has been identified in 50% of victims with unilateral as well as 80%

with bilateral surgically fixed cryptorchidism (Bellenir, 2006). In the interim, sperm that are

exposed to cytokines, for example tumor necrosis factor (TNF) as well as interferon gamma

display damage in motility and lack of ability to infiltrate hamster eggs. In spite of these signs,

the fully developed variety of cellular immune infertility makes it difficult to validate in the

laboratories and the function of this category of immunogenic infertility found in UMI patients is

still hypothetical. Finally, more urbane investigations need thorough illustrations to identify the

impression of cellular immunity in males with unsolved infertility.

Conclusion

With the emphasis on men with mysterious infertility problems as well as normal semen

examinations, the subsequent likelihoods needs consideration:

 sperm dysfunction

 the existence of antisperm antibodies (autoimmune infertility)

 erectile dysfunction

 unfitting coital habits

 existence of a female factor

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By eliminating the last three conditions, the rest need thorough analysis of history in addition

to a comprehensive gynecological assessment while the contemporary andrology may perhaps

assist in handling the first two conditions.

Generally, as the above information dictates, normal semen assessments do not warrant

fertility outcomes. The extrapolative significance of normal semen testing in expectation of

natural pregnancy is merely 60% (Sabanegh, 2011). Presently, there is scarce proof that can be

derived from outdated semen examination for the occurrence of ASA. Respectively, preeminent

titers of ASA are sometimes found even in the aspect of normal semen parameters. The only

viable and highly predictive phenomenon is sperm agglutination, since the experiment that can

be seen in the analysis of semen and especially in circumstances of elevated ASA titers, (Carrell,

2007). Even though much work still needs completion to define the contribution of genes in the

creation of infertile phenotypes, existing research outcomes recommend that accurate diffusion

of genetic and epigenetic materials is vital for fertility. Through the struggles to relate genetic

mutations to definite infertile phenotypes and the practice of global analytical methodologies

such as metabolomics, researchers may be able to define the collaborations of genetics, environs,

and ethnic upbringing on fertility.

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References

Bellenir, K. (2006). Prostate and urological disorders sourcebook. Detroit, MI: Omnigraphics.

Carrell, D. (2007). The genetics of male infertility. Totowa, N.J.: Humana Press.

Sabanegh, E. (2011). Male infertility. Totowa, N.J.: Humana.