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Introduction
The male reproductive system is composed of the penis, scrotum and the testicles which make the external structure of the system . The main function of the male reproductive system is to synthesize, maintain and transfer reproductive cells known as the sperm within the semen fluid to the female equivalent (Crowley, 2009). The system is also the main site for secretion of the male sex hormones. The penis is the organ of copulation. The urethra located inside the penis is tubular in structure and serves as the conduit for transport of urine and seminal fluid. The penis is used for penetration during copulation. Semen is ejaculated during organism through the urethra while urine is blocked. The scrotum contains the testes, nerves and blood vessels (Crowley, 2009). The scrotum protects and maintains the right environment for testicles at a temperature conducive for sperm development. This is achieved through special muscles lining the scrotum wall that facilitate its contraction and relaxation for homeostatic regulation of the testicular temperatures.
Structure and function of reproductive male system
The scrotum contains two testicles connected with the spermatic cord. The sperm cells synthesized in the testes are transported and stored by the epididymis until they are mature. Mature sperms from the epididymis are therefore released from the epididymis during sexual intercourse through muscular contractions. The vas deferens is connected to the epididymis and serves as the passage for mature sperms into the urethra in readiness for ejaculation (Hall, 1998). The urethra runs through the prostate gland which also adds more fluid that nourishes the sperm during ejaculation.
The source of energy for sperm motility is obtained from fructose synthesized by the seminal vesicles which propels the spermatozoa. The male reproductive system is under hormonal regulation. Testosterone and follicle-stimulating hormone are the principle hormones that regulate the functioning of the male reproductive system (Kowalski & Rosdahl, 2007). Follicle stimulating hormone regulates the process of spermatogenesis I combined action of FSH and LH secreted from the anterior pituitary gland. Testosterone is responsible for development male characteristics such sexual vitality, muscular strength and beards.
Testicular function
The testes are both gonads and endocrine glands with respective functions of sperm synthesis and hormone secretion. Sperm-forming and endocrine functions of the testicle are regulated by luteinizing hormone and follicle-stimulating hormones from the pituitary gland. The main hormone produced by the testes is the testosterone. Testes function properly at temperatures which are quite lower than the body temperature. This is the reason why they hang outside the body. Optimum temperature is required in order for spermatogenesis to take place efficiently. The concentration of serum testosterone gradually decreases as men age, a condition known as adropause (Patton & Thibodaux, 2008). The decline in testosterone levels does not lead to serious clinical complications in men unlike the situation witnessed in decrease of estrogen in women.
Aging-related sperm characteristics
Aging is a complex process characterized by progressive and predictable deterioration in coordination of biological tissues and the cellular network. The loss of biological functioning of cells and tissues renders an aging organism incapacitated from not only reproduction but also survival. As a result of aging, males experience reduced numbers of viable spermatozoa whose motility is drastically decreased. Normal men, however, continue to produce viable sperms even in old age and could fertilize the female egg successfully.
Aging also causes rapid reduction of the amount of the seminal fluid whose force of ejaculation also deteriorates. The testes reduce in size and become less firm which results in subsequent decline in testosterone levels in aging males. The firmness of the penis during erection becomes diminished and often requires direct stimulation to remain rigid during copulation. Old men therefore take long to achieve an erection unlike their youthful counterparts. Old men may therefore find it difficult to ejaculate or achieve an orgasm altogether (Harrass, Black& Henshel, 1999). In case of ejaculation, restoring erection even through stimulation becomes complicated. The prostate gland becomes enlarged squeezing the urethra and the flow of urine gets inhibited.
Healthy vs. prostate disease aging related spermatozoa
Prostate enlargement is a common phenomenon with aging in males. The prostate is the sex gland in male reproductive system. In healthy men, the prostate secrets and stores an alkaline fluid which constitutes a proportion of the semen and the spermatozoa that neutralizes the acidic environment of the vaginal tract in order to protect the integrity of the sperm (McElreavey, 2000). The genetic material of spermatozoa which becomes ejaculated together with the prostatic fluid is therefore secured from the hostile acidic environment of the vaginal tract during ejaculation. The prostatic fluid allows for greater motility of the spermatozoa during ejaculation as compared to the seminal vesicular fluid. Smooth muscles in healthy prostate, contract to release semen while they regulate the flow of urine during copulation.
During normal growth and development in healthy males, the prostate doubles in size at puberty and continues to enlarge without causing problems until in old age. Benign prostatic Hyperplasia refers to prostate enlargement among old men which is not accompanied with the expansion of the outer layer (Bentley, 2008). The enlarged prostate therefore presses on the urethra thickening the wall of the urinary bladder. The bladder thickens and it irritates during contraction causing frequent urination. The bladder is progressively weakened reducing its capacity to empty all the urine resulting in accumulation of some urine in the bladder even after urination. The prostate gland is also a male sex gland that should ensure that urine is removed from the urethra being a common passage for both urine and spermatozoa.
Production of spermatozoa in men is a continuous process usually accompanied with small secretions of estrogen. Aging results in decreased secretion of the spermatozoa in men while the blood levels for estrogen remain normal. High levels of estrogen results facilitate increased cell growth (Moon & Mommsen, 2005). The abnormal cell growth is also associated with increased production of dihydrotestosterone, a derivative of testosterone which regulates its production. Reduced testosterone levels leave high amounts of dihydrotestosterone in the blood which stimulates uncontrolled cell growth.
BPH is therefore caused by incomplete emptying of the urinary bladder resulting in urine retention in the bladder for a prolonged period. The problem becomes severe in old age as men either experience frequent urination or unable to empty their bladder at all. Sexual intercourse is also hindered since the urethra is blocked by urine. Seminal fluid and spermatozoa are obstructed from swimming through the urethra as expected. Prostatic fluid which is responsible for neutralizing the acidic media during copulation is no longer significant to sustain the integrity of the spermatozoa within the urethra let alone the vaginal tract (Christen, Epelbaum & Chanson, 2004).
Impaired spermatogenesis and reduction of sertoli cells
Spermatogenesis and leydig cell functioning is turned down during the aging process. The number of sertoli cells and the proportion of spermatids per each sertoli cell decreases with age. Aged testes also decline in number as the sertoli cells resulting in pronounced decrease in production of primary spermatocytes in each of the sertoli cells. Aging is thought to enhance the rate of apoptosis of germ cells resulting in a rapid decline of spermatogenesis. Increased apoptosis is directly related to a higher spermatogenic arrest in aged testes than in normal males suffering from dysfunctional testes. Aged testes are therefore significantly prone to apoptotic spermatogenesis due to impaired regulation of cell death mechanisms (Crowley, 2009). The condition of aged testes is therefore characterized by abnormal apoptosis of germ cells and spermatogonia resulting in arrested production of sperms and hormones of the male reproductive system.
Spermatogenesis is normally reduced as the aging process takes course. The decline in production of spermatogonia is further weakened by the rapid increase in apoptotic cell death of the germ cells. In essence, the few sperm cells that are synthesized in aged testes are destroyed. Male infertility is therefore imminent in old age since the decline in production of sperm cells is amplified by several other biological mechanisms associated with aging. Reduction of sertoli cells is also a product of apoptosis. Apoptosis results in the immediate phagocytosis of synthesized spermatids during aging in a process that inhibits the maturation of spermatogonia (Hall, 1998).
Aging and tunica propria of seminiferous tubules
Aging causes thickening of the tunica propria. Atrophy of the seminiferous tubules also takes place while some which remain normal exhibit active spermatogenesis. Leydig cells increase in number and may even accumulate into huge clusters. Inter-tubular fibrosis of the testes is also a common phenomenon. Decreased spermatogenesis is associated with the thickening of the tunica propria even though testicular volumes remain normal despite of aging. Thickening of the tunica propria, which form the connective tissue of the seminiferous tubules, is thought to regulate movement of fluids into the tubules (Kowalski & Rosdahl, 2007). It is also thought to facilitate movement of spermatozoa by maintaining the right pressure within the seminiferous tubules.
The atrophy of the tubules is the main cause for the decline in volumes of sperms among aging males even though spermatogenesis is maintained. The potential of leydig cells in production of testosterone declines drastically during aging. Decreased amounts of testosterone levels in blood stimulates the production of gonadotrophin which further stimulates increased secretion of leydig cells presumably due to transformation of previous undifferentiated precursor cells(Patton & Thibodaux, 2008). Leydig cell hyperplasia is the condition that arises from the increased gonadotrophin action but unfortunately, it does have a compensatory effect on testosterone levels in blood.
Basement membrane thickening
The basement membrane of the aged testes thickens in association with degeneration of the seminiferous tubules. Thickening is attributed to an increase in the expression of the genes encoding the proteins of the basement membrane.
Deposition of connective tissue and thickening of wall
As biological aging takes place in men, new layers of the connective tissue become deposited in the seminiferous tubules resulting in the thickening of the wall. Senescence is therefore associated with decreased spermatogenesis due to the thickening of the wall (Harrass, Black & Henshel, 1999).
Aging and fibrosis
Fibrosis is maintained during resulting in the separation of the germinal epithelium from the blood vessels. Blood supply to the germinal epithelium is therefore curtailed depriving it of important nutrients.
Testicular tunic and tunic weight
Progressive fibrosis during aging results in the thickening of the testicular tunic and tunic weight with subsequent negative effects on sperm production. The negative effects of the continuing fibrosis are caused by diminished blood supply. Lack of proper blood supply to the germinal epithelium causes metabolic deficiencies such as the decline in supply of oxygen to the testis with subsequent decline in spermatogenesis.
Testicular propensity
Progressive fibrosis is attributed for testicular propensity during aging. The increase in the tunic weight is a reflection of the overall increase in the weight of the testes and tunic thickness.
Metabolic deficiency
Sustained fibrosis separates the germinal epithelium from blood vessels resulting in metabolic deficiency. Diminished blood supply results in a decline in supply of metabolic nutrients and oxygen which is useful in spermatogenesis. Removal of metabolic wastes is also hindered resulting in the accumulation of harmful byproducts of metabolism in the system which reduces its functioning capacity. The result is diminished production of spermatozoa. The few sperms that are secreted are weak since they lack important metabolic constituents and are therefore susceptible to apoptosis. Access to metabolic substrates is reduced due to the distance between the blood vessels and the germinal cells of the testes resulting in reduced metabolism during spermatogenesis (McElreavey, 2000).
Decline production of testosterone and leydig cell population
The decline in leydig cell population associated with aging and production of testosterone leads to depreciated spermatogenesis. This is because sperm production is a factor of the leydig cell population and the concentration of viable testosterone (Söder, 2003). Testosterone is actually involved in the last stage of meiosis during spermatogenesis. The quantity of spermatozoa synthesized during spermatogenesis depends on the rate of cell loss during the prophase stage of meiosis. Since testosterone levels decline with aging, cell loss during post-prophase stage of meiosis becomes pronounced leading to a rapid decline in spermatogenesis.
Environmental endocrine disruption
The endocrine system transforms external stimuli through hormones and related chemical messengers into appropriate enzymatic responses as well as specific gene expression. The endocrine system also coordinates metabolic processes and other developmental mechanisms including sexual differentiation (Bentley, 2008). The hypothalamus controls the production of hormones in response to the external or internal stimuli for a particular response. Secretion of hormones by the pituitary gland is equally under regulation by the hypothalamus. Once secreted, hormones are transported through the bloodstream to target cells where they bind to specific receptor proteins resulting in a conformational change that communicates appropriate physiological responses. The concentration of hormones in the blood regulates its secretion from the hypothalamus and/or the pituitary gland. The response of these gonads to different stimuli is specific although their functioning could be disrupted by certain environmental signals and compounds.
Environmental disruption of the male reproductive system interferes with sexual differentiation. In addition, the manifestations of hormone-induced sex characteristics are hindered as well as the normal functioning of the organs of the male reproductive system. The exposure of the endocrine system to external stimuli exposes it to xenobiotics which could interfere with its functioning. Environmental xenobiotics could disrupt the normal endocrine signaling pathways agonistically by acting as a ligand that subsequently binds to the hormone receptor blocking the actual hormone from doing so (Vernadakis, Quay & Timiras, 2005). The receptor becomes activated in the same manner as hormone binding does but with different physiological responses. Binding of the xenobiotics could also damage the configuration of the receptor transforming its conformational shape thereby inhibiting the actual protein from binding during a normal endocrine mechanism. In essence, the receptor is activated in a different manner during binding of xenobiotics from that of the real hormone.
Xenobiotics actually compete with hormones for the receptor on the target tissue. On the other hand, the xenobiotics could bind to the receptor in a different site from the active site of the hormone. This causes the receptor to become modified resulting in subsequent change in the configuration of the active site. The result is that the hormone cannot bind to the active site as usual reducing the endocrine action. Antagonists which inhibit normal binding and functioning of hormones include drugs such as tamoxifen which is known to compete for the same receptors with androgens and estrogens (Moon & Mommsen, 2005). Other chemical inhibitors include linuron, vinclozolin and their derivative metabolites. The concentration of xenobiotics determines the degree to which endocrine disruption occurs. A high concentration of foreign ligand competing with hormones causes significant inhibition of endocrine activity.
Chemicals also disrupt production of hormones by inhibiting enzymatic catalysis of important reactions. The conversion of testosterone into estrogen is catalyzed by an enzyme aromatase (Christen, Epelbaum & Chanson, 2004). The enzyme can be inhibited by xenobiotics resulting in high concentrations of testosterone while decreasing the concentration of estrogen. This anti-estrogenic activity by the foreign compounds has a negative effect on spermatogenesis. The transport of secreted hormones through the bloodstream can also be inhibited by xenobiotics leading to arrested hormone action since hormones as effecter molecules cannot reach target cells. Hormones become obstructed by xenobiotics circulating in the bloodstream since they cannot be bound by albumins and globulins as usual with small concentrations lipophilic substances (Crowley, 2009).
The degree of interactions between xenobiotics and hormones in the bloodstream depends on the affinity of each for receptor proteins in the target cells as well as the active sites of transport proteins. Steroid hormones both natural and synthetic are potential endocrine disruptors. The effect of environmental endocrine disruptors depends on the rate of exposure and availability of xenobiotics. Xenobiotics which are consumed in the diet are most potent and exhibit the greatest deleterious effects on sperm production.
Environmental estrogens and reduced fertility
Both natural and synthetic estrogens are known to damage or interfere with endocrine system. Environmental estrogen is one the most potent environmental disruptors of the reproductive and developmental systems. Synthetic estrogen is similar to the female sex hormone, estrogen thus it initiates similar actions of the steroid hormone by binding to its receptor (Hall, 1998). Cell signaling pathways that are activated by estrogen are turned on these chemicals inappropriately. Environmental estrogens are obtained from fertilizers such as DDT, endosulfan, dieldrin, kepone, dicofol, toxaphene and birth control pills (Kowalski & Rosdahl, 2007). Polycyclic hydrocarbons and derivatives of plastics are also known environmental estrogens.
Water for drinking can also be contaminated with industrial effluents and pollutants in the air. Toxaphene is one of the air borne pollutants classified as environmental estrogens while the highly chlorinated DDT compound is understood to reduce fertility. Environmental estrogens are the main cause of abnormal testes while high estrogen levels lower the concentration of blood testosterone leading to decline in spermatogenesis. Fertility drastically declines since estrogen blood levels are more than doubled resulting in impairment of the processes involved in sperm production (Patton & Thibodaux, 2008). The testes are also impaired distorting mechanisms for maturation of spermatozoa. Secreted sperms are weak and cannot swim at the same pace as normal ones. The number of synthesized spermatozoa declines as environmental estrogens proliferate within the bloodstream.
Conclusion
The functioning of the reproductive system is dependent on the integrity of the constituent organs and molecules. Coordination of the various systems is important if sexual differentiation and viability of secreted molecules is to be ascertained. The male reproductive system is under regulation by hormones from the anterior pituitary gland and the hypothalamus which work in a coordinated manner. Aging is associated with a decline in biological processes including production of sperms. This is attributed to the rapid decline in cell proliferation in a process referred to as apoptosis (Harrass, Black & Henshel, 1999). The apoptotic cell death of the testicular cells reduces the capacity of the male reproductive system to secrete spermatozoa. There is a decline in spermatogenesis as a result of impaired endocrine function and progressive fibrosis. Viability of the few secreted sperms is reduced since the neutralizing effects of the prostatic fluid are severely depreciated. The volume of the seminal fluid is decreased while testicular function is impaired.
Testicular propensity is a result of continuous fibrosis. Thickening of the basement membrane also takes place resulting in deposition of the connective of layers of connective tissue in the seminiferous tubules. Blood supply to the germinal epithelium is hindered by the thickening of the basement membrane and the rapid increase in the tunic weight. Subsequently, metabolic deficiency arises from the depreciated supply of blood resulting in a decline in spermatogenesis. Aging therefore renders the male reproductive system to numerous clinical disorders which lead to reduced fertility (McElreavey, 2000). One of the clinical conditions associated with aging in men is the notorious benign prostatic hyperplasia. The condition is characterized by the enlargement of the prostate gland leading to the thickening of the walls of the urethra. Eventually, emptying of the bladder becomes a strenuous exercise. Old men are therefore susceptible to episodes of frequent urination and impaired sexual activity. Urine may accumulate in the urethra getting mixed with sperms which is abnormal
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