Spermatogenesis arrest

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Histopathology of various spermatogenesis disorders. Spermatogenesis pathologies.png
Histopathology of various spermatogenesis disorders.

Spermatogenesis arrest is known as the interruption of germinal cells of specific cellular type, which elicits an altered spermatozoa formation. Spermatogenic arrest is usually due to genetic factors resulting in irreversible azoospermia. However some cases may be consecutive to hormonal, thermic, or toxic factors and may be reversible either spontaneously or after a specific treatment. Spermatogenic arrest results in either oligospermia or azoospermia in men. It is quite a difficult condition to proactively diagnose as it tends to affect those who have normal testicular volumes; a diagnosis can be made however through a testicular biopsy. [1]

Contents

Effects

Spermatogenic arrest results in either oligospermia or azoospermia as mentioned above. Oligospermia is when extremely low concentrations of fertile sperm are found in semen or ejaculate, while azoospermia is when no fertile sperm are found in the semen or ejaculate. [2]

Causes

Spermatogenesis is controlled by androgens, namely testosterone and follicle-stimulating hormone (FSH), these are the most important androgens that control the process. FSH uses very specific G-coupled receptors that can be found only on Sertoli cells, this hormone is secreted by the pituitary gland, located in the brain. While testosterone, is produced within the testicles by Leydig cells. This hormone is the main androgenic steroid in the process of spermatogenesis and is regulated by a hormone known as luteinizing hormone. FSH plays a role in the spermatogenic capacity of the adult male as it controls the proliferation of Sertoli cells during either the perinatal or pubertal period, or both. [3] However, testosterone has been found to be the most important hormone that is responsible for both the initiation and the maintenance of spermatogenesis. [4] It is known that spermatogenesis is under the control of androgens, but germ cells (that will become gametes), do not express a functional androgen receptor, which are activated by the binding of androgenic hormones. It has been found through studies that spermatogenetic arrest tends to occur in the late spermatocyte/spermatid stage when the androgen receptor activation in Sertoli cells is interrupted or affected in some way. [3] However, other studies have found that the condition can be due to either genetic factors or a variety of secondary factors.

Chemotherapy

When using chemotherapy treatments, the possibility of azoospermia is dependent on the dose, duration, number and type of drugs used; the male's fertility status before the treatment occurred is also taken into consideration. [5]

Radiotherapy

The use of radiotherapy can cause a temporary bout of azoospermia, this however, is dependant solely on the nature of the dose that are delivered to the testes. Those who experience less than 100 rads will recover in 9–18 months, doses of 200-300 rads will recover in 30 months and doses of 400-600 rads will recover in less than or equal to five years. An irreversible sterility may occur however, for those experiencing a single dose field with 600-800 rads. [6]

Nutritional Factors

Studies have shown that Vitamin A deficiencies in rats [7] , as well as zinc deficiencies in human males may prevent the normal functioning of spermatogenesis. [8]

Heat

Heat may also be the cause of oligozoospermia which can lead to both partial and reversible spermatogenic arrest. [9]

Infections

After the occurrence of an infectious disease in humans, such as hypothermia and/or the presence of toxic or infectious factors spermatogenic arrest is likely to follow, however, the condition may be normalized once antibiotic and anti-inflammatory treatments have been put into effect. [10]

Treatment

Various treatments have been discovered in order to aid those with spermatogenesis arrest, one of these being through the use of arginine. A study done by Jungling and Bunge in 1976 had a small breakthrough in the field by orally distributing arginine, daily to a group of infertile men. Of the eighteen men in the test group only one experienced an increase in sperm count, while others saw no improvement; these men also experienced a decreased sperm motility. However, one of the patients in the group successfully impregnated his wife while taking part in the study. [11] More recently, more successful treatments have been developed, such as through the use of gonadotropin treatment. A study conducted by Selman and El-Danasouri in 2006 proved that using long-term gonadotropin therapy on infertile men can improve sperm production quantitatively and increase sperm population in some patients and can in turn provide a successful in-vitro fertilization treatment. These results were found using men that had normal hormone levels but had spermatogenic arrest. These men were treated using FSH treatments and had testicular biopsy's performed on them before and after the treatment had been administered in order to track progress. [12]

Related Research Articles

Luteinizing hormone is a hormone produced by gonadotropic cells in the anterior pituitary gland. The production of LH is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. In females, an acute rise of LH known as an LH surge, triggers ovulation and development of the corpus luteum. In males, where LH had also been called interstitial cell–stimulating hormone (ICSH), it stimulates Leydig cell production of testosterone. It acts synergistically with follicle-stimulating hormone (FSH).

<span class="mw-page-title-main">Follicle-stimulating hormone</span> Gonadotropin that regulates the development of reproductive processes

Follicle-stimulating hormone (FSH) is a gonadotropin, a glycoprotein polypeptide hormone. FSH is synthesized and secreted by the gonadotropic cells of the anterior pituitary gland and regulates the development, growth, pubertal maturation, and reproductive processes of the body. FSH and luteinizing hormone (LH) work together in the reproductive system.

<span class="mw-page-title-main">Spermatogenesis</span> Production of sperm

Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. This process starts with the mitotic division of the stem cells located close to the basement membrane of the tubules. These cells are called spermatogonial stem cells. The mitotic division of these produces two types of cells. Type A cells replenish the stem cells, and type B cells differentiate into primary spermatocytes. The primary spermatocyte divides meiotically into two secondary spermatocytes; each secondary spermatocyte divides into two equal haploid spermatids by Meiosis II. The spermatids are transformed into spermatozoa (sperm) by the process of spermiogenesis. These develop into mature spermatozoa, also known as sperm cells. Thus, the primary spermatocyte gives rise to two cells, the secondary spermatocytes, and the two secondary spermatocytes by their subdivision produce four spermatozoa and four haploid cells.

<span class="mw-page-title-main">Seminiferous tubule</span> Location of meiosis and creation of spermatozoa

Seminiferous tubules are located within the testes, and are the specific location of meiosis, and the subsequent creation of male gametes, namely spermatozoa.

Fertility medications, also known as fertility drugs, are medications which enhance reproductive fertility. For women, fertility medication is used to stimulate follicle development of the ovary. There are very few fertility medication options available for men.

<span class="mw-page-title-main">Azoospermia</span> Medical condition

Azoospermia is the medical condition of a man whose semen contains no sperm. It is associated with male infertility, but many forms are amenable to medical treatment. In humans, azoospermia affects about 1% of the male population and may be seen in up to 20% of male infertility situations in Canada.

<span class="mw-page-title-main">Buserelin</span> Chemical compound

Buserelin, sold under the brand name Suprefact among others, is a medication which is used primarily in the treatment of prostate cancer and endometriosis. It is also used for other indications such as the treatment of premenopausal breast cancer, uterine fibroids, and early puberty, in assisted reproduction for female infertility, and as a part of transgender hormone therapy. In addition, buserelin is used in veterinary medicine. The medication is typically used as a nasal spray three times per day, but is also available for use as a solution or implant for injection into fat.

Terms oligospermia, oligozoospermia, and low sperm count refer to semen with a low concentration of sperm and is a common finding in male infertility. Often semen with a decreased sperm concentration may also show significant abnormalities in sperm morphology and motility. There has been interest in replacing the descriptive terms used in semen analysis with more quantitative information.

Male infertility refers to a sexually mature male's inability to impregnate a fertile female. In humans it accounts for 40–50% of infertility. It affects approximately 7% of all men. Male infertility is commonly due to deficiencies in the semen, and semen quality is used as a surrogate measure of male fecundity. More recently, advance sperm analyses that examine intracellular sperm components are being developed.

An alternative male contraceptive method involves heating the testicles so that they cannot produce sperm. Sperm are best produced at a temperature slightly below body temperature. The muscles around a male's scrotum involuntarily tighten if the man's body temperature drops, and they loosen, allowing the testes to hang, if the body temperature rises. This is the body's way of keeping the sperm at an ideal temperature. This means that sperm production can be disrupted with increased temperature. Some suggest exposure to high temperatures can affect infertility for months.

<span class="mw-page-title-main">Adjudin</span>

Adjudin (AF-2364) is a drug which is under development as a potential non-hormonal male contraceptive drug, which acts by blocking the production of sperm in the testes, but without affecting testosterone production. It is an analogue of the chemotherapy drug lonidamine, an indazole-carboxylic acid, and further studies continue to be conducted into this family of drugs as possible contraceptives.

Poor ovarian reserve is a condition of low fertility characterized by 1): low numbers of remaining oocytes in the ovaries or 2) possibly impaired preantral oocyte development or recruitment. Recent research suggests that premature ovarian aging and premature ovarian failure may represent a continuum of premature ovarian senescence. It is usually accompanied by high FSH levels.

Sertoli cell-only syndrome is a disorder characterized by male sterility without sexual abnormality. It describes a condition of the testes in which only Sertoli cells line is present in seminiferous tubules.

FNA mapping is an application of fine-needle aspiration (FNA) to the testis for the diagnosis of male infertility. FNA cytology has been used to examine pathological human tissue from various organs for over 100 years. As an alternative to open testicular biopsy for the last 40 years, FNA mapping has helped to characterize states of human male infertility due to defective spermatogenesis. Although recognized as a reliable, and informative technique, testis FNA has not been widely used in U.S. to evaluate male infertility. Recently, however, testicular FNA has gained popularity as both a diagnostic and therapeutic tool for the management of clinical male infertility for several reasons:

  1. The testis is an ideal organ for evaluation by FNA because of its uniform cellularity and easy accessibility.
  2. The trend toward minimally invasive procedures and cost-containment views FNA favorably compared to surgical testis biopsy.
  3. The realization that the specific histologic abnormality observed on testis biopsy has no definite correlation to either the etiology of infertility or to the ability to find sperm for assisted reproduction.
  4. Assisted reproduction has undergone dramatic advances such that testis sperm are routinely used for biological pregnancies, thus fueling the development of novel FNA techniques to both locate and procure sperm.
<span class="mw-page-title-main">Mild androgen insensitivity syndrome</span> Medical condition

Mild androgen insensitivity syndrome (MAIS) is a condition that results in a mild impairment of the cell's ability to respond to androgens. The degree of impairment is sufficient to impair spermatogenesis and / or the development of secondary sexual characteristics at puberty in males, but does not affect genital differentiation or development. Female genital and sexual development is not significantly affected by the insensitivity to androgens; as such, MAIS is only diagnosed in males. The clinical phenotype associated with MAIS is a normal male habitus with mild spermatogenic defect and / or reduced secondary terminal hair.

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism or primary gonadal failure, is a condition which is characterized by hypogonadism which is due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production. As compensation and the lack of negative feedback, gonadotropin levels are elevated. Individuals with HH have an intact and functioning hypothalamus and pituitary glands so they are still able to produce FSH and LH. HH may present as either congenital or acquired, but the majority of cases are of the former nature. HH can be treated with hormone replacement therapy.

<span class="mw-page-title-main">Leydig cell hypoplasia</span> Medical condition

Leydig cell hypoplasia (LCH), also known as Leydig cell agenesis, is a rare autosomal recessive genetic and endocrine syndrome affecting an estimated 1 in 1,000,000 genetic males. It is characterized by an inability of the body to respond to luteinizing hormone (LH), a gonadotropin which is normally responsible for signaling Leydig cells of the testicles to produce testosterone and other androgen sex hormones. The condition manifests itself as pseudohermaphroditism, hypergonadotropic hypogonadism, reduced or absent puberty, and infertility.

Hypogonadotropic hypogonadism (HH), is due to problems with either the hypothalamus or pituitary gland affecting the hypothalamic-pituitary-gonadal axis. Hypothalamic disorders result from a deficiency in the release of gonadotropic releasing hormone (GnRH), while pituitary gland disorders are due to a deficiency in the release of gonadotropins from the anterior pituitary. GnRH is the central regulator in reproductive function and sexual development via the HPG axis. GnRH is released by GnRH neurons, which are hypothalamic neuroendocrine cells, into the hypophyseal portal system acting on gonadotrophs in the anterior pituitary. The release of gonadotropins, LH and FSH, act on the gonads for the development and maintenance of proper adult reproductive physiology. LH acts on Leydig cells in the male testes and theca cells in the female. FSH acts on Sertoli cells in the male and follicular cells in the female. Combined this causes the secretion of gonadal sex steroids and the initiation of folliculogenesis and spermatogenesis. The production of sex steroids forms a negative feedback loop acting on both the anterior pituitary and hypothalamus causing a pulsatile secretion of GnRH. GnRH neurons lack sex steroid receptors and mediators such as kisspeptin stimulate GnRH neurons for pulsatile secretion of GnRH.

Follicle-stimulating hormone (FSH) insensitivity, or ovarian insensitivity to FSH in females, also referable to as ovarian follicle hypoplasia or granulosa cell hypoplasia in females, is a rare autosomal recessive genetic and endocrine syndrome affecting both females and males, with the former presenting with much greater severity of symptomatology. It is characterized by a resistance or complete insensitivity to the effects of follicle-stimulating hormone (FSH), a gonadotropin which is normally responsible for the stimulation of estrogen production by the ovaries in females and maintenance of fertility in both sexes. The condition manifests itself as hypergonadotropic hypogonadism, reduced or absent puberty, amenorrhea, and infertility in females, whereas males present merely with varying degrees of infertility and associated symptoms.

<span class="mw-page-title-main">Side effects of radiotherapy on fertility</span>

The side effects of radiotherapy on fertility are a growing concern to patients undergoing radiotherapy as cancer treatments. Radiotherapy is essential for certain cancer treatments and often is the first point of call for patients. Radiation can be divided into two categories: ionising radiation (IR) and non-ionising radiation (NIR). IR is more dangerous than NIR and a source of this radiation is X-rays used in medical procedures, for example in radiotherapy.

References

  1. ↑ Martin-du Pan, RC; Campana, A (1993). "Physiopathology of spermatogenic arrest". Fertil Steril. 60 (6): 937–46. doi: 10.1016/S0015-0282(16)56388-2 . PMID   8243695.
  2. ↑ Franchimont, P; Millet, D; Vendrely, E; Letawe, J; Legros, JJ; Netter, A (June 1972). "Relationship between spermatogenesis and serum gonadotropin levels in azoospermia and oligospermia". The Journal of Clinical Endocrinology and Metabolism. 34 (6): 1003–8. doi:10.1210/jcem-34-6-1003. PMID   5020414.
  3. 1 2 Gendt, KD; Swinnen, JV; Saunders, P; Schoonjans, L; Dewerchin, M; Devos, A; Tan, K; Atanassova, N; Claessens, F; Lecureuil, C; Heyns, W; Carmeliet, P; Guilou, F; Sharpe, RM; Verhoeven, G (2004). "A Sertoli cell-selective knockout of the androgen receptor causes spermatogenic arrest in meiosis". PNAS. 101 (5): 1327–1332. Bibcode:2004PNAS..101.1327D. doi: 10.1073/pnas.0308114100 . PMC   337052 . PMID   14745012.
  4. ↑ Sharpe, RM (1994). "Physiopathology of Reproduction": 1363–2434.{{cite journal}}: Cite journal requires |journal= (help)
  5. ↑ Damewood, MD; Grochow, LB (1986). "Prospects for fertility after chemotherapy or radiation for neoplastic disease". Fertil Steril. 45 (4): 443–59. doi: 10.1016/S0015-0282(16)49268-X . PMID   3082680.
  6. ↑ Ash, P (1966). "The influence of radiation on fertility in man". Br. J. Radiol. 39: 901–6.
  7. ↑ Ismail, N; Morales, C; Clermont, Y (1990). "Role of spermatogonia in the stage-synchronization of the seminiferous epithelium in vitamin-A deficient rats". Am. J. Anat. 188 (1): 57–63. doi:10.1002/aja.1001880107. PMID   2346119.
  8. ↑ Abbasi, AA; Prasad, AS; Rabbani, P; DuMouchelle, E (1980). "Experimental zinc deficiency in man: effect on testicular function". J. Lab. Clin. Med. 96 (3): 544–49. PMID   6772723.
  9. ↑ Kandeel, FR; Swerdloff, RS (1988). "Role of temperature in regulation of and the use of heating as a method for contraception". Fertil. Steril. 49 (1): 1–23. doi: 10.1016/S0015-0282(16)59640-X . PMID   3275550.
  10. ↑ Osegbe, DN (1991). "Testicular function after unilateral bacterial epididymo-orchitis". Eur. Urol. 19 (3): 2014–8. doi:10.1159/000473620. PMID   1855525.
  11. ↑ Jungling, ML; Bunge, RG (1976). "The treatment of spermatogenic arrest with arginine". Fertility and Sterility. 27 (3): 282–3. doi: 10.1016/S0015-0282(16)41718-8 . PMID   1254025.
  12. ↑ Sleman, H; El-Danasouri, I (2006). "Rescue of spermatogenesis arrest in azoospermic men after long-term gonadotropin treatment". Fertility and Sterility. 86 (2): 446–468. doi: 10.1016/j.fertnstert.2005.12.055 . PMID   16753161.
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