TABLE OF CONTENTS
Factors Affecting Spermatogenesis in Male Animals
Factors affecting spermatogenesis in male animals include a combination of hormonal, environmental, nutritional, genetic, and physiological influences.
The factors affecting spermatogenesis in animals are:
- Physical factors
- Chemical factors
- Nutritional factors
- Hormonal factors
- Genetic factors
- Pathological factors
- Age factors
1. Physical Factors
Irradiation
Irradiation interferes with spermatogenesis by damaging spermatogonia, spermatocytes, and spermatids. Among these, spermatocytes are the most sensitive to irradiation, while Leydig and Sertoli cells are quite resistant. Steroidogenesis is not significantly affected by X-rays, and testosterone levels are generally maintained.
Hyperthermia
High ambient temperatures can lead to testicular degeneration, which adversely affects spermatogenesis. A number of conditions can elevate testicular temperature, including cryptorchidism, ectopic testes, inguinal hernia, scrotal dermatitis due to irritants, chorioptic mange, and myiasis in sheep. Localized infections, wounds, contusions, and hematomas of the scrotum or testes also contribute to increased testicular heat.
Prolonged fever caused by infectious diseases, as well as persistently high environmental temperatures—particularly when associated with high humidity—can further impair testicular function. Males that are unable to stand often experience testicular degeneration and atrophy due to the testes being held close to the body, which leads to prolonged heat exposure.
A testicular temperature exceeding 41°C has a detrimental effect on spermatogenesis. Cells actively undergoing meiosis are more sensitive to heat than resting sperm cells. However, steroidogenesis remains largely unaffected. Among the germ cells, late pachytene primary spermatocytes and early round spermatids are the most heat-sensitive.
Hypothermia
Spermatogenesis appears to be more resistant to cold than to heat. In response to low temperatures, the tunica dartos and cremaster muscle contract to draw the testes closer to the body, helping to maintain an optimal temperature for sperm production.
However, damage to spermatogenic function has been observed at temperatures below -25°F. In cases of hypothermia, the stagnation of blood flow and resulting hypoxia are likely more harmful than the actual drop in temperature itself.
Light
The influence of light on control of spermatogenesis is brought through the capacity of it to control the pituitary gonadotrophin.
The pineal body operated as a neuroendocrine transducer mediating light effects on the testes. The shortened photoperiod (below 12 hours) decrease the capacity of the pituitary to release of gonadotrophin, possibly by reducing sensitivity to gonadal steroid hormone feedback. Thereby it brings about effect on spermatogenesis.
Low Oxygen Tension
Spermatogenesis is severely impaired when adopted males are subjected to low oxygen tension at high attitude or in experimental chambers.
2. Chemical Factors
Antispermatogenic Drugs
Cadmium
Cadmium salts, in small doses produce marked necrosis in the testis which probably results from a marked increase in testicular blood flow and increase in permeability of the blood vessels by increasing the intercellular cleft and the blood-testis barrier. It affects both the spermatogenic and androgenic functions of the testis but after about one month, the damaged testis gradually regains full androgenic activity.
Alkylating Agents
Alkylating agents such as Busulfan destroy spermatogonia; in later stages, the germinal epithelium is depleted through a process known as maturation depletion.
Diamines
Diamines drugs affect spermatocytes followed by ‘maturation depletion’.
Nitrogen Containing Compounds
Administration of nitrogen containing compounds cause arrest of spermatogenesis at primary spermatocyte stage with histological castration changes in the pituitary.
Effects of Environment Agents
Recent evidence suggests that the pesticides used in agricultural might alter the male reproductive function.
Organochlorine Derivatives
DDT (Dichlorodiphenyl Trichloro Ethene)
DDT (Dichlorodiphenyltrichloroethene) causes spermatogenic cell degeneration and spermatogenic activity appeared to be decreased. It causes progressive histological deterioration followed by loss of germinal cells, karyopyknotic nuclei, cytoplasmic vacuolization, abnormal spermatids and multinucleated spermatocytes.
Cyclodienes
Dieldrin, aldrin and some indane derivatives may cause germ cell damage, lowered plasma testosterone levels and degreased prostatic secretion and these alterations may lead to decrease in spermatogenic activity.
Benzene Hexachloride
Benzene hexachloride decreases the number of mature sperms and the testis show degenerative changes, necrosis and cellular proliferation. The seminiferous tubules are severely damaged and multinucleated giant cells are commonly found.
Miscellaneous Organochlorine Compounds
Kepone
Kepone (used to control a wide range of inset pests). It produces atropic or greatly enlarged testes associated with seminiferous histopathology and thereby interfere with spermatogenesis.
Polychloroprene (Insecticide)
Polychloroprene causes degeneration of seminiferous tubules with lack of mature spermatozoa, spermatids and spermatocytes. However sertoli cells and spermatogonia are present.
Organophosphates
Dichlorvos
Dichlorvos causes degeneration of seminiferous tubules but sertoli cells and Leydig cells appear normal.
Carbamates
Carbaryl at various doses increased testosterone hydroxynation and carbaryl stimulate the conversion of testosterone to dihydrotestosterone.
Food Additives and Contaminants
Diethylstilbestrol
Diethylstilbestrol produces atrophy of seminiferous tubule and leydig cells.
Food Colourings
Metanil yellow which is an commonly used dye in India produces vascular damage and irreversible damage to seminiferous epithelium and thereby produce spermatogenic cell changes in testes.
Alcohol
Most important cause of male feminization. The effect of alcohol is characterized by atrophy and pathology of testes, prostate and seminal vesicles, lowered plasma testosterone levels, germ cell immaturity and seminiferous tubule pathology.
The changes occur in the absence of liver disease suggesting that alcohol is a direct testicular toxin. Ethanol inhibits testicular retinal alcohol dehydrogenase activity. Vitamin A plays an important of spermatogenesis.
Alcohol inhibits the rate of formation of retinol from retinal liver and retina. If this inhibition occurs in the testes, steroidogenesis might be reduced followed by alteration in spermatogenesis and accessory gland morphology and function.
Atmospheric Pollutants
Increased atmospheric pressure of carbondioxide reduces spermatid concentrations in seminiferous tubules and prematurely releases spermatozoa, presumably by carbondioxide effects on sertoli cells.
3. Nutritional Factors
Low Plane of Nutrition
The low plane of nutrition or malnutrition cause a greater stress on prepubertal animals than in postpubertal animals. It causes hypoplasia of the testes and accessory sex glands and delays puberty. Adversely affect gonadotropins secretion i.e FSH and LH and thereby reduces the spermatogenic activity.
High Plane of Nutrition
High plane of nutrition is frequently cited as a cause of infertility especially in fatty, overfed and obese animals. It indicated that excessively fatty bulls may have enough fat around the testes in the scrotum, especially the dorsal part to insulate the testes and possibly affect spermatogenesis.
Vitamins Deficiencies
Hypovitaminosis A
Germinal and ledig cells are both affected by hypovitaminosis A resulting in poor semen quality, testicular atrophy, hypoplasia of accessory sex glands and delayed puberty.
Vitamin A is epitheliotropic and the severe deficiency produce degeneration of seminiferous tubule and interfere with spermatogenesis.
Hypovitaminosis E
Hypovitaminosis E causes testicular damage in rats but in domestic animals the role of vitamin E on spermatogenesis is insignificant.
4. Hormonal Factors
Exogenous Steroids
Exogenous steroids affect testicular function by altering the secretion of gonadotropins. Small doses of testosterone may impair spermatogenesis to a greater degree than larger doses due to ability of the larger dose to maintain the seminiferous epithelium.
In some species steroid suppression of testis has been followed by a rebound phenomenon after steroid withdrawal.
Pituitary Factors
Reduced spermatogenesis with testicular atrophy may be caused by failure of FSH and LH. Many stress factors affect LH and FSH release, the most important being inanition due to low plane of nutrition.
Tumors of the pituitary gland also cause atrophy of the pituitary gland and failure of gonadotropic production.
5. Genetic Factors
Heredity
Sperm production is grossly affected by genetic abnormality like testicular hypoplasia and congenital aplasia of wolffian duct. Testicular hypoplasia in cattle is due to single recessive autosomal gene with incomplete penetrance.
Hereditary defects in sperm production or maturation cause abnormality of the acrosome and separation of the head and tail.
Inbreeding
It increases the abnormal seminiferous tubules and hypoplasia which will affect the spermatogenesis. This may be due to autosomal recessive gene.
Cytogenetic Disturbances
Cytogenetic disturbances causes two abnormalities in the primary spermatocytes including:
- Stickness of chrosome in which they failed to separate at anaphase.
- A pyknotic nuclei and multiple spindle formation due to a dysfunction of the mechanism of cell division due to extra centrosome divisions resulting in the formation of giant cells with a number of nucleus.
Hybridization
Example: Donkey(Jack) (62) X Horse (mare) (64) = Mule (63)
The germ cells of hybrids proceed through mitosis, but there is a block to meiosis since ‘pairing’ of homologous chromosomes is impossible due to ‘uneven chromosome number’ having come from parents with different chromosome numbers.
Freemartinism
In this condition there will be non inflammatory degeneration of testes which will affect the spermatogenesis.
6. Pathological Factors
The pathological factors affecting spermatogenesis are divided into two namely congenital factors and acquired factors.
Congenital Factors
Testicular Hypoplasia
Testicular hypoplasia is congenital or hereditary in origin caused by single recessive autosomal gene with incomplete penetrance leading to lack of miotic division and block in spermatogenesis.
Cryptorchidism
Spermatogenesis is inhibited by elevation of temperature of the affected testis. The affected testis is usually small in size, soft, flaccid and do not produce any spermatozoa.
Imperfect Descent of the Testes
Thermoregulatory system is affected and hence spermatogenesis is impaired.
Scrotal or Inguinal Hernia
Scrotal or inguinal hernia interferes with the normal thermoregulatory mechanism and thereby affect the spermatogenesis.
Acquired Factors
Testicular Degeneration
Several factors like heat, cold, trauma, excessive physical strain, unilateral castration, irradiation, fever, toxaemia, hot environment, insect bites on the scrotum, diseases like foot and mouth and other viral diseases, vaccination against rinderpest and FMD, Vitamin A deficiency, injection of autologous or homologous testicular material can cause testicular degeneration.
Here spermatogenesis is affected and there will be presence pf spermatocytes in the semen. The tubules are reduced in size.
Testicular Fibrosis
A marked degenerative change in the germinal epithelium together with increased interstitial tissue is noticed. Semen is usually watery containing few or no sperms.
7. Age Factors
Degenerative changes in seminiferous tubules of mammals have been noticed in aging. Focal degeneration and calcification of tubules has been noticed.
A decline in germinal tissue, an arrest of the later stages of spermatogenesis and increase in connective tissue are associated with aging.
