Veterinary Andrology and Reproductive Techniques

Chemical factors

II: CHEMICAL FACTORS AFFECTING SPERMATOGENESIS

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: Eg. Busulfan. These drugs destroy spermatogonia and in later stages the germinal epithelium are removed by ‘maturation depletion’.
• Diamines: these drugs affect spermatocytes followed by ‘maturation depletion’.
• Nitrogen-containing compounds: Administration of these drugs cause arrest of spermatogenesis at primary spermatocyte stage with histological castration changes in the pituitary.
• Drugs affecting cell division: Drugs like hydroxyurea, interferes with DNA synthesis and thereby it affects the spermatogenesis

Effects of Environment Agents

• Recent evidence suggests that the pesticides used in agricultural might alter the male reproductive function.

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Organochlorine derivatives

• DDT (Dichlorodiphenyl Trichloro Ethane): It 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 vascuolization, abnormal spermatids and multinucleated spermatocytes.
• Cyclodines: Dieldrin, aldrin and some indane derivatives may cause germ cell damage, lowered plasma testosterone levels and decreased prostatic secretion and these alterations may lead to decrease in spermatogenic activity.
• Benzene hexachloride: It 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: (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
  • Polychlorpinene: (Insecticide) It causes degeneration of seminiferous tubules with lack of mature spermatozoa, spermatids and spermatocytes. However sertoli cells and spermatogonia are present.
• Organophosphates: eg.Dichlorovos and carbamates
  • Dichlorovos: It 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.

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Food additives and contaminants

• Diethyl stilbesterol: Diethyl stilbesterol produces atrophy seminiferous tubule histopathology and atrophic 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.

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