Effects of high doses of testosterone propionate and testosterone enanthate on rat seminiferous tubules — a stereological and cytological study

Abstract

The effects of exogenous testosterone on various testicular variables has become of increasing significance because of its potential use in male contraception. For this reason, high doses of two testosterone esters [testosterone propionate (TP) and testosterone enanthate (TE)] were used in a study of their influence on the morphology, length and curvature of the seminiferous tubules of the rat testis, and on cytological smears of the seminiferous tubules epithelium. TP was given for 14 days (3 mg/100 g body weight, i.m.) to assess the acute effects of testosterone on the seminiferous tubules. TE was administered for 60 days (in the same manner as TP) to study possible chronic effects on the rat testis. After TP and TE treatment the seminiferous tubule epithelium showed disorganization and desquamation of spermatogenic cells. In the TP-treated testes the tubules lined with Sertoli cells only were observed. The values for the length and curvature of seminiferous tubules of the TP- and TE-treated rats were significantly reduced (p < 0.001). All these changes were observed earlier in the TP-treated than in the TE-treated animals. In cytological smears of the testis of the TP- and TE-treated rats an increase of vacuoles and residual bodies in Sertoli cell cytoplasm was noted. In addition, a reduction of spermatogenic cells, particularly sperms, was manifest in the smears after treatment. Large groups of Sertoli cells were seen in the smears from these testes.

Histological changes induced by testosterone abuse in the testis and the skeletal muscle of adult male albino rats

“…Similar results were detected by other investigators with different testosterone overloads in rats [18] and Syrian hamsters [20]. Most of the tubules were irregular and atrophied, with marked damage in the germinal epithelium in the form of vacuolization, apoptosis, and depleted cells except for the basal apoptotic cells.…”

“…Although the exact concentration of testosterone that leads to spermatogenesis remains a matter of discussion, it is generally accepted that the seminiferous epithelium is normally exposed to high concentrations of this hormone [18]. AAS administration is often associated with various adverse effects that are generally dose related.…”

“…Some of the Sertoli cell vacuolization could be the result of a metabolic disturbance in the Sertoli cells and a subsequent change in their morphology [18]. Thus, these vacuoles were possibly extracellular in relation to the Sertoli cell, due to the lack of elements of the seminiferous epithelium.…”

Effects of organotin compounds on pubertal male rats

“…This is in agreement with reports which have described decreased testis and epididymal weights after treatment with different androgens like testosterone, methyltestosterone and others in adult mice and rats (Heywood et al, 1977;Banasal and Davies, 1986;Sun et al, 1990;Gao and Short, 1993;Jezek et al, 1993;Bronson, 1996;Okazaki et al, 2002). Depressed spermatogenesis has been discussed as one possible mechanism (Sun et al, 1990), downregulation of testosterone production in the Leydig cells due to the inhibition of FSH release in the pituitary as result of negative feedback of testosterone has also been suggested (Yamasaki et al, 2000).…”

A repeated 28-day oral dose toxicity study of 17α-methyltestosterone in rats, based on the 'Enhanced OECD Test Guideline 407' for screening the endocrine-disrupting chemicals

“…Changes in sexual organs in males included decrease in testis and epididymis weights, atrophy of seminiferous tubules and Leydig cells and increased degeneration of pachytene spermatocytes in the testes and of germ cells in epididymides in the 80 mg/kg group. There have been a number of reports of decreased testis weights after many kinds of testosterone treatment such as with testosterone itself, methyltestosterone, and testosterone cypionate, enanthate or propionate (Banasal and Davies 1986;Sun et al 1990; Gao and Short 1993;Jezek et al 1993;Bronson 1996), as a result of depressed spermatogenesis (Sun et al 1990). Histopathologically, atrophy of seminiferous tubules and Leydig cells has been described with testosterone given by intraperitoneal administration of 10 or 20 mg/kg per day for 15 days, which was accompanied by a decline in LH and FSH (Jezek et al 1993), or with methyltestosterone in the diet at approximately 34.5 lg/ g body weight per day for 90 days (Gao and Short 1993).…”