Effects of Cisplatin on Testicular Tissue and the Leydig Cell-Pituitary Axis

Abstract

The mechanisms responsible for the rapid increases in levels of gonadotropin and steroid hormones upon administration of cisplatin to rats are not clearly understood. In the present study, the morphologic effects of cisplatin on the testis and the relationship of these changes to serum hormone levels were studied in adult rats. Upon administration of a single dose (5 mg/kg) of cisplatin, the levels of testosterone in the peripheral blood decreased and the level of luteinizing hormone (LH) increased. After 3 days, significant damage to the germinal epithelium became detectable by morphologic examination. In Ley-dig and Sertoli cells, dilatation of the endoplasmic reticulum, structural changes in mitochondria and an increase in the numbers of inclusion bodies were detected. Although blood-testis barriers between Sertoli cells were normal, the relationship between germinal cells and the relationship between germinal cells and Sertoli cells were distorted. It is concluded that damage to Ley-dig cells and withdrawal of the controlling effects of the germinal epithelium on the LH-Leydig cell axis could explain the changes in serum hormone levels.

The possible protective role of royal jelly against cisplatin-induced testicular lesions in adult albino rats

“…Similar findings were also seen by other researchers [8,23]. Moreover, it was reported that a decrease in testosterone production might occur after CP treatment and might directly or indirectly affect the interstitial tissue and lymphatic space, provoking interstitial testicular edema [28]. It was also reported that capillary filtration participates in interstitial fluid formation; thus, changes in capillary permeability and blood/lymph flow could modify the interstitial fluid [29].…”

“…Similarly, it was reported that CP could decline the testosterone levels [35], which might be related to Leydig cell morphological alterations [28]. This was against findings by other researchers who reported that the testosterone level in the CP group was not significantly different from that of the control group [36].…”

Persistent Impairment of Testicular Histology and Sperm Motility in Adult Rats Treated with Cisplatin at Peri-Puberty

“…Post-natal sexual development in the male rat has been divided into four phases: neonatal (post-natal day -PND 1-7), infantile (PND 8-21), juvenile (PND [22][23][24][25][26][27][28][29][30][31][32][33][34][35] and peripubertal (PND 36-55 or 60) [1,2]. Male rats reach puberty, a dynamic physical, behavioural and hormonal event of sexual development [3], around the 50 days of age, when the first spermatozoa are observed in the cauda epididymis [4] and reproductive capacity is attained [3].…”

Amifostine Protective Effect on Cisplatin‐Treated Rat Testis

“…In mammals, spermatogonia are sensitive to cisplatin and other different chemotherapeutic drugs (Meistrich et al,1982). Moreover, cisplatin also seems to inhibit Leydig cell testosterone secretion (Vawda,1994; Malarvizhi and Mathur,1995) and usual changes in hormonal levels observed during cisplatin treatment may be related to Leydig cell damage (Aydiner et al,1997). Cisplatin also induces germ cell death in several different phases of spermatogenesis (Meistrich et al,1982; Vawda and Davies,1986; Handelsman et al,1988; Huang et al,1990; Kinkead et al,1992) and has been associated with an increase in the frequency of programmed germ cell death (apoptosis; Zhang et al,2001; Seaman et al,2003).…”