Effects of scrotal hyperthermia on Leydig cells in long-term: a histological, immunohistochemical and ultrastructural study in rats

Abstract

We have previously demonstrated that scrotal hyperthermia induce Leydig cell (LC) damage in short-term. The objectives of this pilot study were to investigate morphological changes and regulation of steroidogenesis on LC in long-term and the time of observation were extended to investigate whether the LC would eventually make a recovery after scrotal hyperthermia. The rats were randomly allotted into one of four groups: A (control), B (70 days after scrotal hyperthermia), C (105 days after scrotal hyperthermia), D (140 days after scrotal hyperthermia); each group contain seven animals. Scrotal hyperthermia was carried out in a thermostatically controlled water bath at 43 degrees C for 30 min once daily for six consecutive days. Control rats were treated in the same way, except the testes were immersed in a water bath maintained at 22 degrees C. Hyperthermia applied rats were sacrificed under 50 mg/kg ketamine anaesthesia after 70, 105 and 140 days, and biopsy materials of testes were obtained for light and electron microscopic examinations. Morphologically normal and the number of testosterone positive LC was significantly higher in 140 days after last heat than all other heat treatment groups. In heat treated groups, a dilated smooth endoplasmic reticulum, swollen mitochondria, and vanished mitochondrial cristae were observed. In the 140 days after scrotal hyperthermia, the severities of degenerative changes of LC were less than that observed in the other heat treated groups. We conclude that, scrotal hyperthermia cause morphological damaging and impaired steroidogenesis in LC and recovery of these findings were noted first time in 140 days after the last heat treatment.

Thresholds for thermal damage to normal tissues: An update

“…This shows substantial decrease in testosterone levels, even at this early time point. In rats, the percentage of testosterone positive Leydig cells decreases dramatically at day 1, similar to the mouse study, but follow up data show a subsequent recovery period lasting until 140 days, at which time the study ended but full recovery was not achieved [37, 38] (Supplementary Figure 5). …”

“…In light of the other data showing decreased sperm production and increased cell damage following heat treatments, the testicular mass likely decreases due to cell death and/or decrease in proliferation. The thermal dose delivered in rat studies was much higher than that for mice, at CEM 43 =180 min [37, 38]. Rats appear to be less sensitive to thermal dose than mice, as this high dose did not cause appreciably more damage than an equivalent mouse dose of CEM 43 =7.5–15 min.…”

Seasonal Changes of Serum Gonadotropins and Testosterone in Men Revealed by a Large Data Set of Real-World Observations Over Nine Years

“…Increasing environmental temperatures, testosterone raises, reaching the highest values in summer. In this setting, there is large evidence of the detrimental effect of local heat on Leydig cells activity and survival in animal models (44,45). In particular, heat-induced testicular damage is mediated by the activation of specific apoptotic pathways in animal models (46,47).…”

Cryptorchidism Is Not a Risk Factor for Antisperm Antibody Production in Post-Orchidopexy Males with Infertility

“…Scrotal hyperthermia can induce Leydig cell damage and cause disruptions in Sertoli cell tight junctions [8,16,17]. Therefore, it is speculated that males with cryptorchidism should have developed ASA due to the heat-induced breaches in the BTB.…”