Apoptotic balance during testicular detorsion after one hour induced torsion in rats

Abstract

Testicular torsion (TT) is an emergency complication that leads to oxidative stress and adversely affects spermatogenesis. Although immediate treatment consists of testicular detorsion (TD) to reverse TT-induced ischemia, mechanisms underlying recovery have yet to be fully understood. The current study aimed to investigate TD effects after a one-hour experimental TT by evaluating testicular antioxidant status and apoptosis-related proteins. Forty male Wistar rats were submitted to TT by testicular rotation, for one hour. Following TT, 32 rats were submitted to TD for 1, 2, 4, and 8 h (N = 8/group), the other 8 rats euthanized as TT-only. For controls, 8 rats were sham-operated. Testicular tissues were aseptically dissected for biochemical, histopathological, and immunohistochemistry analyses. The TD groups, especially after 4 h of TD, exhibited diminished MDA and increased TAC and GPX levels in testicular tissue. Levels of p53 and Caspase-3 were down-regulated in T1D4 and T1D8 groups versus torsion group. Bcl-2 was increased in T1D4 and T1D8 groups compared to the TT group. Moreover, spermatogenesis was recovered in T1D4 and T1D8 groups compared to the TT group. It can be concluded that after 1 h TT in rats, at least 4 h post-TD is needed for testicular tissue to initiate recovery.

Testicular torsion in vivo models: Mechanisms and treatments

“…49 During the last decades, various studies including those from our group revealed that oxidative stress plays a pivotal role in TTinduced damages. 14,39,42 The ischemia/reperfusion (I/R)-induced condition results in testicular lipid peroxidation increment, reduced total antioxidant capacity (TAC), superoxide dismutase (SOD), catalase, and glutathione (GSH) peroxidase (GPx) enzyme activity in testicular tissue. Thus, induced oxidative stress does not only happen due to reduced oxygen supply but also can be more severe when the testicular antioxidant defense mechanism suppresses.…”

“…Thus, induced oxidative stress does not only happen due to reduced oxygen supply but also can be more severe when the testicular antioxidant defense mechanism suppresses. 14,39 It should be noted that TT-induced oxidative stress has the potential to induce cell cycle arrest in germ cells. 44 Talebi and Farahpour conducted a study illustrating an increase in p21 protein expression in a TT model experiment.…”

“…66 Studies by our group showed that TD-induced injuries start soon after the operation. 14,39,42 Thus, the protective protocol, which is to start using antioxidant treatment before TD and continue the treatment for a couple of days after TD, might be the most effective protocol to protect the testis. Despite various studies focusing on the protective effects of different antioxidant agents in I/R condition, it is still unclear which antioxidant administration protocol can protect testis more efficiently, and finding the best antioxidant with a sufficient protective mechanism against TT warrants further studies with different antioxidants and the TT model.…”

“…40 Induced TT in this manner is sufficient to induce blood flow obstruction, 17,41 spermatogenesis dysfunction, 14 germ cell arrest, 42 and apoptosis. 39 However, in order to induce the same condition in mice, at least 2 h of 720 o torsion is required. 43 Moreover, Shamsi et al illustrated that more than 4 h of 720 o TT induction in rats causes testicular necrosis, which could be the source of irreversible damage to the tissue.…”

“…Although time is an important factor in TT induction, TT degree and ischemia (I)-induced damages are also playing key roles in the induction of TT condition. 14,38,39 Prolonged TT induction leads to testicular infarction and necrosis, making a kind of limitation for a proper evaluation of TT condition. For instance, it has been revealed that atrophied testis )half of the normal testicular mass) represents a complete spermatogenesis arrest and aspermatogenic condition.…”