Testicular torsion is an emergent condition. The protective effect of medical hypothermia in ischemia/reperfusion injury is well defined.

To evaluate the late results of hypothermia through a rat testicular torsion/detorsion model compatible with human testicular torsion.

Rats were divided into 5 groups (n = 7): (1)Sham (S) group, (2)T/D group: right testis was torted for 1-h, (3)T/D + H30 group: hypothermia at 4 °C was applied for 30 min before detorsion, (4)T/D + H90 group: hypothermia at 4 °C was applied for a total of 90 min (30 min before and 1-h after detorsion), (5)H group: hypothermia at 4 °C was applied to right testis for 90 min. Testicular diameters at preoperative period and 8th postoperative week were measured. Biochemically, MPO, NO, 3-NT and 4-HNE in testicular tissue and serum levels of NO, PGF 2α, 3-NT, 8-OHdG and 4-HNE were studied. Histopathologic examination and TUNEL assay were also performed.

Biochemical and macroscopical parameters of both T/D + H30 and T/D + H90 groups were statistically different from group T/D with respect to protective effects of hypothermia. Johnsen's score was also statistically different in group T/D + H90.

Hypothermia can easily be applied with ice bags both in perioperative period. This is the first study evaluating the effect of hypothermia applied postoperatively. Tissue level of protein oxidation marker (3-NT) and serum levels of DNA damage (8-OHdG), lipid peroxidation (4-HNE), protein oxidation (3-NT) and oxidative stress (PGF-2α) markers were measured for the first time.

Hypothermia has been shown to be macroscopically, biochemically and histopathologically beneficial in the long-term experimental testicular torsion model.

This study was designed to evaluate the protective and therapeutic efficacy of platelet-rich plasma (PRP) against testicular degeneration and germ cell apoptosis after induced spermatic cord torsion/detorsion (TD) in rats.

Forty rats were allocated into 5 groups: 1) control, 2) short torsion/detorsion (STD), 3) long torsion detorsion (LTD), 4) protective (PRP/P) and 5) treatment (PRP/T). Testicular ischemia was induced by twisting the right testis 1080° clockwise for 2.5 h. PRP (10 μl) was injected intra-testicular 5 min before (PRP/P) and 3 h after (PRP/T) detorsion. At the end of the experiment, rats were euthanized at 2, 30, 2, and 30 days for groups 2-5 respectively. Nitric oxide, malondialdehyde, catalase, total antioxidant capacity, reduced glutathione, glutathione-S-transferase, interleukin1 beta, tumor necrosis factor, caspase-3, and B-cell lymphoma 2 expressions were assessed in the testes. Moreover, histological examination was performed.

PRP treatment significantly mitigated the torsion-detorsion induced testicular degeneration. Particularly, by improving the state of oxidative stress (NO, P = 0.0001) and antioxidant markers (TAC, GSH, GST, P = 0.0001-0.01) and decreasing the expression of IL-1β, TNF-α and cas 3 and increase the BCL2 fold changes (P = 0.0001). The protective use of PRP is superior to the therapeutic use of PRP in the restoration of the testicular histoarchitecture following TD.

This study illustrates the cyto-protective role of PRP against TD induced testicular cell injury that highlight possible application of PRP as a complementary therapy in different testicular degenerative diseases which might attribute to its ability to ameliorate the oxidative stress and inhibit induced apoptosis.

Testicular torsion is an urological emergency and an important cause of male infertility. Recent studies have shown that not only ischemia, but also the restoration of blood flow creates a deleterious situation for the testis. The goal of this work was to evaluate the role of systemic epithelial growth factor application and its association with decompressive fasciotomy in tissue recovery of the testes undergoing the torsion of the spermatic cord.

Torsion of the spermatic cord was induced in 40 Wistar pubescent testes for a period of 4 h. At the time of detorsion systemic epithelial growth factor and decompressive fasciotomy were applied as treatment alternatives. After 21 days, the testicles were examined macro and microscopically.

The variables evaluated were weight, testicular volume and the degree of histological alterations by optical microscopy. The rate of healing of testicular torsion showed significant difference between the groups. It was noted that in terms of testicular weight and volume the animals treated with systemic epithelial growth factor resembled the control group and had a better histological classification than the other groups. The mean Johnsen score was significantly higher in the group treated with systemic growth factor and decompressive testicular fasciotomy than in the group without fasciotomy. No significant changes were noted in the contralateral testes.

Although decompressive testicular fasciotomy improved spermatogenesis, recovery was limited. Systemic epithelial growth factor administered in combination with decompressive testicular fasciotomy was more effective for spermatogenesis than fasciotomy alone. Administering epithelial growth factor after reperfusion might have the potential to decrease long-term histologic damage after testicular torsion. The combination of decompressive testicular fasciotomy and epithelial growth factor had a synergistic effect on the healing of these testes.

The purpose of the study was to determine the effect of (-)-epigallocatechin gallate (EGCG) on testicular ischemia-reperfusion injury in rats.

Forty male Wistar rats were assigned to 5 groups. A sham operation was performed on the animals in group 1. In group 2, after 4 hours of unilateral testicular ischemia, 4 hours of testicular reperfusion was performed with EGCG administered 1 hour before reperfusion. In group 3, the same surgical procedure as in group 2 was performed, but without EGCG. Serum superoxide dismutase activity, creatine kinase, and lactate dehydrogenase were then measured in blood samples from groups 1 to 3. In group 4, after 4 hours of unilateral testicular ischemia, testicular reperfusion was performed. In group 5, the same procedure as in group 4 was performed, but with EGCG administered 1 hour before reperfusion. For groups 4 and 5, bilateral orchiectomy was performed for histologic examination 4 weeks after reperfusion was started.

Serum superoxide dismutase activity was significantly higher in group 2 than in group 3. The ratios of bilateral testicular weight, mean seminiferous tubule diameter, and germinal epithelial cell thickness were significantly higher in group 5 than in group 4.

Therapy with EGCG before reperfusion might exert protective effects via antioxidant activities in a rat experimental model of testicular ischemia-reperfusion injury.

Serum- and glucocorticoid-inducible kinase-1 (SGK1) is a serine/threonine protein kinase that responds to various stimuli and mediates cell survival. Although it is known that testicular torsion leads to testicular damage and male infertility, the role of SGK1 in torsion remains unclear. This study investigated whether torsion-induced apoptosis is associated with changes in phosphoinositide-dependent protein kinase-1 (PDK1), SGK1 and forkhead transcription factor FOXO3a expression and/or phosphorylation in rats. Sprague-Dawley rats were divided into four groups: sham (control), 1, 2 and 4 h of unilateral torsion. Bilateral testes, testicular interstitial fluid (TIF) and blood samples were collected immediately after torsion. Our results revealed that SGK1 protein and mRNA were abundantly present in testes and were induced by 2 h of torsion, but that phosphorylation of SGK1, PDK1 and FOXO3a decreased simultaneously. After 2 h of torsion, the testosterone secretion capacity of the primary Leydig cells and testicular interstitial cells (TICs) was impaired and apoptotic spermatogonia and TICs were observed; in addition, the mean seminiferous tubular diameter was decreased. Torsion increased plasma corticosterone levels, but decreased plasma luteinizing hormone and testosterone levels. However, the testosterone levels of the TIF in the ipsilateral testes were significantly enhanced after 2 h of torsion, but suppressed in the contralateral testes. This animal study suggests that PDK1, SGK1 and FOXO3a are involved in torsion-induced apoptosis and that medical therapy should be performed as early as 2 h after the occurrence of torsion to prevent further damage.