Effect of dexamethasone on germ cell apoptosis in the contralateral testis after testicular ischemia−reperfusion injury in the rat

Elenberg, Yigal; Lurie, M.; Shiloni, Eitan; Coran, Arnold G.; Sukhotnik, Igor

doi:10.1016/j.fertnstert.2005.10.021

Cited by 47 publications

(47 citation statements)

References 23 publications

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“…This data fits with reports of other investigators who have also noted minimal or no contralateral damage following ipsilateral experimental torsion [4,17,18]. Consistent with our previous studies [7,8], in the present experiment we also observed a significant (twofold) increase in germ cell apoptosis in the contralateral testis compared to sham animals. Although germ cell apoptosis in the contralateral testis increased less significantly when compared to the ischemic testis, which exerted an eightfold increase in the apoptotic rate, this increase may be responsible for decrease in the number of germ cell layers.…”

Section: Discussionsupporting

confidence: 94%

“…Consistent with our previous studies [7,8], in the present study testicular IR caused severe damage in the ischemic testis, induced degeneration in germ cells, and impaired spermatogenesis. A marked decrease in the average number of germinal epithelial cell layers and Johnsen's criteria in the ischemic testis support this conclusion.…”

Section: Discussionsupporting

confidence: 93%

“…Consistent with the result of our previous experiments [7,8], testicular ischemia resulted in a significant increase in germ cell apoptosis in the contralateral testis (Fig. 2).…”

Section: Contralateral Testissupporting

confidence: 92%

“…In a recent experiment, we have demonstrated that germ cells in the contralateral testis undergo apoptosis 24 h after testicular IR and that the extent of apoptosis increases with the duration of the ischemia [7]. Additionally, we have shown that 96 h after IR germ cell apoptosis in the contralateral testis remains significantly increased [8]. The catalyst for increased germ cell apoptosis in the contralateral testis following testicular IR is currently unknown and the pathways involved are poorly characterized.…”

Section: Introductionmentioning

confidence: 93%

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Effect of testicular ischemia-reperfusion on recruitment of neutrophils, E-selectin expression and germ cell apoptosis in the contralateral testis in a rat

et al. 2007

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Recent evidence suggests that neutrophil recruitment may initiate germ cell apoptosis in the ischemic testis. The purpose of the present study was to examine the relationship between germ cell apoptosis and neutrophil recruitment in the contralateral testis following testicular ischemia-reperfusion (IR) injury in a rat. Adult male Sprague-Dawley rats were divided randomly into two experimental groups: Group A: Sham operated animals; Group B: IR rats underwent 90 min of unilateral testicular ischemia following by 96 h of reperfusion. The rats were sacrificed and testes were harvested. Johnsen's criteria and the number of germinal cell layers were measured to categorize the spermatogenesis. TUNEL assay was used to determine germ cell apoptosis in both the ischemic and contralateral testis. The recruitment of neutrophils was calculated per 100 venules. Expression of E-selectin was determined using immunohistochemical analysis. Statistical analysis was performed using Student's t test, with P less than 0.05 considered statistically significant. Germ cell apoptosis in both the ischemic and the contralateral testis increased significantly after IR. E-selectin expression was significantly greater in ischemic testis from IR rats compared to sham animals. The small increase in E-selectin expression and the concomitant increase in neutrophil recruitment in the contralateral testis of the IR rats (vs. sham animals) were not statistically significant. In conclusion, testicular ischemia causes an increase in germ cell apoptosis in the contralateral testis. Mechanisms other than neutrophil recruitment apparently initiate this process.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 93%

“…Consistent with the result of our previous experiments [7,8], testicular ischemia resulted in a significant increase in germ cell apoptosis in the contralateral testis (Fig. 2).…”

Section: Contralateral Testissupporting

confidence: 92%

Section: Introductionmentioning

confidence: 93%

See 2 more Smart Citations

Effect of testicular ischemia-reperfusion on recruitment of neutrophils, E-selectin expression and germ cell apoptosis in the contralateral testis in a rat

et al. 2007

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“…The loss of germ cells after testicular I/R is due to germ cell-specific apoptosis. Germ cell apoptosis is a significant process in normal spermatogenesis but it is becoming clear that the process is massively up-regulated in a number of conditions disrupting spermatogenesis, including testicular torsion [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

The protective effects of trimetazidine on testicular ischemia and reperfusion injury in rats

et al. 2007

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This study was designed to investigate the protective effect of trimetazidine [TMZ; 1-(2, 3, 4-trimethhoxibenzyl)-piperazine dihydrochloride], as an antioxidant agent, on torsion-detorsion-induced biochemical and histopathological changes in experimental testicular ischemia/reperfusion injury in rats. Twenty-seven male Wistar rats weighing 180-220 g were divided into five groups: control (C, n = 4), sham-operated (S, n = 4), ischemia (I, n = 6), ischemia-reperfusion (I/R, n = 6) and ischemia-reperfusion + trimetazidine (I/R + TMZ; n = 7). Control rats were used for basal normal values. In group I, 2 h torsion of the left testis was performed. In I/R and I/R + TMZ groups, following 2 h of torsion, 4 h detorsion of the testis was performed. In ischemia and I/R groups, physiologic saline was administered orally for 7 days, and the rats in I/R + TMZ group were pretreated orally with 5 mg/kg day TMZ for 7 days before inducing ischemia. At the end of each experiment, ipsilateral orchiectomies were performed for the tissue levels of malondialdehyde (MDA), glutathione peroxidase (GPx) enzyme activities and histopathological examinations in all groups. MDA levels were significantly reduced and GPx enzyme activities were significantly increased in testes in I/R+TMZ pretreated group compared to group I and I/R. The mean seminiferous tubular diameter (MSTD) and Johnsen's score were significantly better in I/R+TMZ group than groups I and I/R. Pretreatment with TMZ decreased germ cell apoptosis and caspase-3 expression in the ischemic testis. The present results show that TMZ has a protective activity in the testicular injury caused by I/R, and provide the first evidence of the role of TMZ for the prevention of I/R-induced testicular injury.

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Dysfunction in Sertoli cells participates in glucocorticoid‐induced impairment of spermatogenesis

Ren

Zhang

Xin

et al. 2021

Molecular Reproduction Devel

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The effect of stress on male fertility is a widespread public health issue, but less is known about the related signaling pathway. To investigate this, we established a hypercortisolism mouse model by supplementing the drinking water with corticosterone for four weeks. In the hypercortisolism mice, the serum corticosterone was much higher than in the control, and serum testosterone was significantly decreased. Moreover, corticosterone treatment induced decrease of sperm counts and increase of teratozoospermia. Increased numbers of multinucleated giant cells and apoptotic germ cells as well as downregulated meiotic markers suggested that corticosterone induced impaired spermatogenesis. Further, upregulation of macrophage‐specific marker antigen F4/80 as well as inflammation‐related genes suggested that corticosterone induced inflammation in the testis. Lactate content was found to be decreased in the testis and Sertoli cells after corticosterone treatment, and lactate metabolism‐related genes were downregulated. In vitro phagocytosis assays showed that the phagocytic activity in corticosterone‐treated Sertoli cells was downregulated and accompanied by decreased mitochondrial membrane potential, while pyruvate dehydrogenase kinase‐4 inhibitor supplementation restored this process. Taken together, our results demonstrated that dysfunctional phagocytosis capacity and lactate metabolism in Sertoli cells participates in corticosterone‐induced impairment of spermatogenesis.

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Effect of dexamethasone on germ cell apoptosis in the contralateral testis after testicular ischemia−reperfusion injury in the rat

Cited by 47 publications

References 23 publications

Effect of testicular ischemia-reperfusion on recruitment of neutrophils, E-selectin expression and germ cell apoptosis in the contralateral testis in a rat

Effect of testicular ischemia-reperfusion on recruitment of neutrophils, E-selectin expression and germ cell apoptosis in the contralateral testis in a rat

The protective effects of trimetazidine on testicular ischemia and reperfusion injury in rats

Dysfunction in Sertoli cells participates in glucocorticoid‐induced impairment of spermatogenesis

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