H2O2 at physiological concentrations modulates Leydig cell function inducing oxidative stress and apoptosis

Gautam, D. K.; Misro, M. M.; Chaki, Sankar P.; Sehgal, Neeta

doi:10.1007/s10495-005-3087-1

Cited by 72 publications

(42 citation statements)

References 44 publications

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“…On the other hand, it is well-known that normal testosterone synthesis and secretion are necessary for spermatogenesis. ROS, particularly H 2 O 2 interfere with leydig cell function through a variety of actions like decrease in steroidogenic enzyme activity and apoptosis [10]. Therefore, ghrelin might also be able to prevent I/R detrimental effects on germ and leydig cells and improve sperm quality via its antioxidant properties.…”

Section: Discussionmentioning

confidence: 99%

The effect of ghrelin pretreatment on epididymal sperm quality and tissue antioxidant enzyme activities after testicular ischemia/reperfusion in rats

et al. 2011

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Ghrelin, the endogenous ligand for growth hormone secretagogue receptor, has been reported to prevent ischemia/reperfusion (I/R) injury in various tissues by its antioxidant activity. Therefore, this study was aimed to investigate the effect of ghrelin on sperm quality and antioxidant enzyme activity in a rat testicular ischemia/reperfusion injury model. Forty-two male Wistar rats were divided into groups control, I/R, and I/R plus ghrelin. The right testes were rotated 720° for 1 h and were allowed to reperfuse for 4 h and 30 days thereafter. Ghrelin (40 nmol/kg IP) or vehicle (physiological saline) was administrated 15 min before reperfusion. After 4 h of reperfusion, a right orchiectomy was performed to measure the biochemical parameters. In addition, the sperm was collected from the epididymis after 30 days of reperfusion, and sperm characteristics were examined. The malondialdehyde levels of the testis tissues were significantly increased, but a statistically significant decrease was found in the superoxide dismutase, glutathione peroxidase, and catalase activities in the I/R group as compared with the control, indicating I/R injury. The sperm evaluation showed a significant reduction in all characteristics resulted from I/R compared with the control. In the ghrelin-treated group, the malondialdehyde values were significantly lowered, and only enzyme activity of glutathione peroxidase showed significant increases compared with the I/R group. Ghrelin significantly enhanced sperm motility, movement, and concentration but did not prevent I/R-induced reduction in membrane integrity in the testes of rats compared to the I/R group. Our results suggest that ghrelin treatment has a protective role on IR-induced testicular injury, and this effect may be due to its antioxidant properties.

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Section: Discussionmentioning

confidence: 99%

The effect of ghrelin pretreatment on epididymal sperm quality and tissue antioxidant enzyme activities after testicular ischemia/reperfusion in rats

et al. 2011

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“…Assay for caspase-8 activity Caspase-8 activity was measured using a caspase-8 colorimetric assay kit (Alexis, San Diego, CA, USA) [22]. In brief, frozen testes in liquid nitrogen were grinded in lysis buffer (100 mg/200 µl) and incubated on ice for 10 min.…”

Section: Cell Viabilitymentioning

confidence: 99%

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

et al. 2006

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In order to understand the pathogenesis of estradiol induced effects in the seminiferous epithelium, studies were undertaken in adult rats with estradiol-3-benzoate administered for different durations. After 30 d of treatment, a significant rise in lipid peroxidation with concomitant fall in the activities of superoxide dismutase and catalase was observed. Both, serum and intra-testicular testosterone levels were found severely depleted. Seminiferous epithelium was devoid of elongated spermatids and spermatozoa by 30 d of treatment. Number of spermatocytes and round spermatids were significantly (p < 0.001) reduced. Flowcytometric analysis confirmed a drastic reduction of the haploid cell population (1c peak). Beginning from day 10 of treatment, there was a consistent rise in the number of pyknotic/apoptotic germ cells in the seminiferous epithelium. A gradual increase in Bax protein expression was observed with the duration of treatment. The shift in Bax immunostaining from the cytoplasm and nucleus of germ cells (at 10 d of treatment) to only nuclei of cells by 30 d of treatment was also noticed. By this time testicular tissue showed three-fold increase in caspase-8 enzyme activity. Viable testicular cells isolated in vitro decreased drastically subsequent to different periods of estradiol treatment. The above findings substantiate the fact that the testicular pathogenesis of estradiol benzoate treatment may be primarily because of altered reproductive hormone levels and high oxidative stress leading to germ cell apoptosis and subsequent germ cell loss in the seminiferous epithelium.

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“…Among antioxidants, only catalase, a scavenger of H 2 O 2 , provided a significant protective effect against either heat or oxidative stress induced apoptosis. An appropriate concentration of H 2 O 2 has been shown to induce apoptosis in a variety of cell types including testicular cells [17]. Further, as compared to the liver, the rat testis expresses equivalent levels of SOD activity but only 5% of the glutathione peroxidase activity and 2% of the catalase activity [46].…”

Section: Discussionmentioning

confidence: 99%

“…Activity of caspase-3 was measured using a caspase-3 colorimetric assay kit (Alexis, San Diego, CA, USA) as described [17]. In brief, frozen testis was grinded in liquid nitrogen (100 mg/200 µl lysis buffer) and incubated on ice for 10 min.…”

Section: Assay For Caspase-3 Activitymentioning

confidence: 99%

“…But, other factors such as, testicular oxidative stress coupled with production of reactive oxygen species are also implicated with impaired spermatogenesis [15,16]. H 2 O 2 , one of the potent reactive oxygen species, is able to induce cell apoptosis even at physiological concentrations [17]. However, the mechanisms involved in apoptosis occurring during normal spermatogenesis and in response to different pathological or experimentally induced situations may not be the same and are still largely unknown [18].…”

Section: Introductionmentioning

confidence: 99%

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hCG treatment raises H2O2 levels and induces germ cell apoptosis in rat testis

et al. 2007

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The clinical significance of exogenous hCG treatment is to stimulate steroidogenesis and spermatogenesis in the testis. However, the pathogenesis of detrimental effects on the testis arising out of chronic hCG treatment is yet to be clearly ascertained. In the present study we have shown that hCG treatment (100 IU/day) to rats for 30 days raises testicular oxidative stress leading to germ cell apoptosis and impairment of spermatogenesis. The treatment raises testicular H(2)O(2) levels along with increase in lipid peroxidation and concomitant decrease in the enzymatic antioxidant activities like superoxide dismutase, catalase and glutathione-s-transferase. The rise in the number of apoptotic germ cells was associated with up regulation of Fas protein expression and caspase-3 activity in the testis. However, serum testosterone which was elevated by 15 days of hCG treatment declined to pretreatment levels by 30 days. No significant alteration in serum gonadotropins was observed. The above findings indicate that the pathogenesis of deleterious effects following chronic hCG treatment is due to increase in testicular oxidative stress with high H(2)O(2) availability leading to apoptosis among germ cells.

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H2O2 at physiological concentrations modulates Leydig cell function inducing oxidative stress and apoptosis

Cited by 72 publications

References 44 publications

The effect of ghrelin pretreatment on epididymal sperm quality and tissue antioxidant enzyme activities after testicular ischemia/reperfusion in rats

The effect of ghrelin pretreatment on epididymal sperm quality and tissue antioxidant enzyme activities after testicular ischemia/reperfusion in rats

Estradiol treatment induces testicular oxidative stress and germ cell apoptosis in rats

hCG treatment raises H2O2 levels and induces germ cell apoptosis in rat testis

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