Ghrelin attenuates heat-induced degenerative effects in the rat testis

Kheradmand, Arash; Dezfoulian, Omid; Tarrahi, Mohammadali

doi:10.1016/j.regpep.2010.12.002

Cited by 39 publications

(19 citation statements)

References 58 publications

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“…Likely, a prolong time is needed for possible repair in testicular cytoarchitecture. This hypothesis is completely in consistent with our previous report, by which ghrelin significantly stimulated testicular regeneration just after 30 days upon oxidative stress induced by local scrotal hyperthermia (Kheradmand et al ., ). It seems that despite pre‐treatment by ghrlin with higher dose in the current study compared with our earlier study, 10 days is too short period and is not sufficient for protecting of degenerated seminiferous tubules after severe toxicity of Cd, and therefore, further time is required for testicular regeneration.…”

Section: Discussionmentioning

confidence: 97%

Biochemical and histopathological evaluations of ghrelin effects following cadmium toxicity in the rat testis

2014

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Numerous reports demonstrate that cadmium (Cd) induces oxidative stress by increasing lipid peroxidation and altering antioxidative enzymes status. Thirty male rats were subdivided into control-saline, Cd-saline and Cd-ghrelin groups. A single dose of Cd was injected to induce testicular injury and also ghrelin for 10 consecutive days to group 3. SOD activity decreased and lipid peroxidation increased by Cd administration. The mean activities of GPx and CAT as well as GSH content were lower in the Cd-saline rats; however, they did not statistically differ compared with the controls. Exposure to Cd resulted in complete degeneration of seminiferous tubules with severe depletion of germ cells and arrest in spermatogenesis. Notably, ghrelin treatment not only prevented reduction in SOD, GPx, CAT and GSH level, but also increased enzyme activities form their normal values. Moreover, TBARS concentration was significantly reduced by ghrelin administration. Furthermore, ghrelin pre-treatment resulted in partial but not significant prevention in testicular histopathological features damaged by Cd. In conclusion, the obtained results indicate for the first time the novel evidences of ghrelin ability in promotion of antioxidant enzyme activities and reduction of lipid peroxidation following Cd-induced oxidative stress in the rat testis. These observations also demonstrate that ghrelin may be considered as promising antioxidant agent in prevention and attenuation of testicular injury upon Cd toxicity.

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Section: Discussionmentioning

confidence: 97%

Biochemical and histopathological evaluations of ghrelin effects following cadmium toxicity in the rat testis

2014

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“…Recent reports suggest that ghrelin prevents testicular damage induced by heat, cadmium or ionizing radiation, and a reduction of oxidative stress has been postulated as a possible mechanism, although the specific pathway remains to be fully elucidated. [19,21,44,45]. Ghrelin prevents apoptosis in a number of tissues including adipocytes, endothelial cells and others [22][23][24]46] but whether these actions are mediated through p53 has not been well-established.…”

Section: Discussionmentioning

confidence: 99%

Ghrelin Prevents Cisplatin-Induced Testicular Damage by Facilitating Repair of DNA Double Strand Breaks Through Activation of p53 in Mice1

García

Chen

Guillory

et al. 2015

Biology of Reproduction

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Cisplatin administration induces DNA damage resulting in germ cell apoptosis and subsequent testicular atrophy. Although 50 percent of male cancer patients receiving cisplatin-based chemotherapy develop long-term secondary infertility, medical treatment to prevent spermatogenic failure after chemotherapy is not available. Under normal conditions, testicular p53 promotes cell cycle arrest, which allows time for DNA repair and reshuffling during meiosis. However, its role in the setting of cisplatin-induced infertility has not been studied. Ghrelin administration ameliorates the spermatogenic failure that follows cisplatin administration in mice, but the mechanisms mediating these effects have not been well established. The aim of the current study was to characterize the mechanisms of ghrelin and p53 action in the testis after cisplatin-induced testicular damage. Here we show that cisplatin induces germ cell damage through inhibition of p53-dependent DNA repair mechanisms involving gamma-H2AX and ataxia telangiectasia mutated protein kinase. As a result, testicular weight and sperm count and motility were decreased with an associated increase in sperm DNA damage. Ghrelin administration prevented these sequelae by restoring the normal expression of gamma-H2AX, ataxia telangiectasia mutated, and p53, which in turn allows repair of DNA double stranded breaks. In conclusion, these findings indicate that ghrelin has the potential to prevent or diminish infertility caused by cisplatin and other chemotherapeutic agents by restoring p53-dependent DNA repair mechanisms.

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“…Ghrelin has been identified as an endogenous ligand for growth hormone secretagogue receptor (GHSR) that regulates growth hormone (GH) secretion, regulates food intake, increases appetite and contributes to insulin release and energy homeostasis (Kojima and Kangawa 2005;Obay et al 2008;Kheradmand et al 2010Kheradmand et al , 2011Neamati et al 2011). It has been detected in a large number of tissues and cell types, including hypothalamus, small intestine, pancreas, placenta, pituitary, brain, lung, and kidney (Fernandez-Fernandez et al 2005;Ghelardoni et al 2006;Takeda et al 2006;Neamati et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Novel Antioxidant Properties of Ghrelin and Oleuropein Versus Lipopolysaccharide-Mediated Renal Failure in Rats

Alirezaei

Dezfoulian

Kheradmand

2015

Int J Pept Res Ther

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Ghrelin and oleuropein have recently been shown to bear beneficial effects against oxidative stress in our reports. The aim of this study was to evaluate the antioxidant abilities of ghrelin and oleuropein in a lipopolysaccharide (LPS)-induced nephrotoxicity model. The Sprague-Dawley male rats were divided into LPS, the ghrelin 1 plus LPS (Ghr 1 ?LPS), the ghrelin 4 plus LPS (Ghr 4 ?LPS), the oleuropein 10 plus LPS (Ole 10 ?LPS) and the oleuropein 15 plus LPS (Ole 15 ?LPS) groups. 1 or 4 nmol/ rat of ghrelin as subcutaneous and oleuropein 10 or 15 mg/kg as oral were administrated to ghrelin and oleuropein pretreated rats and vehicle injected to LPS group for ten consecutive days. All of the groups received LPS (once; 5 mg/ kg) in the 11th day of the treatment as intraperitoneally. LPSinduced nephrotoxicity was manifested by a significant elevation in renal function tests (BUN and creatinine; P \ 0.001) and histopathology findings in LPS group in comparison with the ghrelin and oleuropein pretreated rats. Renal lipid peroxidation was significantly higher in the LPStreated animals than the ghrelin and oleuropein pretreated groups (P \ 0.05). In contrast, glutathione peroxidase (GPx), catalase and superoxide dismutase activities were significantly higher in Ghr 4 ?LPS-treated rats than LPS group (P \ 0.05). GPx activity was also significantly higher in Ole 15 ?LPS-treated rats than LPS group (P \ 0.05). Regarding nitrosative stress, renal nitrite content was significantly lower in Ghr 4 ?LPS and Ole 15 ?LPS groups than LPS group (P \ 0.05). These results suggest that ghrelin and oleuropein have beneficial antioxidant properties versus LPS-induced renal failure in rats.

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Ghrelin attenuates heat-induced degenerative effects in the rat testis

Cited by 39 publications

References 58 publications

Biochemical and histopathological evaluations of ghrelin effects following cadmium toxicity in the rat testis

Biochemical and histopathological evaluations of ghrelin effects following cadmium toxicity in the rat testis

Ghrelin Prevents Cisplatin-Induced Testicular Damage by Facilitating Repair of DNA Double Strand Breaks Through Activation of p53 in Mice1

Novel Antioxidant Properties of Ghrelin and Oleuropein Versus Lipopolysaccharide-Mediated Renal Failure in Rats

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