Investigation of the effects of curcumin, vitamin E and their combination in cisplatin-induced testicular apoptosis using immunohistochemical technique

Gevrek, Fıkret; Erdemır, Fikret

doi:10.5152/tud.2017.95752

Cited by 20 publications

(24 citation statements)

References 31 publications

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“…The histopathological examination of the testicular tissue after CDDP injection showed irregularities in seminiferous tubules, apoptosis, and necrosis in interstitial cells of Leydig, and degenerative changes in germ cells. These findings were observed also in other studies 1,3,4,16,29 confirming the cytotoxic effect of CDDP.…”

Section: Discussionsupporting

confidence: 87%

“…These findings were in coupe with other studies that showed a marked increase in immunostaining intensity of caspase-3 in CDDP group and decreased intensity in control group. 16,45 The CDDP induces the Bax translocation to mitochondria releasing ROS and cytochrome c which then stimulates caspases 3,8,9 triggering apoptosis. 44 Caspase-3 is the executive caspase that induces apoptosis and its activation by CDDP confirmed the CDDP apoptotic damage in the testicular tissue.…”

Section: Discussionmentioning

confidence: 99%

“…11,15 Finally, all animals were weighed, and then sacrificed after anesthesia using a mixture of ketamine 60 mg/kg/ip and xylazine 10 mg/kg/ip. 16…”

Section: Methodsmentioning

confidence: 99%

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Candesartan in a rat model of testicular toxicity: New insight on its protective mechanism

Sherif

Sarhan

2019

Exp Biol Med (Maywood)

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Cisplatin (CDDP) is widely used as an effective chemotherapy; nevertheless, its use is associated with male reproductive system damage. Candesartan (Cand) is an angiotensin II receptor blocker which showed a protective effect against CDDP-induced testicular toxicity. This study was implemented to investigate further novel molecular protective effect of Cand. Animals were divided into four groups and treated for 10 days as: Group I (Normal control): received saline, Group II (Cand control): treated with Cand (10 mg/kg/day) orally, Group III (CDDP): injected with a single dose of 10 mg/kg CDDP intraperitoneally (ip), Group IV (Cand + CDDP): treated with Cand (10 mg/kg/day) orally plus a single ip dose of 10 mg/kg CDDP at day 3. Blood and testicular tissue collections were done at the end of the experiment. A marked decrease in testicular, body, and relative body weights in addition to testosterone level was observed in the CDDP group when compared with normal rats. In addition, exposure to CDDP showed a marked upregulation of testicular TNF-α mRNA level and a significant rise in testicular levels of total oxidant status, oxidative stress index (OSI) ratio, pro-apoptotic protein Bax, Bax/Bcl-2 ratio alongside with a marked reduction in testicular levels of total antioxidant status, antiapoptotic protein Bcl-2, and a significant upregulation of the testicular caspase-3 expression in comparison to normal group. Histopathological findings after CDDP injection showed apoptosis and necrosis in testicular tissues. Administration of Cand ameliorated these biochemical and histopathological findings. Cand exhibited a novel protective mechanism against CDDP induced-gonadal damage via antioxidant, anti-inflammatory, and anti-apoptotic activities. Impact statement Cisplatin is a commonly used drug in the treatment of solid tumors and its application is associated with testicular toxicity. The effect of candesartan in cisplatin-induced testicular toxicity and its fundamental mechanism of action were investigated. Candesartan had certainly repaired the testicular injury and ameliorated both biochemical and histopathological changes. Candesartan mitigated the gonadotoxicity induced by cisplatin via antioxidative, anti-inflammatory, and antiapoptotic actions.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

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Candesartan in a rat model of testicular toxicity: New insight on its protective mechanism

Sherif

Sarhan

2019

Exp Biol Med (Maywood)

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“…The high polyunsaturated membrane lipid content of the testes makes the testes more susceptible to the effects of oxidative agents such as CP (Gevrek & Erdemir, ). The protective effect of various natural substances, including fish oil (Ciftci et al, ), curcumin (Gevrek & Erdemir, ), resveratrol (Reddy et al, ), hesperidin (Kaya et al, ) and rutin (Aksu et al, ), against CP‐induced reproductive system damage has also been demonstrated in many studies. To our knowledge, the potential beneficial effects of β‐glucans against CP‐induced reproductive toxicity have not been studied previously.…”

Section: Introductionmentioning

confidence: 99%

Favourable effect of β‐glucan treatment against cisplatin‐induced reproductive system damage in male rats

et al. 2019

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The aim of this study was to investigate the potential beneficial effects of β‐glucan treatment against oxidative, histological and spermatological damage caused by cisplatin on the male reproductive system. Twenty‐eight Sprague Dawley male rats were used in the study. The rats were randomly divided into four equal‐sized groups: a control group, cisplatin group (7 mg/kg in a single‐dose cisplatin administered intraperitoneally), β‐glucan group (β‐glucan given at a dose of 50 mg kg−1 d−1 for 14 day) and a cisplatin plus β‐glucan group (cisplatin and β‐glucan administered together at the same dose). Cisplatin administration induced an increase in the level of thiobarbituric acid‐reactive substances, a lipid peroxidation indicator. It induced a decrease in enzymatic (superoxide dismutase, catalase and glutathione peroxidase) activities and nonenzymatic (reduced glutathione) antioxidant levels. In addition, cisplatin caused both histological and spermatological damage, as shown by a decrease in sperm motility and epididymal sperm concentrations and an increase in abnormal sperm rates. The β‐glucan treatment improved cisplatin‐induced oxidative, histological and spermatological damage. This study revealed that β‐glucan treatment provided prevention against male reproductive system damage caused by cisplatin. These preventative effects were likely due to its antioxidant properties.

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“…Previous studies demonstrated that Cis inhibits tumor growth by inducing apoptosis in patients [30] and Cis induces apoptosis in rat testis and spermatozoa [31][32][33]. Several studies showed that Cis treatment increases the formation of oxidative stress, DNA fragmentation and induceses apoptosis in testis, and different antioxidants and antioxidant rich extracts such as rutin [34], Ginkgo biloba extract [27], and Eugenia jambolana extract [35] inhibits apoptosis in Cis induced testis damage.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol treatment reduces apoptosis and morphological alterations in cisplatin induced testis damage

Nagehan¹,

Şener²,

Ercan³

2019

jrp

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Cisplatin commonly used as a chemotheropotic agent however, it is associated with numerous side effects such as reproductive cytotoxicity. It causes spermatogenic cell death and DNA damage in spermatozoa via the formation of reactive oxygene species. Resveratrol (3,5,4'-trans-trihydroxystilbene), a natural phytoalexin, is a potent antioxidant agent, present in a wide variety of dietary sources including grapes, plums and peanuts. The aim of present study to evaluate the beneficial effects of resveratrol on cisplatin induced testis damage. Male Sprague Dawley rats were used in the study and four experimental groups were formed as: 1-saline applied control, 2-resveratrol applied control, 3-cisplatin and 4-cisplatin+resveratrol groups. Following a single dose of cisplatin (7 mg/kg i.p.), either saline or resveratrol (10 mg/kg, orally) was administered for 5 days. Testis samples were prepared for histopathological and ultrastructural evaluations, cell proliferation and apoptosis. Tissue malondialdehyde (MDA), glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined biochemically. Degenerated and atrophic tubules of tissue, apoptotic cells, MDA level and MPO activity were increased although proliferation index and GSH level were decreased in cisplatin group. Degenerated tight junctions between the Sertoli cells and vacuole formation in germinal epithelial cells were also revealed at this group. However, resveratrol treatment reduced degenerated and atrophic tubules, apoptotic cells, vacuole formation in germinal epithelial cells, MDA level and MPO activity and increased proliferation index and GSH level in testis. These results showed that resveratrol ameliorates cisplatin induced testis injury by the impairment of oxidative stress and apoptosis.

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Investigation of the effects of curcumin, vitamin E and their combination in cisplatin-induced testicular apoptosis using immunohistochemical technique

Cited by 20 publications

References 31 publications

Candesartan in a rat model of testicular toxicity: New insight on its protective mechanism

Candesartan in a rat model of testicular toxicity: New insight on its protective mechanism

Favourable effect of β‐glucan treatment against cisplatin‐induced reproductive system damage in male rats

Resveratrol treatment reduces apoptosis and morphological alterations in cisplatin induced testis damage

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