Ameliorative effect of selenium in cisplatin-induced testicular damage in rats

Şimşek, Nejdet; Koç, Akif; Karadeniz, Ali; Yıldırım, Mehmet; Çelik, Hüseyin; Sarı, Esin Söğütlü; Kara, Adem

doi:10.1016/j.acthis.2016.02.002

Cited by 18 publications

(13 citation statements)

References 45 publications

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“…CP is one of the most effective and widely used chemotherapeutic agents against many types of cancers (e.g., testicular, ovarian, breast, lung, bladder, sarcomas and lymphomas; Eid et al, ). CP is thought to interact with DNA in cancer cells, which in turn leads to apoptosis by altering apoptosis‐related signals and the activation of signalling pathways (Simsek et al, ). Toxic effects of CP on many tissues and organs, such as the liver, kidney and gonads, limit its clinical usage (Aksu et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Testicular tissue has a high content of polyunsaturated membrane lipids and a low antioxidant capacity. Thus, it is more susceptible to oxidative stress than other tissues and organs, making the testis one of the most vulnerable organs to CP treatment (Ciftci et al, ; Simsek et al, ). Many previous studies have clearly demonstrated the adverse effects of CP on testes (Aksu et al, ; Hussein, Mohamed, Shalaby, Abd El‐Haleem, & Abd El Motteleb, ; Kaya et al, ; Saral et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…Many previous studies have clearly demonstrated the adverse effects of CP on testes (Aksu et al, ; Hussein, Mohamed, Shalaby, Abd El‐Haleem, & Abd El Motteleb, ; Kaya et al, ; Saral et al, ). A number of studies have investigated the efficacy of antioxidants, such as rutin (Aksu et al, ), hesperidin (Kaya et al, ), selenium (Simsek et al, ) and fish oil (Ciftci et al, ), against CP‐induced testicular damage. To our knowledge, no studies have focused on the impact of β‐glucans on CP‐induced testicular damage.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

et al. 2019

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“…Se protects the normal cells against apoptosis through down‐regulation of apoptosis, whereas it is inducing apoptosis through up‐regulation of oxidative stress in cancer cells. Up‐regulation of apoptosis, casp‐3 and casp‐9 through cisplatin treatment was further increased in breast cancer cell line by Se treatment (Simsek et al, ). In the current study, we found negative synergism between MEL, Se and DTX in the casp‐3, casp‐9 and apoptosis analyses of normal kidneys and testes.…”

Section: Discussionmentioning

confidence: 99%

“…The presence of an inverse relationship between plasma Se levels and mortality in patients with prostate cancer treated with/without taxanes has been reported (Niraula et al, ). Recent studies have demonstrated the protective role of Se on cisplatin‐induced oxidative stress and apoptosis in kidneys (Aksoy et al, ; Nazıroğlu, Karaoğlu, & Aksoy, ; Saif‐Elnasr, Abdel‐Aziz, & Ibrahim, ) and testes (Simsek et al, ) in rats. In addition, synergic interaction between Se and chemotherapeutic agent (cisplatin) on the same intracellular toxic cascade in breast cancer cell line was recently reported (Sakallı Çetin, Nazıroğlu, Çiğ, Övey, & Aslan, ).…”

Section: Introductionmentioning

confidence: 99%

Treatment with melatonin and selenium attenuates docetaxel‐induced apoptosis and oxidative injury in kidney and testes of mice

Baş

Nazıroğlu

2019

Andrologia

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Docetaxel (DTX) has been used in cancer treatments for several decades, but it results in many adverse apoptotic effects through excessive production of reactive oxygen species (ROS) in some tissue including the kidney and testes. We aimed to investigate potential modulatory roles of melatonin (MEL) and selenium (Se) against DTX-induced apoptosis and oxidative injury in the testes and kidney of mice. Thirtytwo mice were divided into four equal groups as control, DTX, DTX + MEL and DTX + Se. DTX group was treated with a single intraperitoneal dose of DTX. After DTX treatment, MEL and Se were administered to the mice in the DTX + MEL and DTX + Se groups for 7 days respectively. Increased lipid peroxidation, ROS, apoptosis, caspase-3 and caspase-9 activities in the kidney and testes of the DTX group were diminished by treatment with MEL and Se. DTX-induced decreases in vitamin E (α-and γ-tocopherol), glutathione peroxidase and reduced glutathione levels in the kidney and testis were increased following MEL and Se treatments. In conclusion, our data show that MEL and Se can act as modulators against DTX-induced apoptosis and oxidative damage in the kidney and testis through up-regulation of glutathione and vitamin E and down-regulation of caspase pathways. K E Y W O R D Scancer, caspase, docetaxel, oxidative injury, testis

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Tranilast abrogates cisplatin‐induced testicular and epididymal injuries: An insight into its modulatory impact on apoptosis/proliferation

Makled

Said

2021

J Biochem & Molecular Tox

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Cisplatin is a chemotherapeutic agent whose therapeutic use is greatly limited by the associated organs' toxicity and particularly, testicular toxicity. Cisplatin‐induced testicular damage reported being mediated through mitochondria‐mediated apoptosis, inflammation, and oxidative stress. Evidence showed that tranilast (TRN) has the ability to restore the oxidative status and modulate TRAIL/caspase‐8 signaling. This led us to hypothesize that TRN could abrogate cisplatin‐induced testicular and epididymal injuries via inhibiting oxidative stress and modulating proliferation and TRAIL/caspase‐8/cJNK signaling. Cisplatin injection induced oligospermia and abnormalities in testicular and epididymal structure along with impaired oxidative status. TRN administration (100 or 300 mg/kg) for 7 days post‐cisplatin injection preserved spermatogenesis and restored testicular and epididymal architecture, but restoration was more so in TRN300 than TRN100. This was in line with the restoration of balanced oxidative status as indicated by the increased total antioxidant capacity, glutathione and superoxide dismutase activity, and the decreased malondialdehyde content in testes (p < 0.05 vs. cisplatin). TRN increased the cell proliferation revealed by the increased expression of proliferating cell nuclear antigen in a dose‐dependent manner (p < 0.05 vs. cisplatin) whereas only TRN300 decreased testicular cJNK, TRAIL, and caspase‐8 expression (p < 0.05 vs. cisplatin). Moreover, TRN dose‐dependently inhibited the pro‐inflammatory transcription factor NF‐kB and the cytokine TNF‐α expressions in testes. In conclusion, TRN300 was more effective than TRN100 in alleviating cisplatin‐induced testicular and epididymal injuries and in enhancing spermatogenesis. This curative effect of TRN might be mediated through its antioxidant and anti‐inflammatory impacts along with its modulatory impact on cJNK/TRAIL/caspase‐8 signaling favoring proliferation rather than apoptosis.

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Ameliorative effect of selenium in cisplatin-induced testicular damage in rats

Cited by 18 publications

References 45 publications

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

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

Treatment with melatonin and selenium attenuates docetaxel‐induced apoptosis and oxidative injury in kidney and testes of mice

Tranilast abrogates cisplatin‐induced testicular and epididymal injuries: An insight into its modulatory impact on apoptosis/proliferation

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