Protective effects of amifostine, curcumin and caffeic acid phenethyl ester against cisplatin-induced testis tissue damage in rats

Mercantepe, Tolga; Ünal, Deniz; Tümkaya, Levent; Yazıcı, Zihni Açar

doi:10.3892/etm.2018.5819

Cited by 40 publications

(51 citation statements)

References 63 publications

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“…Testicular dysfunction caused by cisplatin is notified to be a major cause of infertility in males subjected to chemotherapy [44]. In this study, the body weight and the absolute testes weight were significantly diminished in response to cisplatin treatment.…”

Section: Discussionmentioning

confidence: 56%

Cisplatin induced testicular damage through mitochondria mediated apoptosis, inflammation and oxidative stress in rats: impact of resveratrol

Aly

Eid

2020

Endocr J

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The target of this study was to explore the role of mitochondria mediated apoptosis and inflammation in cisplatininduced testicular damage and to evaluate the ameliorative effect of resveratrol. Adult male Wistar rats were randomly allocated to 4 groups. Group I (Control) received normal saline, Group II (Resveratrol) received resveratrol (50 mg/kg/day), Group III (Cisplatin) received cisplatin (7.5 mg/kg/week, i.p.) and Group IV (Resveratrol + Cisplatin) received resveratrol and cisplatin in the same regimen of treatment. Treatment with resveratrol in Groups II and IV started 48h before cisplatin injection and continued for further 4 successive weeks. Cisplatin-treated rats showed reduced body weight, absolute testes weight and sperm count, motility and viability. On the other hand, cisplatin treatment increased the percentage of sperm abnormalities. It also decreased serum testosterone level, mitochondrial membrane potential while, increased cytochrome C liberation from the mitochondria into the cytosol. The activities of caspase-3 &-9 were increased. The level of TNF-α, IL-6 and Bax were increased whereas Bcl-2 was decreased. Oxidative stress markers were found to increase with a concomitant reduction in the antioxidant enzymes and GSH levels. These results were confirmed by immunohistochemical and histopathological analysis. Contrary to all these results, there were improvements in cisplatin induced testicular damage through attenuation of mitochondria mediated apoptosis, inflammation, and oxidative stress owing to resveratrol pretreatment. Thus, resveratrol, as a potential therapeutic agent, may hold promise in preventing mitochondria mediated apoptosis and inflammation in cisplatin-induced testicular damage in rats.

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Section: Discussionmentioning

confidence: 56%

Cisplatin induced testicular damage through mitochondria mediated apoptosis, inflammation and oxidative stress in rats: impact of resveratrol

Aly

Eid

2020

Endocr J

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“…Group 5 (MB) received 4 mg/kg of MB (IP) for 7 days. The doses, administration period of CP and MB were selected according to previous studies (Karimi et al, 2018;Liao et al, 2002;Mercantepe et al, 2018). CP and MB at these doses demonstrated harmful and protective effects respectively.…”

Section: Experimental Designmentioning

confidence: 99%

The ameliorative effects of methylene blue on testicular damage induced by cisplatin in rats

et al. 2020

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Cisplatin (CP) is a chemotherapeutic drug widely used for the treatment of different types of solid tumours (Wang & Lippard, 2005). However, clinical uses of CP are restricted due to severe side effects like nephrotoxicity, ototoxicity, hepatotoxicity and neurotoxicity (Florea & Büsselberg, 2011). Also, the toxic effect of CP on the reproductive system is well established (Howell & Shalet, 2005). Studies have revealed that the consumption of CP leads to several tissue injuries and biochemical changes in the reproductive system (Türk et al., 2008). The toxicity caused by CP can induce meiotic arrest which may consequently contribute to azoospermia (Martin-du Pan & Campana, 1993). However, the exact mechanism by which the deleterious effects of CP are ameliorated is not yet understood. The formation of reactive oxygen species (ROS) is one of the principal mechanisms involved in the destruction of the reproductive system through the consumption of CP. Thus, various supportive antioxidant components, such as hesperidin, melatonin, amifostine, ellagic acid, lycopene, vitamin E, Kigelia africana fruit extract, Ginkgo biloba, Nigella sativa oil and quercetin, have been used against CP-induced damages (Ateşşahin et al., 2006). Therefore, the use of antioxidants can be a substantial strategy to attenuate oxidative stress induced by CP consumption.

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“…Accumulating evidence is demonstrating CIS-induced impairment on antioxidant defence mechanism and promotion of inflammatory cytokine expression (Kaygusuzoglu et al, 2018;Mercantepe et al, 2018). Natural agents with antioxidant and anti-inflammatory potentials have been suggested to combat chemotherapy-associated toxicity (Bairi, Atanasov, Amrani, & Afqir, 2019;Famurewa et al, 2019).…”

mentioning

confidence: 99%

Ginger juice prevents cisplatin‐induced oxidative stress, endocrine imbalance and NO/iNOS/NF‐κB signalling via modulating testicular redox‐inflammatory mechanism in rats

Famurewa¹,

Ekeleme‐Egedigwe²,

Onwe

et al. 2020

Andrologia

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Chemotherapy is a cornerstone option in cancer treatment owing to its efficacy and effect on quality of life of cancer patients. The action mechanism of anticancer agents is targeted at deregulating cell cycle machinery and inhibiting unscheduled proliferation of cancer cells (Lin et al., 2020). Unfortunately, chemotherapeutic anticancer drugs often exert deleterious effect on healthy cells and tissues leading to systemic toxicity (Negrette-Guzmán, 2019). The toxicity may become unbearable that the treatment regimen has to be disrupted, even when achieving tumoricidal efficacy (Lin et al., 2020). Cisplatin (CIS) is an efficacious anticancer agent; it is the first choice for the treatment of advanced nonsmall-cell lung cancer cells, breast cancer and ovarian cancer (Browning et al., 2017; Lin et al., 2020; Manohar & Leung, 2018). It is of significant value also in the treatment of germ cell and testicular cancers (Thurston, 2007). It unleashes its anticancer action through formation of cisplatin-DNA adduct by intrastrand cross-links due to interaction with cancer cell DNA purine bases eventually leading to p53 activation, cell cycle arrest and induction

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Protective effects of amifostine, curcumin and caffeic acid phenethyl ester against cisplatin-induced testis tissue damage in rats

Cited by 40 publications

References 63 publications

Cisplatin induced testicular damage through mitochondria mediated apoptosis, inflammation and oxidative stress in rats: impact of resveratrol

Cisplatin induced testicular damage through mitochondria mediated apoptosis, inflammation and oxidative stress in rats: impact of resveratrol

The ameliorative effects of methylene blue on testicular damage induced by cisplatin in rats

Ginger juice prevents cisplatin‐induced oxidative stress, endocrine imbalance and NO/iNOS/NF‐κB signalling via modulating testicular redox‐inflammatory mechanism in rats

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