Assessment of the Effectiveness of Quercetin on Cisplatin-Induced Ototoxicity in Rats

Gündoğdu, Ramazan; Erkan, Mustafa; Aydın, Mesut; Sönmez, Mehmet Fatih; Vural, Alperen; Kökoğlu, Kerem; Karabulut, Derya; Şahin, Mehmet İlhan

doi:10.5152/iao.2019.5902

Cited by 10 publications

(2 citation statements)

References 32 publications

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“…Each group contained eight randomly selected rats. The sample size of the study was determined according to similar studies previously conducted (5,15,16).…”

Section: Experimental Designmentioning

confidence: 99%

Protective Effect of Carvacrol against Paclitaxel-Induced Ototoxicity in Rat Model

Atalay

Tatar

Dinçer

et al. 2021

Turk Arch Otorhinolaryngol

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Objective: This study aimed to explore whether carvacrol (CV) had a protective effect on paclitaxel-induced ototoxicity from biochemical, functional, and histopathological perspectives.Methods: Forty Wistar albino male rats were randomly separated into five groups of eight rats. Group 1 was the control group, so Paclitaxel or CV was not administered. Group 2 was administered i.p. CV at 25 mg/kg once a week; Group 3, was administered i.p. paclitaxel at 5 mg/kg once a week; Group 4 was administered i.p. paclitaxel at 5 mg/kg followed (30 min later) by CV at 25 mg/kg once a week; and Group 5 was administered i.p. CV at 25 mg/kg followed (1 day later) by paclitaxel at 5 mg/kg. once a week. The drugs were administered intraperitoneally once a week for four consecutive weeks, and distortion product otoacoustic emissions (DPOAE) tests were performed at the beginning of the study before the first drug administration and at the end of the study after the last drug administration. All rats were sacrificed, and cochleae were removed for biochemical and histopathological analysis. Results: Biochemical data indicated that paclitaxel caused oxidative stress in the cochlea. Histopathological findings revealed the loss of outer hair cells in the organ of Corti (CO) and moderate degenerative changes in the stria vascularis (SV). It was observed that DPOAE measurements were significantly reduced at high frequencies. In groups which CV was administered together with paclitaxel, these biochemical, histopathological, and functional changes were favorably reversed. Conclusion: CV may have a protective effect against paclitaxel-induced ototoxicity when given.

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“…Each group contained eight randomly selected rats. The sample size of the study was determined according to similar studies previously conducted (5,15,16).…”

Section: Experimental Designmentioning

confidence: 99%

Protective Effect of Carvacrol against Paclitaxel-Induced Ototoxicity in Rat Model

Atalay

Tatar

Dinçer

et al. 2021

Turk Arch Otorhinolaryngol

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“…For instance, chrysin offers protection against cisplatin-induced hepatotoxicity and colon toxicity [340]. Luteolin, kaempferol, chrysin, and quercetin also prevent ototoxicity and nephrotoxicity damage induced by cisplatin [340][341][342][343][344][345]. Resveratrol offered protection against cisplatin-induced epididymal toxicity, testicular toxicity, and toxicity in ovarian and cavity cancer cells [346,347].…”

Section: Other Cardiotoxic Cancer Treatments Cisplatinmentioning

confidence: 99%

CYP1B1 as a therapeutic target in cardio-oncology

2020

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Cardiovascular complications have been frequently reported in cancer patients and survivors, mainly because of various cardiotoxic cancer treatments. Despite the known cardiovascular toxic effects of these treatments, they are still clinically used because of their effectiveness as anti-cancer agents. In this review, we discuss the growing body of evidence suggesting that inhibition of the cytochrome P450 1B1 enzyme (CYP1B1) can be a promising therapeutic strategy that has the potential to prevent cancer treatment-induced cardiovascular complications without reducing their anti-cancer effects. CYP1B1 is an extrahepatic enzyme that is expressed in cardiovascular tissues and overexpressed in different types of cancers. A growing body of evidence is demonstrating a detrimental role of CYP1B1 in both cardiovascular diseases and cancer, via perturbed metabolism of endogenous compounds, production of carcinogenic metabolites, DNA adduct formation, and generation of reactive oxygen species (ROS). Several chemotherapeutic agents have been shown to induce CYP1B1 in cardiovascular and cancer cells, possibly via activating the Aryl hydrocarbon Receptor (AhR), ROS generation, and inflammatory cytokines. Induction of CYP1B1 is detrimental in many ways. First, it can induce or exacerbate cancer treatment-induced cardiovascular complications. Second, it may lead to significant chemo/radio-resistance, undermining both the safety and effectiveness of cancer treatments. Therefore, numerous preclinical studies demonstrate that inhibition of CYP1B1 protects against chemotherapy-induced cardiotoxicity and prevents chemo- and radio-resistance. Most of these studies have utilized phytochemicals to inhibit CYP1B1. Since phytochemicals have multiple targets, future studies are needed to discern the specific contribution of CYP1B1 to the cardioprotective and chemo/radio-sensitizing effects of these phytochemicals.

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Exploring the bioactive ingredients of three traditional Chinese medicine formulas against age-related hearing loss through network pharmacology and experimental validation

Shi,

Zhao,

Gao

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Assessment of the Effectiveness of Quercetin on Cisplatin-Induced Ototoxicity in Rats

Cited by 10 publications

References 32 publications

Protective Effect of Carvacrol against Paclitaxel-Induced Ototoxicity in Rat Model

Protective Effect of Carvacrol against Paclitaxel-Induced Ototoxicity in Rat Model

CYP1B1 as a therapeutic target in cardio-oncology

Exploring the bioactive ingredients of three traditional Chinese medicine formulas against age-related hearing loss through network pharmacology and experimental validation

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