Ebselen attenuates cisplatin-induced ROS generation through Nrf2 activation in auditory cells

Kim, Se-Jin; Park, Channy; Han, A Lum; Youn, Myung-Ja; Lee, Jeong-Han; Kim, Yunha; Kim, Eun-Sook; Kim, Hyungjin; Kim, Jin‐Kyung; Lee, Ho-Kyun; Chung, Sung Tae; So, Hong-Seob; Park, Raekil

doi:10.1016/j.heares.2009.03.003

Cited by 99 publications

(76 citation statements)

References 39 publications

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“…Several studies reported that the hair cells were damaged by cisplatin in vitro. The concentrations ranged from 3.3 to 40 μmol/l in rat [12,21,22], and 13.3-26.6 μmol/l in mouse [13,23]. In these studies, severer ototoxicity induced by higher doses was noticed similarly to what was observed in this study when the concentration was less than 100 μmol/l.…”

Section: Discussionsupporting

confidence: 78%

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Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Zeng

Xianlin²,

Chen³

et al. 2016

ORL

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Aims: The purpose of this study was to investigate the characteristics of cisplatin-induced C57 mouse cochlear hair cell damage in vitro. Methods: Forty-seven cochleae harvested from 2- to 4-day-old C57 mice were used. Forty specimens were treated with different concentrations of cisplatin (10, 25, 50, 100, 400, and 1,000 μmol/l) for 48 h. The remaining seven specimens were used as a control group. Results: The rate of hair cell loss increased from 14.5 to 78.4% over cisplatin concentrations of 10 to 100 μmol/l, whereas hair cell loss decreased to 48.8 and 8.77% at concentrations of 400 and 1,000 μmol/l, respectively. Apoptosis was detected by DAPI staining in the areas of hair cell damage. Hair cell loss rates differed significantly among the cisplatin-treated groups. Linear regression analysis of cisplatin dose versus hair cell number showed a significant negative correlation for cisplatin doses up to 100 μmol/l and a positive correlation with further increases up to 1,000 μmol/l. Conclusions: We conclude that cisplatin-induced hair cell damage was concentration dependent only up to a certain dose and that injury resistance may occur in cochlear cells treated with higher doses of cisplatin.

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Section: Discussionsupporting

confidence: 78%

“…Similar results have been reported in some animal studies [12,13]. These studies support the idea of a dose-dependent pattern of cisplatin-mediated damage [2,11,12].…”

Section: Introductionsupporting

confidence: 91%

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Zeng

Xianlin²,

Chen³

et al. 2016

ORL

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“…Two of these agents, the antioxidants sodium thiosulfate and 4-methyl-thiobenzoic acid, are applied systemically [41]. Other agents interfere only with the ototoxicity of cisplatin, including Gingko biloba [42], ebselen (a synthetic compound with an activity similar to that of glutathione peroxidase) [43], and amifostine [24]. Other protective compounds, whose antineoplastic effects have not been evaluated, include metformin [3] and silymarin, a lipophilic extract derived from the plant Silybum marianum [23].…”

Section: Discussionmentioning

confidence: 99%

Effect of Remote Ischemic Preconditioning on Systemic Toxicity and Ototoxicity Induced by Cisplatin in Rats: Role of TNF-α and Nitric Oxide

Mjb

Ama²,

Ynf³

et al. 2017

ORL

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Background/Aims: Cisplatin is a chemotherapeutic agent. The use of remote ischemic preconditioning (RIPC) was proposed after the observation that ischemic preconditioning of a cardiac vascular area could protect another completely distinctly. Methods: This is an experimental study. Male Wistar rats were anesthetized, and they underwent a hearing evaluation via measurement of the brainstem auditory evoked potential (BSAEP). Then, cisplatin was administered intraperitoneally (IP) at a dose of 8 mg/kg/day for 4 consecutive days to group 1, whereas saline solution was administered IP to group 2. In groups 3 and 4, ischemia of the right hind paw was performed for 10 min, followed by reperfusion for 30 min, after which cisplatin or saline was administered IP to group 3 or group 4, respectively. Afterwards, all animals were evaluated via the BSAEP. The right cochlea was dissected for immunohistochemistry. Results: RIPC lowered the increase in BSAEP of the animals treated with cisplatin (p = 0.0146). Weight loss decreased in the animals subjected to RIPC (p < 0.005). In group 3, RIPC reversed immunostaining for tumor necrosis factor-α and inducible nitric oxide synthase in the stria vascularis injured by cisplatin (p < 0.05). Conclusion: RIPC protects against systemic toxicity and ototoxicity induced by cisplatin in rats.

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“…Although our present study did not determine the mechanism of protection by the organoselenium compounds against CEES toxicity, Kim et al (43) have suggested that EB-1 activates nuclear transcription via Nrf2. This in turn increases the expression of many phase II enzymes such as heme oxygenase (HO-1), NAD(P)H:quinone oxidoreductase, and gammaglutamylcysteine synthetase (gamma-GCS), which act against oxidants.…”

Section: Discussionmentioning

confidence: 58%

Ebselen Analogues Reduce 2-chloroethyl Ethyl Sulphide Toxicity in A-431 Cells

Pino

Pįętka-Ottlik

Billack

2013

Archives of Industrial Hygiene and Toxicology

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Vesicants are potent blistering agents. The prototype vesicant is sulphur mustard gas, fi rst used in World War I, which still has no effective antidote. We used a mustard gas surrogate 2-chloroethyl ethyl sulphide (CEES) to study the ability of resveratrol (RES) and pterostilbene (PTS), two well-established stilbene antioxidants, ebselen (EB-1), an organoselenium compound, and three EB-1 analogues (EB-2, EB-3, and EB-4) to reduce CEES toxicity in human epidermoid carcinoma cells (A-431). Following a 24-hour incubation of a toxic concentration of CEES (1000 μmol L ) did not decrease cell viability. Treatment with CEES and test antioxidants for 24 h showed that only EB-1 and its analogues EB-2, EB-3, and EB-4 but not the stilbene compounds could rescue the cells from death. EB-1 and EB-4 were the most effective at reducing CEES cytotoxicity and did so in a concentration-dependent manner, while EB-2 and EB-3 demonstrated the least protective effect. In summary, the data described herein indicate that organoselenium antioxidants, especially EB-4, may prove useful as countermeasures to blistering agents.

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Ebselen attenuates cisplatin-induced ROS generation through Nrf2 activation in auditory cells

Cited by 99 publications

References 39 publications

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Low, but Not High, Doses of Cisplatin Damage Cochlear Hair Cells in C57 Mouse Organotypic Cultures

Effect of Remote Ischemic Preconditioning on Systemic Toxicity and Ototoxicity Induced by Cisplatin in Rats: Role of TNF-α and Nitric Oxide

Ebselen Analogues Reduce 2-chloroethyl Ethyl Sulphide Toxicity in A-431 Cells

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