Prevention and Restoration of Hearing Loss Associated with the Use of Cisplatin

Chirteş, Felician; Albu, Silviu

doi:10.1155/2014/925485

Cited by 53 publications

(54 citation statements)

References 40 publications

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“…The cytokines involved in the lesion induced by cisplatin, such as TNF-α, IL-1, and iNOS, are affected by preconditioning, indicating a possible mode of action of RIPC. The decreased generation of ROS by RIPC can explain the decrease in cisplatin-induced cell damage in the DNA damage-independent pathway, and the main mechanism of action may be a decrease in oxidative stress [10]. We evaluated the BSAEP because this evaluation is easy to perform and has less variability and greater reproducibility than assessment of distortion product otoacoustic emissions [44], though many studies still use the latter method [45].…”

Section: Discussionmentioning

confidence: 99%

“…The protection against the ototoxic effects of cisplatin by RIPC in mice is related to the modulation of these cytokines, as shown in other organs [35]. Moreover, the production of ROS is essential in cisplatin-induced lesions [10] and is most likely decreased by RIPC, as demonstrated in other organs [46]. The effect of RIPC on cisplatin-induced ototoxicity in rats also depends on the modulation of other cytokines, such as iNOS.…”

Section: Discussionmentioning

confidence: 99%

“…The independent pathways are important in cochlear injury [9] and occur via formation of reactive oxygen species (ROS), depletion of the glutathione system, increase in lipid peroxidation, oxidative modification of proteins, and nitrosylation of cochlear proteins [10]. The cytokines involved in the formation of lesions induced by cisplatin are proinflammatory and include tumor necrosis factor-α (TNF-α) [11], interleukin (IL)-1β, and IL-6 [12].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…It is used clinically for head and neck, lung, bladder, cervical, ovarian, testicular, and gastrointestinal cancers as well as childhood cancers such as neuroblastoma and medulloblastoma [ 14 ]. One of its major side effects is irreversible sensorineural hearing loss that occurs with an average incidence of 62 % of patients treated with cisplatin [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Development of Cell-Based High-Throughput Chemical Screens for Protection Against Cisplatin-Induced Ototoxicity

Teitz

Goktug

Chen

et al. 2016

Methods in Molecular Biology

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Various compounds have been tested in recent years for protection against cisplatin-induced hearing loss, but no compound has yet been FDA approved for clinical use in patients. Towards this goal, we developed an unbiased, high-throughput, mammalian cochlear cell-based chemical screen that allowed quantification of the protection ability of bioactive compounds and ranked them for future testing ex vivo in cochlear explant cultures and in vivo in animal models. In our primary screens, protection in the HEI-OC1 organ of Corti immortalized cell line was measured by the ability of each compound to inhibit caspase-3/7 activity triggered by cisplatin treatment (50 μM cisplatin for 22 h). A total of 4385 unique bioactive compounds were tested in a single dose of 8 μM and promising compounds were validated by dose response curves covering ten, 1:3 serial diluted concentrations. Primary hits were defined as having more than 60 % inhibition of the caspase-3/7 activity. Toxicity of the top compounds was measured by a CellTiter-Glo (CTG) assay that measured the viability of the cells in the presence of compound alone in similar dose responsive analysis. A combination of the caspase-3/7 inhibition activity assay (as measured by IC50) and the CTG viability assay (as determined by LD50) identified the top protective compounds in the HEI-OC1 cells. In the future, the top hits in our screens will be tested for their protective ability ex vivo in mouse cochlear explants and in vivo in animal models. Our mammalian cochlear cell-based, high-throughput chemical screening assays described here can be further modified and represent an initial successful step towards therapeutic intervention of hearing disorders, an unmet medical need of our society.

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“…Recent strategies to avoid the ototoxic effect of cisplatin are mostly about ROS (Deavall et al 2012). Numerous studies have been conducted on prevention and restoration of the ototoxicity related to cisplatin (Chirtes & Albu 2014;Harrison et al 2015). These studies have suggested that antioxidants prevent ototoxicity.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of Pycnogenol on cisplatin-induced ototoxicity in rats

Eryılmaz

Eliyatkın

Demirci

et al. 2016

Pharmaceutical Biology

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Context: PycnogenolV R , which is French maritime pine bark extract, is a potent antioxidant. It is used in medical conditions caused by oxidative stress. Cisplatin (cis-diamminedichloroplatinum II) is an antineoplastic agent. However, its serious side effects such as ototoxicity limit its usage. Objective: Antioxidants can be used to prevent ototoxicity. We investigated the effect of Pycnogenol V R on cisplatin-induced ototoxicity. Materials and methods: Rats were randomly assigned to four groups of five. Distortion product-evoked otoacoustic emissions (DPOAE) test was performed for each rat. The experimental groups were as follows: Control Group, Pycnogenol V R Group: 10 mg/kg Pycnogenol V R intraperitoneally for 7 days, Cisplatin Group: intraperitoneally 15 mg/kg single injection of cisplatin on the fifth day, Cisplatin þ Pycnogenol V R Group: intraperitoneally 10 mg/kg Pycnogenol V R treatment for 7 days, additionally on the fifth day, 15 mg/kg single injection of cisplatin was given. On the eighth day, DPOAE was re-performed and rats were sacrificed. Apoptosis was evaluated histopathologically. Results: Mean percentage of apoptotic cells was 1.5, 3, 30 and 11% in organ of Corti and 2, 2, 40, 15% in spiral ganglion neurons in Control Group, Pycnogenol V R Group, Cisplatin Group and Cisplatin þ Pycnogenol V R Group, respectively. Cisplatin Group and Cisplatin þ Pycnogenol V R Group were significantly different when compared to Control Group histopathologically both in organ of Corti and spiral ganglion neuron (p <0.001, p ¼ 0.019, p ¼ 0.001, p ¼ 0.015). DPOAE results showed that Cisplatin þ Pycnogenol V R Group was significantly different when compared to Cisplatin Group at 3, 6 and 8 kHz (p < 0.05). Conclusion: Pycnogenol protected against cisplatin ototoxicity. Also, pycnogenol is not ototoxic. ARTICLE HISTORY

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Prevention and Restoration of Hearing Loss Associated with the Use of Cisplatin

Cited by 53 publications

References 40 publications

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

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

Development of Cell-Based High-Throughput Chemical Screens for Protection Against Cisplatin-Induced Ototoxicity

Protective effect of Pycnogenol on cisplatin-induced ototoxicity in rats

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