Cisplatin Ototoxicity and Protection: Clinical and Experimental Studies

Rybak, Leonard P.; Mukherjea, Debashree; Jajoo, Sarvesh; Ramkumar, Vickram

doi:10.1620/tjem.219.177

Cited by 306 publications

(244 citation statements)

References 91 publications

(102 reference statements)

Supporting

Mentioning

238

Contrasting

Unclassified

Order By: Relevance

“…These events can cause apoptosis and consequently to a decrease the cochlear cells of the inner ear [2][3][4][5].…”

Section: Discussionmentioning

confidence: 99%

“…Cisplatin progressively destroys outer hair cells, from the base to the apex and ototoxicity may occur within hours. Hearing loss appears to be bilateral, usually permanent, dose-related, and initially at higher frequencies [2]. Recently it was reported that an increase in hearing thresholds may occur in up to 75-100 % of patients [22].…”

Section: Discussionmentioning

confidence: 99%

“…Although cisplatin treatment is highly effective, significant adverse effects appear such as vomiting, nausea, bone marrow depression, nephrotoxicity, hepatotoxicity, and ototoxicity [2].…”

Section: Introductionmentioning

confidence: 99%

“…The suggested mechanism of ototoxicity is the production of reactive oxygen species (ROS) that main cause of cell injury or death [2,3]. Cisplatin administration also decreases antioxidant enzymes in the cochlea [4].…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The Protective Role of Molsidomine on the Cisplatin-Induced Ototoxicity

Toplu

Parlakpınar

Sapmaz

et al. 2014

Indian J Otolaryngol Head Neck Surg

View full text Add to dashboard Cite

This experimental study was designed to investigate the protective effects of molsidomine (MOL) on against cisplatin-induced ototoxicity (CIO). To examine this effect, distortion product otoacoustic emissions (DPOAEs) measurements and serum levels of oxidative and antioxidant status [including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPX), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI)] were evaluated. Thirty-two female wistar albino rats were divided into four groups including; control (Group K), cisplatin (Group C), cisplatin plus MOL group (Group CM), and MOL group (Group M). DPOAEs measurements between 0.9961 and 8.0003 Hz as DP-gram and input/output (I/O) functions were performed in the same (left) ear of all rats on days 0, 1st, 5th and 12th. Prior to death, the last DPOAEs measurements and blood samples were taken. In the C group, statistically significant DPOAE amplitude reductions were detected at 2. 5195, 3.1758, 3.9961, 5.0391, 6.3516 and 8.0039 Hz frequencies (p \ 0.05) between 0th and 1st, 0th and 5th and 0th and 12th days' measurements (p \ 0.05). Serum level of MDA, TAC and OSI levels were significantly higher in the C group versus K group (p \ 0.05). In the CM group, there were no significant differences at all frequencies between 0th and other days' measurements (p [ 0.05) and the serum levels of all biochemical parameters were shifted toward normal values, similar to the K group (p \ 0.05). No significant differences were detected in the either M or K group's measurements. According to these results, cisplatin-related ototoxicity has been significantly prevented by MOL.

show abstract

“…These events can cause apoptosis and consequently to a decrease the cochlear cells of the inner ear [2][3][4][5].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Although cisplatin treatment is highly effective, significant adverse effects appear such as vomiting, nausea, bone marrow depression, nephrotoxicity, hepatotoxicity, and ototoxicity [2].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Protective Role of Molsidomine on the Cisplatin-Induced Ototoxicity

Toplu

Parlakpınar

Sapmaz

et al. 2014

Indian J Otolaryngol Head Neck Surg

View full text Add to dashboard Cite

show abstract

“…Several lines of evidence suggest that the generation of reactive oxygen species (ROS) are involved in the toxicity associated with cisplatin therapy 18 . ROSmediated damage occurs as a consequence of antioxidant depletion and increased lipid peroxidation in the cochlea.…”

Section: Mechanisms Influencing Outcomesmentioning

confidence: 99%

Clinical Practice Recommendations for the Management and Prevention of Cisplatin-Induced Hearing Loss Using Pharmacogenetic Markers

Lee

Pussegoda

Rassekh

et al. 2016

Therapeutic Drug Monitoring

View full text Add to dashboard Cite

Abstract:Currently no pharmacogenomics-based criteria exist to guide clinicians in identifying individuals who are at risk of hearing loss from cisplatin-based chemotherapy. This review summarizes findings from pharmacogenomic studies that report genetic polymorphisms associated with cisplatin-induced hearing loss and aims to (1) provide up-to-date information on new developments in the field; (2) provide recommendations for the use of pharmacogenetic testing in the prevention, assessment and management of cisplatin-induced hearing loss in children and adults; and (3) identify knowledge gaps to direct and prioritize future research. These practice recommendations for pharmacogenetic testing in the context of cisplatin-induced hearing loss reflect a review and evaluation of recent literature and are designed to assist clinicians in providing optimal clinical care for patients receiving cisplatin based chemotherapy.

show abstract