Time sequence of degeneration pattern in the guinea pig cochlea during cisplatin administration.

Ruijven, Marjolein W.M. van; Groot, John C.M.J. de; Smoorenburg, Guido F.

doi:10.1016/j.heares.2004.07.014

Cited by 81 publications

(47 citation statements)

References 50 publications

(93 reference statements)

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“…Low-dose, long-term exposure (1.5-2 mg/kg, daily) resulted in a loss of outer hair cells and shrinkage of the spiral ganglion cells with (Tange and Vuzevski, 1984) or without degeneration of strial marginal cells (van Ruijven et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

High Accumulation of Platinum-DNA Adducts in Strial Marginal Cells of the Cochlea Is an Early Event in Cisplatin but Not Carboplatin Ototoxicity

Thomas

Lautermann²,

Liedert³

et al. 2006

Mol Pharmacol

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Ototoxicity is a typical dose-limiting side effect of cancer chemotherapy with cisplatin but much less so with carboplatin. To elucidate the underlying molecular pathological mechanisms, we have measured the formation and persistence of druginduced DNA adducts in the nuclei of inner ear cells of guinea pigs after short-term exposure to either cisplatin or carboplatin using immunofluorescence staining and quantitative image analysis. After application of carboplatin, all cells of the cochlea exhibited a similar burden of guanine-guanine intrastrand cross-links in DNA. In contrast, we observed a pronounced 3-to 5-fold accumulation of this cytotoxic adduct exclusively in the marginal cells of the stria vascularis between 8 and 48 h after treatment with cisplatin. In the kidney, the other critical target tissue of cisplatin toxicity, a similar high preferential formation of cytotoxic DNA adducts was measured in the tubular epithelial cells but not in other renal cell types. As for the ear, this excessive formation of DNA damage in a particular cell type was seen in animals treated with cisplatin but not those treated with carboplatin. Because cisplatin ototoxicity is often attributed to oxidative stress mediated by the generation of radical oxygen species (ROS), we have measured in parallel the levels of the lead DNA oxidation product 8-oxoguanine (8-oxoG) in cochlear cryosections. Compared with basal levels in untreated control cochleas, no additional formation of 8-oxoG was detectable up to 48 h after cisplatin treatment in the DNA of either inner-ear cell type. This suggests that the generation of ROS may be a secondary event in cisplatin ototoxicity.Platinum derivatives are frequently used in cancer chemotherapy for patients with malignancies of, for example, the urogenital tract, the lung, the colon, the stomach, or the head and neck region. It is widely accepted that the antineoplastic efficiency of cisplatin [cis-diamminedichloroplatinum (II)] as well as carboplatin (diammine-cyclobutane-dicarboxylatoplatinum) results from their interaction with the nuclear DNA of tumor cells (reviewed in Siddik, 2003). The drugs harboring two reactive groups initially induce monoadducts at nucleophilic sites (e.g., of guanine or adenine) and can lead subsequently to intra-and interstrand cross-links in the DNA. Once formed, these lesions can trigger apoptotic cascades (McKeage, 1995;Boulikas and Vougiouka, 2003) predominantly via the mitochondrial pathway (McDonald and Windebank, 2002;Lee et al., 2004). The vital role of DNA adducts in this process is confirmed by observations in human cells differing in their ability to repair drug-induced damage to their genome. Cells with impaired nucleotide excision repair functions are clearly more sensitive to cisplatin than their proficient counterparts (Furuta et al., 2002;Wu et al., 2003).On the other hand, the frequently dose limiting side effects of cisplatin on normal cells and tissues (e.g., in the inner ear and the kidney) were mainly ascribed until now to pathways not ...

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Section: Discussionmentioning

confidence: 99%

High Accumulation of Platinum-DNA Adducts in Strial Marginal Cells of the Cochlea Is an Early Event in Cisplatin but Not Carboplatin Ototoxicity

Thomas

Lautermann²,

Liedert³

et al. 2006

Mol Pharmacol

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“…Cochleas were processed as described in detail by De Groot et al (1987). Cochleas were embedded in toto in Spurr's low-viscosity resin and divided into two halves along a standardized midmodiolar plane (Van Ruijven et al, 2004). Semithin (1 lm) sections were stained with methylene blue and azur II in sodium tetraborate and examined with a Zeiss Axiophot light microscope.…”

Section: Histologymentioning

confidence: 99%

“…The number of inner hair cells (IHCs) and outer hair cells (OHCs) was counted in each individual transection of the respective half-turn (b1, b2, m1, m2, a1, a2, a3; see Fig. 6A), as described in Van Ruijven et al (2004). Digitized light-microscopical images of the spiral ganglia from each individual transection were analysed using the software program NIH Image, version 1.63 (http:// www.rsb.info.nih.gov/nih-image).…”

Section: Histologymentioning

confidence: 99%

Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

et al. 2007

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In animal models of deafness, administration of an aminoglycoside in combination with a loop diuretic is often applied to produce a rapid loss of cochlear hair cells. However, the extent to which surviving hair cells remain functional after such a deafening procedure varies. In a longitudinal electrocochleographical study, we investigated the variability of cochlear function between and within guinea pigs after combined administration of kanamycin and furosemide. Concurrently, histological data were obtained at 1, 2, 4 and 8 weeks after deafening treatment. The main measures in our study were compound action potential (CAP) thresholds, percentage of surviving hair cells and packing density of spiral ganglion cells (SGCs). One day after deafening treatment, we found threshold shifts widely varying among animals from 0 to 100 dB. The variability decreased after 2 days, and in 18 out of 20 animals threshold shifts greater than 55 dB were found 4-7 days after deafening. Remarkably, in the majority of animals, thresholds decreased by up to 25 dB after 7 days indicating functional recovery. As expected, final thresholds were negatively correlated to the percentage of surviving hair cells. Notably, the percentage of surviving hair cells might be predicted on the basis of thresholds observed one day after deafening. SGC packing density, which rapidly decreased with the period after deafening treatment and correlated to the percentage of surviving inner hair cells, was not a determining factor for the CAP thresholds.

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“…The increase in ROS has been reported to lead to morphological and functional changes in the organ of Corti 19 . The production of ROS changes acoustic transduction by modulating the outer hair cell motility in the organ of Corti resulting in cell death 20 .…”

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

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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.

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Time sequence of degeneration pattern in the guinea pig cochlea during cisplatin administration.

Cited by 81 publications

References 50 publications

High Accumulation of Platinum-DNA Adducts in Strial Marginal Cells of the Cochlea Is an Early Event in Cisplatin but Not Carboplatin Ototoxicity

High Accumulation of Platinum-DNA Adducts in Strial Marginal Cells of the Cochlea Is an Early Event in Cisplatin but Not Carboplatin Ototoxicity

Time course of cochlear electrophysiology and morphology after combined administration of kanamycin and furosemide

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

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