Glutathione-dependent antioxidant systems in the mammalian inner ear: effects of aging, ototoxic drugs and noise

Lautermann, J.; Crann, Sherry A.; McLaren, James; Schacht, Jochen

doi:10.1016/s0378-5955(97)00154-8

Cited by 116 publications

(75 citation statements)

References 44 publications

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“…It is well known that glutathione and glutathione-related enzymes protect against oxidative cell injury caused by free radicals. Specific changes in glutathione levels and enzymes in glutathione metabolism have been found with cisplatin treatment [14] . These findings are in agreement with the proposed mechanism of action based on oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Instability Due to Drug-Induced Vestibulotoxicity

Sánchez-Sellero

Soto-Varela²

2016

Int Adv Otol

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OBJECTIVE:The therapeutic use of ototoxic drugs is relatively common, particularly in patients with severe diseases. It is likely that disturbances of balance in these patients are underestimated by clinicians. MATERIALS and METHODS:The purpose of this study was to identify drugs involved in the vestibulotoxic origin of instability in a group of 18 patients. RESULTS:Six patients showed both cochlear and vestibular damage, while 12 were affected only by posterior labyrinthine damage. Four groups of drugs were identified: antibiotics (nine patients), cytostatics (four), anti-tuberculosis medicinal products (three), and other drugs (two). Cytostatics were involved in many cases studied, a fact scarcely reported before. CONCLUSION:It is important to ensure an early diagnosis to prevent ototoxic effects induced by drugs. We propose that patients receiving potential ototoxic drugs undergo cochlear and vestibular assessments. Further, we recommend that patients with instability undergo vestibular rehabilitation.

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Section: Discussionmentioning

confidence: 99%

Instability Due to Drug-Induced Vestibulotoxicity

Sánchez-Sellero

Soto-Varela²

2016

Int Adv Otol

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“…Insults such as neurotrophin withdrawal, ototoxin exposure, and hypoxia/ischemia lead to oxidative stress, which then leads to apoptosis [Lautermann et al, 1997]. Reactive oxygen species (ROS) including free radicals are formed as by-products of several metabolic pathways and these molecules can themselves cause cell damage by reacting with cellular proteins, lipids and DNA.…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Mechanisms of Cell Death in the Injured Auditory System: Otoprotective Strategies

et al. 2002

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Oxidative stress insults such as neurotrophin withdrawal, sound trauma, hypoxia/ischemia, ototoxic antibiotics, and chemotherapeutic agents have been shown to induce apoptosis of both auditory hair cells and neurons. In this paper, we review some components of the apoptotic pathways leading to the death of hair cells and auditory induced by growth factor withdrawal or cisplatin intoxication: (1) reactive oxygen species and free radicals are formed as by-products of several metabolic pathways and these molecules can themselves cause cell damage by reacting with cellular proteins; (2) activation of caspases, and (3) activation of calpain. These mechanisms have several different points at which inhibitors could be targeted to protect cells from programmed cell death, including the prevention of oxidative stress-induced apoptosis and the activation of caspases and calpains.

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“…PBN is able to form adducts with ROS thereby reducing the likelihood of oxidative stress. The role of oxidative stress in cochlear injury has also been underscored as a consequence of aminoglycoside antibiotic (Garetz et al 1994;Hester et al 1998;Lautermann et al 1997) and cisplatin (Rybak et al 1995Campbell et al 1996Campbell et al , 1999Kopke et al 1997;Dehne et al 2001). Both of these agents are widely recognized as promoting NIHL (e.g., Bone and Ryan 1978;Brown et al 1980;Bhattacharyya and Dayal 1991;Gratton et al 1990).…”

Section: Introductionmentioning

confidence: 99%

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

Fechter

Gearhart

Shirwany

2004

JARO - Journal of the Association for Research in Otolaryngolog

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Acrylonitrile, one of the 50 most commonly produced industrial chemicals, has recently been identified as a promoter of noise-induced hearing loss (NIHL). This agent has the potential to produce oxidative stress through multiple pathways. We hypothesize that acrylonitrile potentiates NIHL as a consequence of oxidative stress. The objectives of this study were to characterize acrylonitrile exposure conditions that promote permanent NIHL in rats and determine the ability of this nitrile to produce auditory dysfunction by itself. Additionally, we sought to determine whether a spin-trap agent that can form adducts with ROS would protect against the effects of acrylonitrile. Acrylonitrile administration produced significant elevation in NIHL detected as a loss in compound action potential sensitivity. The effect was particularly robust for high-frequency tones and particularly when acrylonitrile and noise were given on repeated occasions. Acrylonitrile by itself did not disrupt threshold sensitivity. Administration of the spin-trap agent phenyl-N-tert-butylnitrone (PBN), given to rats prior to acrylonitrile and noise, did block the elevation of NIHL by acrylonitrile. However, PBN at the dose and time interval given was ineffective in protecting auditory function in subjects exposed to noise alone. The results suggest that oxidative stress may play a role in the promotion of NIHL by acrylonitrile.

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Glutathione-dependent antioxidant systems in the mammalian inner ear: effects of aging, ototoxic drugs and noise

Cited by 116 publications

References 44 publications

Instability Due to Drug-Induced Vestibulotoxicity

Instability Due to Drug-Induced Vestibulotoxicity

Mechanisms of Cell Death in the Injured Auditory System: Otoprotective Strategies

Acrylonitrile Potentiates Noise-Induced Hearing Loss in Rat

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