Prevention of noise- and drug-induced hearing loss with d-methionine

Campbell, Kathleen C.M.; Meech, Robert P.; Klemens, James J.; Gerberi, Michael T.; Dyrstad, Sara S.W.; Larsen, Deb L.; Mitchell, Diana; El-Azizi, Mohammed; Verhulst, Steven J.; Hughes, Larry F.

doi:10.1016/j.heares.2006.11.012

Cited by 195 publications

(176 citation statements)

References 56 publications

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“…D-Met has been shown to prevent or ameliorate peripheral cisplatininduced hearing threshold shifts, outer hair cell loss, loss of hair cell function, loss of spiral ganglion cell neurons, and damage to the stria vascularis in animals (Campbell et al, 1996(Campbell et al, , 1999(Campbell et al, , 2007Gabaizadeh et al, 1997;Wimmer et al, 2004). However, to our knowledge, this investigation is the first evidence of direct cisplatin damage to the cortical neurons, in vitro, and the amelioration of this damage by an over-thecounter supplement -D-Met.…”

Section: Discussionmentioning

confidence: 70%

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d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

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Cisplatin is a platinum-based chemotherapeutic agent widely used for the treatment of various types of cancer. Patients undergoing cisplatin treatment often suffer from a condition known as "chemobrain", ototoxicity, peripheral neuropathy, weight loss, nausea, vomiting, nephrotoxicity, seizures, hearing loss and tinnitus.D-Methionine (D-Met), a sulfur-containing nucleophilic antioxidant, has been shown to prevent cisplatininduced side effects in animals without antitumor interference. In this study, we have used an in vitro model of cortical networks (CNs), enriched in auditory cortex cells; to quantify cisplatin neurotoxicity and the protective effects of D-Met. Dissociated neurons from auditory cortices of mouse embryos were grown on microelectrode arrays with 64 transparent indium-tin oxide electrodes, which enabled continuous optical and electrophysiological monitoring of network neurons. Cisplatin at 0.10-0.25 mM induced up to a 200% increase in spontaneous spiking activity, while concentrations at or above 0.5 mM caused irreversible loss of neuronal activity, accompanied by cell death. Pretreatment with D-Met, at a concentration of 1.0 mM, prevented the cisplatin-induced excitation at 0.10-0.25 mM, caused sustained excitation without occurrence of cell death at 0.5 mM, and delayed cell death at 0.75 mM cisplatin. L-Methionine, the optical isomer, showed lower potency and less efficacy than D-Met, was less protective against 0.1 mM cisplatin, and proved ineffective at a concentration of 0.5 mM cisplatin. Pre-exposure time of D-Met was associated with the protective effects at 0.1 and 0.5 mM cisplatin, with longer pre-exposure times exhibiting better protection. This study quantifies as a function of concentration and time that D-Met protects central nervous system tissue from acute cisplatin toxicity.

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Section: Discussionmentioning

confidence: 70%

“…D-Met, which can effectively be delivered orally (Campbell et al, 2007) can presumably help circumvent the deleterious effects of cisplatin treatment if taken at an optimal period of time. It is possible that the required pretreatment time for patients in vivo will be longer than what is observed in cell culture.…”

Section: Discussionmentioning

confidence: 99%

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Gopal

Shrestha

et al. 2012

Neurotoxicology and Teratology

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“…In addition, some otoprotectants may be able to rescue damaged cells once injury has occurred, thereby minimizing hearing loss. There have been numerous studies of various compounds used to protect hearing loss, ranging from antioxidants that scavenge free radicals to agents that increase blood flow and drugs that block cell-death-pathway signaling factors [69][70][71]. Despite the potential these investigations bring for protection from hearing damage, the translation of animal studies of otoprotectants to clinical treatment has been limited.…”

Section: Preventionmentioning

confidence: 99%

Auditory and vestibular dysfunction associated with blast-related traumatic brain injury

Fausti¹,

Wilmington²,

Gallun³

et al. 2009

JRRD

186

117

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Abstract-The dramatic escalation of blast exposure in military deployments has created an unprecedented amount of traumatic brain injury (TBI) and associated auditory impairment. Auditory dysfunction has become the most prevalent individual service-connected disability, with compensation totaling more than 1 billion dollars annually. Impairment due to blast can include peripheral hearing loss, central auditory processing deficits, vestibular impairment, and tinnitus. These deficits are particularly challenging in the TBI population, as symptoms can be mistaken for posttraumatic stress disorder, mentalhealth issues, and cognitive deficits. In addition, comorbid factors such as attention, cognition, neuronal loss, noise toxicity, etc., can confound assessment, causing misdiagnosis. Furthermore, some auditory impairments, such as sensorineural hearing loss, will continue to progress with age, unlike many other injuries. In the TBI population, significant clinical challenges are the accurate differentiation of auditory and vestibular impairments from multiple, many times overlapping, symptoms and the development of multidisciplinary rehabilitation strategies to improve treatment outcomes and quality of life for these patients.

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“…While many drugs have been demonstrated to successfully protect hair cells against damage (e.g., antioxidants, caspase inhibitors, Stat-1, etc. ; Matsui et al 2002;Wang et al 2003Wang et al , 2004Sha et al 2006;Campbell et al 2007;Schmitt et al 2009), there is currently no FDA-approved drug used for the prevention of hearing loss. Aspirin was demonstrated to protect against aminoglycoside-induced hair cell death (Sha et al 2006), but required high daily doses (3 g/day).…”

Section: Introductionmentioning

confidence: 99%

Quinoline Ring Derivatives Protect Against Aminoglycoside-Induced Hair Cell Death in the Zebrafish Lateral Line

Keating

et al. 2012

JARO

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We have previously published results from a screen of 1,040 FDA-approved drugs and bioactives (NINDS Custom Collection) for drugs that protect against neomycin-induced hair cell death (Ou et al., J Assoc Res Otolaryngol 10:191-203, 2009). Further evaluation of this drug library identified eight protective drugs that shared a common quinoline scaffold. These drugs were tested further in terms of their protection against other aminoglycosides, as well as their effect on aminoglycoside uptake. All of the eight quinolines that protected against neomycin were found to protect against shortand long-term gentamicin damage protocols. We then tested the structurally related compounds quinoline, isoquinoline, naphthalene, and indole for protective effects. Of these compounds, indole demonstrated a small but significant amount of protection against neomycin, while quinoline and isoquinoline partially protected against long-term gentamicin damage. We examined whether the protective activity of this group of compounds was related to known targets of the quinoline derivatives. The protective effects did not seem linked to either the cholinergic or histaminergic pathways that are regulated by some members of the quinoline family. However, all eight protective drugs were found to reduce the uptake of aminoglycosides into hair cells. Subsequent experiments suggest that reduction of uptake is the primary mechanism of protection among the quinoline drugs.

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Prevention of noise- and drug-induced hearing loss with d-methionine

Cited by 195 publications

References 56 publications

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

d-Methionine protects against cisplatin-induced neurotoxicity in cortical networks

Auditory and vestibular dysfunction associated with blast-related traumatic brain injury

Quinoline Ring Derivatives Protect Against Aminoglycoside-Induced Hair Cell Death in the Zebrafish Lateral Line

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