The Potentiation of Noise‐Induced Hearing Loss by Neomycin

Vernon, J; Brown, Jeffrey J.; Meikle, Mary B.; Re, Brummett

doi:10.1177/019459987808600129

Cited by 7 publications

(8 citation statements)

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“…These observations were confirmed by Jack Vernon's group who reported a very prominent synergistic effect of noise and neomycin in the guinea pig 44,45. The well-controlled experiment included conditions of 1) high intensity noise alone (115 dB SPL, 10 hours), 2) 200 mg/kg/day neomycin with low intensity noise (45 dB SPL), and 3) neomycin with high intensity noise.…”

Section: Aminoglycosides and Noisesupporting

confidence: 52%

Synergistic ototoxicity due to noise exposure and aminoglycoside antibiotics

Steyger

2009

Noise Health

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Acoustic exposure to high intensity and/or prolonged noise causes temporary or permanent threshold shifts in auditory perception, reflected by reversible or irreversible damage in the cochlea. Aminoglycoside antibiotics, used for treating or preventing life-threatening bacterial infections, also induce cytotoxicity in the cochlea. Combined noise and aminoglycoside exposure, particularly in neonatal intensive care units, can lead to auditory threshold shifts greater than simple summation of the two insults. The synergistic toxicity of acoustic exposure and aminoglycoside antibiotics is not limited to simultaneous exposures. Prior acoustic insult which does not result in permanent threshold shifts potentiates aminoglycoside ototoxicity. In addition, exposure to sub-damaging doses of aminoglycosides aggravates noise-induced cochlear damage. The mechanisms by which aminoglycosides cause auditory dysfunction are still being unraveled, but likely include the following: 1) penetration into the endolymphatic fluid of the scala media, 2) permeation of non-selective cation channels on the apical surface of hair cells and 3) generation of toxic reactive oxygen species and interference with other cellular pathways. Here we discuss the synergistic effect of combined noise and aminoglycoside exposure to identify pivotal synergistic events that can potentiate ototoxicity, in addition to a current understanding of aminoglycoside trafficking within the cochlea. Preventing the ototoxic synergy of noise and aminoglycosides is best achieved by using non-ototoxic bactericidal drugs, and by attenuating perceived noise intensity when life-saving aminoglycoside therapy is required.

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Section: Aminoglycosides and Noisesupporting

confidence: 52%

Synergistic ototoxicity due to noise exposure and aminoglycoside antibiotics

Steyger

2009

Noise Health

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“…This was first observed in the 1960s when animals receiving aminoglycosides appeared to be more susceptible to noise-induced hearing loss [11] and confirmed by subsequent studies [12], [13], [14], [15]. The same ototoxic mechanism is likely responsible for the increased deafness risk in pre-term infants from neonatal intensive care units [16], [17] and in wounded soldiers [18], [19], [20], [21], [22].…”

Section: Introductionmentioning

confidence: 79%

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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BackgroundExposure to intense sound or high doses of aminoglycoside antibiotics can increase hearing thresholds, induce cochlear dysfunction, disrupt hair cell morphology and promote hair cell death, leading to permanent hearing loss. When the two insults are combined, synergistic ototoxicity occurs, exacerbating cochlear vulnerability to sound exposure. The underlying mechanism of this synergism remains unknown. In this study, we tested the hypothesis that sound exposure enhances the intra-cochlear trafficking of aminoglycosides, such as gentamicin, leading to increased hair cell uptake of aminoglycosides and subsequent ototoxicity.MethodsJuvenile C57Bl/6 mice were exposed to moderate or intense sound levels, while fluorescently-conjugated or native gentamicin was administered concurrently or following sound exposure. Drug uptake was then examined in cochlear tissues by confocal microscopy.ResultsProlonged sound exposure that induced temporary threshold shifts increased gentamicin uptake by cochlear hair cells, and increased gentamicin permeation across the strial blood-labyrinth barrier. Enhanced intra-cochlear trafficking and hair cell uptake of gentamicin also occurred when prolonged sound, and subsequent aminoglycoside exposure were temporally separated, confirming previous observations. Acute, concurrent sound exposure did not increase cochlear uptake of aminoglycosides.ConclusionsProlonged, moderate sound exposures enhanced intra-cochlear aminoglycoside trafficking into the stria vascularis and hair cells. Changes in strial and/or hair cell physiology and integrity due to acoustic overstimulation could increase hair cell uptake of gentamicin, and may represent one mechanism of synergistic ototoxicity.

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“…28,29 Potentiation of aminoglycoside-induced ototoxicity by simultaneous exposure to noise has been occasionally investigated since it was first described by Gannon and Tso in 1969 and confirmed in subsequent animal studies. [30][31][32][33][34][35][36][37][38] Interestingly, noise exposure followed by aminoglycoside treatment also induced enhanced auditory dysfunction, but this was not observed for aminoglycoside treatment followed by noise exposure. 31,32,35 These studies are clinically relevant because aminoglycosides are systemically administered for prophylaxis to casualties with blast and gunshot wounds during medical evacuation from battlefields and relocation to major medical centers.…”

Section: Synergism Between Noise and Clinical Drugsmentioning

confidence: 95%

“…Thus, short-term exposure to moderate levels of noise (i.e., > 80 dBA) potentiates the ototoxic effects of aminoglycosides, and this potentiation is greater than additive, 43 corroborating conclusions derived from a variety of animal studies that noise potentiates aminoglycoside-induced ototoxicity. [30][31][32][33][34][35][36][37][38] In contrast, exposure to noise in the absence of aminoglycosides did not generally cause hearing loss, unless noise levels themselves were ototoxic.…”

Section: Synergism Between Noise and Clinical Drugsmentioning

confidence: 97%

Potentiation of Chemical Ototoxicity by Noise

Steyger¹

2009

Semin Hear

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High-intensity and/or prolonged exposure to noise causes temporary or permanent threshold shifts in auditory perception. Occupational exposure to solvents or administration of clinically important drugs, such as aminoglycoside antibiotics and cisplatin, also can induce permanent hearing loss. The mechanisms by which these ototoxic insults cause auditory dysfunction are still being unraveled, yet they share common sequelae, particularly generation of reactive oxygen species, that ultimately lead to hearing loss and deafness. Individuals are frequently exposed to ototoxic chemical contaminants (e.g., fuel) and noise simultaneously in a variety of work and recreational environments. Does simultaneous exposure to chemical ototoxins and noise potentiate auditory dysfunction? Exposure to solvent vapor in noisy environments potentiates the permanent threshold shifts induced by noise alone. Moderate noise levels potentiate both aminoglycoside- and cisplatin-induced ototoxicity in both rate of onset and in severity of auditory dysfunction. Thus, simultaneous exposure to chemical ototoxins and moderate levels of noise can potentiate auditory dysfunction. Preventing the ototoxic synergy of noise and chemical ototoxins requires removing exposure to ototoxins and/or attenuating noise exposure levels when chemical ototoxins are present.

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The Potentiation of Noise‐Induced Hearing Loss by Neomycin

Cited by 7 publications

References 0 publications

Synergistic ototoxicity due to noise exposure and aminoglycoside antibiotics

Synergistic ototoxicity due to noise exposure and aminoglycoside antibiotics

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Potentiation of Chemical Ototoxicity by Noise

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