Interaction of kanamycin and noise exposure

Gannon, R. P.; Tso, S. S.; Chung, David Y.

doi:10.1017/s0022215100087119

Cited by 20 publications

(15 citation statements)

References 10 publications

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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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Section: Introductionmentioning

confidence: 79%

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Wang

Steyger

2011

PLoS ONE

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“…However, synergism did occur if the noise was introduced within 20 days after the cessation of drug use 42. Collins (1988) also reported mild drug-then-noise synergism with 10 days in between insults.…”

Section: Aminoglycosides and Noisementioning

confidence: 98%

“…Potentiation of aminoglycoside-induced ototoxicity by concurrent exposure to noise has been investigated since the 1960's when animals receiving aminoglycosides appeared to be more susceptible to noise-induced hearing loss 41 and reported conclusively by Gannon and Tso in 1969 and in subsequent animal studies 42,43. 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.…”

Section: Aminoglycosides and Noisementioning

confidence: 99%

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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“…There appears to be injurious synergy when noise is combined with ototoxic medications. Animal studies have demonstrated this effect with kanamycin [72,73], but this has not been substantiated in children when evaluated in two studies [74,75]. While there appears to be no demonstrated synergistic interaction between noise and loop‐inhibiting diuretics [76], there does appear to be some synergistic interaction between the carboplatinum agents and noise.…”

Section: Synergism With Noise and Other Ototoxic Agentsmentioning

confidence: 99%

Noise in the Pediatric Intensive Care Unit

Berens¹

1999

J Intensive Care Med

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The pediatric intensive care unit is an environment filled with dedicated caregivers, state‐of‐the‐art monitors, and machines that collectively work to provide the best care possible for critically ill children. A previously unappreciated result of having these resources mingled together is the elevated level of environmental noise. Although the levels of noise do not reach OSHA levels (>85 dB for 8 continuous hours) that cause noise‐induced hearing loss, the patients are exposed to continuous moderate noise levels that may cause hearing impairment if mixed with other ototoxic agents. In addition, these noise exposures may result in abnormalities in the stress response as well as in sleep patterns. This article reviews the physiology of hearing, the consequences of noise pollution as it relates to pediatric patients, and preventive measures used to reduce noise pollution in a pediatric intensive care setting. Considerations for further research efforts are also discussed.

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Interaction of kanamycin and noise exposure

Cited by 20 publications

References 10 publications

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Acoustic Trauma Increases Cochlear and Hair Cell Uptake of Gentamicin

Synergistic ototoxicity due to noise exposure and aminoglycoside antibiotics

Noise in the Pediatric Intensive Care Unit

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