Elsevier

Neuroscience

Volume 134, Issue 2, 2005, Pages 633-642
Neuroscience

Sensory systems
Post-exposure treatment attenuates noise-induced hearing loss

https://doi.org/10.1016/j.neuroscience.2005.04.015Get rights and content

Abstract

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are involved in sensory cell and neural death in the peripheral nervous system, including damage induced by noise trauma. Antioxidant administration prior to or concomitant with noise exposure can prevent auditory deficits, but the efficacy of a delayed treatment is not known. We have recently found continued reactive oxygen species/reactive nitrogen species formation in the ear for 7–10 days following noise exposure and reasoned that antioxidant intervention during this period should also reduce noise-induced hearing loss.

Guinea-pigs were subjected to 4 kHz octave band noise at 120 decibels sound- pressure-level (dB SPL) for 5 hours and received treatment with ROS and RNS scavengers (salicylate and trolox) beginning 3 days prior, 1 hour, 1, 3, or 5 days after noise exposure. Auditory thresholds were assessed by sound-evoked auditory brainstem response at 4, 8, and 16 kHz, before and 10 days after noise exposure. Hair cell damage was analyzed by quantitative histology, and free radical activity was determined immunohistochemically via 4-hydroxynonenal and nitrotyrosine as markers of reactive oxygen species and reactive nitrogen species action. Delivered up to 3 days after noise exposure, salicylate and trolox significantly reduced auditory brainstem response deficits, reduced hair cell damage, and decreased reactive oxygen species and reactive nitrogen species formation. Earlier drug treatment was more effective than later treatment. Our results detail a window of opportunity for rescue from noise trauma, and provide evidence for both morphological and functional protection by delayed pharmacological intervention.

Section snippets

Animals

Pigmented male guinea-pigs (250–300g; Elm Hill Breeding Laboratories, Chelmsford, MA, USA) with a normal Preyer's reflex were used in this study. Male guinea-pigs were selected as sex differences have been associated with differing ability to detoxify ROS (Julicher et al., 1984) and with varying activity of glutathione S-transferase in the cochlea (El Barbary et al., 1993). The experimental protocol was reviewed and approved by the Animal Care and Use Committee at the University of Michigan and

Baseline ABR thresholds

Pre-treatment baseline ABR thresholds did not differ between the seven assigned treatment groups. They were also consistent with normative data previously obtained in our laboratory (mean thresholds±S.D. from 112 animals: 4 kHz, 50±2 dB; 8 kHz, 29±2 dB; 16 kHz, 10±1 dB).

Functional protection: threshold shifts after noise exposure

Noise exposure induced significant ABR threshold shifts as determined 10 days following the exposure (Fig. 1). Control animals exhibited shifts ranging from about 28 dB (at 4 kHz) to 50 dB (at 16 kHz). There was no significant

Discussion

The salient finding of this study is the attenuation of NIHL and noise-induced sensory cell death by a combination of antioxidants (i.e. salicylate and trolox) during a window of time following noise exposure. While pretreatment was most effective, treatment initiated up to 3 days after noise exposure significantly attenuated the functional and morphological consequences of noise trauma. Consistent with the involvement of ROS and RNS in NIHL, the expression of two indicators of free radical

Acknowledgments

Supported by the National Institutes of Health, National Institute on Deafness and Other Communication Disorders (NIH-NIDCD) grant DC 04058, General Motors Corporation, the Ruth and Lynn Townsend Professorship of Communication Disorders, and a core center grant (P30 DC-05188) from the NIH-NIDCD. The authors thank Dr. Richard Altschuler for helpful discussions.

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