Acrylonitrile potentiates noise-induced hearing loss in rat

• Published in: Journal of the Association for Research in Otolaryngology 2004-03, Vol.5 (1), p.90-98
• Main Authors: Fechter, Laurence D, Gearhart, Caroline, Shirwany, Najeeb A
• Format: Article
• Language: English
• Subjects: Acrylonitrile - toxicity; Animals; Auditory Threshold - drug effects; Carcinogens - toxicity; Hearing Loss, Noise-Induced - metabolism; Hearing Loss, Noise-Induced - physiopathology; Male; Noise - adverse effects; Oxidative Stress - drug effects; Rats; Rats, Long-Evans
• ISSN: 1525-3961; 1438-7573
• DOI: 10.1007/s10162-003-4028-8

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.