Selective vulnerability of the cochlear Basal turn to acrylonitrile and noise.

Exposure to acrylonitrile, a high-production industrial chemical, can promote noise-induced hearing loss (NIHL) in the rat even though this agent does not itself produce permanent hearing loss. The mechanism by which acrylonitrile promotes NIHL includes oxidative stress as antioxidant drugs can partially protect the cochlea from acrylonitrile + noise. Acrylonitrile depletes glutathione levels while noise can increase the formation of reactive oxygen species.

Lipoic acid and 6-formylpterin reduce potentiation of noise-induced hearing loss by carbon monoxide: preliminary investigation.

Potentiation of noise-induced hearing loss (NIHL) by specific chemical contaminants and therapeutic drugs represents a distinct public health risk. Prediction of chemicals that yield such potentiation has not been successful because such agents differ markedly in structure. One mechanism for this potentiation that has garnered support is oxidative injury to the cochlea.

Depletion of liver glutathione levels in rats: a potential confound of nose-only inhalation.

Nose-only inhalation exposure chambers offer key advantages to whole-body systems, particularly when aerosol or mixed aerosol-vapor exposures are used. Specifically, nose-only chambers provide enhanced control over the route of exposure and dose by minimizing the deposition of particles either on the subjects skin/fur or on surfaces of a whole-body exposure system. In the current series of experiments, liver, brain, and lung total glutathione (GSH) levels were assessed following either nose-only or whole-body exposures to either jet fuel or to clean, filtered air.

Promotion of noise-induced cochlear injury by toluene and ethylbenzene in the rat.

Ethylbenzene + toluene are known individually to have ototoxic potential at high exposure levels and with prolonged exposure times generally of 4-16 weeks. Both ethylbenzene + toluene are minor constituents of JP-8 jet fuel; this fuel has recently been determined to promote susceptibility to noise-induced hearing loss. Therefore, the current study evaluates the ototoxic potential of combined exposure to ethylbenzene + toluene exposure in a ratio calculated from the average found in three laboratories.

JP-8 jet fuel can promote auditory impairment resulting from subsequent noise exposure in rats.

We report on the transient and persistent effects of JP-8 jet fuel exposure on auditory function in rats. JP-8 has become the standard jet fuel utilized in the United States and North Atlantic Treaty Organization countries for military use and it is closely related to Jet A fuel, which is used in U.S.