Perinatal exposure to Aroclor 1254 impairs distortion product otoacoustic emissions (DPOAEs) in rats.
Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that are a potential health hazard to human and wildlife populations. Low-frequency auditory impairments have previously been documented in Aroclor 1254 (A 1254)-exposed rats, including elevated behavioral auditory thresholds and decreased amplitude and prolonged latency auditory evoked brain stem responses (ABRs). Furthermore, outer hair-cell loss on the basilar membrane of the cochlea has been documented, demonstrating that the cochlea is a target organ for PCB ototoxicity. The current experiment assessed the effects of A1254 on cochlear function by measuring distortion product otoacoustic emissions (DPOAEs). ABRs were measured to determine the effects of A1254 on the central nervous system auditory pathways. Pregnant Long-Evans rats received either 0 or 6 mg/kg A1254 (po) in corn oil from gestation day 6 to lactational day 21. The auditory function of male and female offspring was assessed at approximately 18 months of age. The rats were anesthetized and a probe-unit, consisting of 2 insert earphones and a microphone, was positioned in the ear canal. DPOAE amplitudes were reduced and thresholds increased in the A1254-exposed rats. The deficits were most pronounced at the lowest frequencies tested (2.1-3.2 kHz), but deficits were also observed at higher frequencies (3.7-8.6 kHz). Males and females were equally affected at the lower frequencies, but females were more impaired at the higher frequencies. In contrast, ABR latencies and amplitudes were not altered by A1254 exposure. These findings provide the first functional evidence supporting a cochlear site of damage in PCB-induced hearing loss.[1]References
- Perinatal exposure to Aroclor 1254 impairs distortion product otoacoustic emissions (DPOAEs) in rats. Lasky, R.E., Widholm, J.J., Crofton, K.M., Schantz, S.L. Toxicol. Sci. (2002) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
