Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2005 Sep;207(1-2):35-42.
doi: 10.1016/j.heares.2005.03.025.

Damage and threshold shift resulting from cochlear exposure to paraquat-generated superoxide

Eric C Bielefeld  1 , Bo Hua Hu, Kelly Carney Harris, Donald Henderson
Affiliations

Damage and threshold shift resulting from cochlear exposure to paraquat-generated superoxide

Eric C Bielefeld et al. Hear Res. 2005 Sep.

Abstract

Superoxide has been implicated as a contributing factor to cochlear pathology from a number of sources, including noise and ototoxic drugs. The effects of NADPH oxidase-dependent superoxide on the cochlea were investigated in the current study using paraquat (PQ). PQ is a toxic herbicide that causes tissue damage by generating superoxide through reduction of molecular oxygen in a reaction catalyzed by NADPH oxidase. The current study examined the effects of round window PQ administration on inferior colliculus (IC) evoked potential thresholds (EVP) and hair cell damage. Using implanted IC electrodes, chinchillas were tested for IC EVP thresholds before and after PQ exposure. Ears were exposed to PQ at one of four concentrations: 10, 5, 3 mM, and vehicle control. Thresholds were increased in a dose-dependent manner, and peaked between one and seven days post-exposure. Thresholds then showed a small amount of recovery before reaching PTS by Day 22. Outer and inner hair cell losses were consistent with PTS. The similarities between PQ ototoxicity and noise-induced hearing loss suggest the possibility of similar biochemical pathways involving superoxide.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
Recovery patterns of the 10 mM concentration group for the five frequencies tested, plotted as threshold shift in dB against the Day of testing post-exposure. Error bars are +1 standard deviation.
Fig. 2
Fig. 2
Recovery patterns of the 5 mM concentration group for the five frequencies tested, plotted as threshold shift in dB against the Day of testing post-exposure. Error bars are +1 standard deviation.
Fig. 3
Fig. 3
Recovery patterns of the 3 mM concentration group for the five frequencies tested, plotted as threshold shift in dB against the Day of testing post-exposure. Error bars are +1 standard deviation.
Fig. 4
Fig. 4
PTS for the four experimental groups plotted as dB PTS across frequency. Error bars are +1 standard deviation.
Fig. 5
Fig. 5
Mean OHC loss cochleograms for the four concentration groups, plotted as % OHC lost against % distance from the apex of the cochlea.
Fig. 6
Fig. 6
Mean IHC loss cochleograms for the four concentration groups, plotted as % IHC lost against % distance from the apex of the cochlea.
See this image and copyright information in PMC

References

    1. Böheim K, Bichler E. Cisplatin-induced ototoxicity: Audiometric findings and experimental cochlear pathology. Arch. Otorhinolaryngol. 1985;242:1–6. - PubMed
    1. Bus JS, Gibson JE. Paraquat: Model for oxidant-initiated toxicity. Environ. Health Perspect. 1984;55:37–46. - PMC - PubMed
    1. Campbell KC, Rybak LP, Meech RP, Hughes L. d-methionine provides excellent protection from cisplatin ototoxicity in the rat. Hear. Res. 1996;102:90–98. - PubMed
    1. Clerici WJ, Yang L. Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function. Hear. Res. 1996;101:14–22. - PubMed
    1. Clerici WJ, Hensley K, DiMartino DL, Butterfield DA. Direct detection of ototoxicant-induced reactive oxygen species generation in cochlear explants. Hear. Res. 1996;98:116–124. - PubMed

Publication types

MeSH terms