Mechanisms of noise-induced hearing loss potentiation by hypoxia

Potentiation of noise-induced permanent threshold shift (PTS) by hypoxia has been reported [Hear. Res. 172 (1-2) (2002) 186]. In this study in rats, effects of noise (110 dB SPL), hypoxia (10% O2), and their combination have been determined on different cochlear potentials and on the expression of genes coding proteins in the outer hair cell (OHC) membrane skeleton (β-actin) and in the mitochondrial respiratory chain (SDHa & b). The noise exposure alone caused CAP threshold shift only in the noise-band. The combined exposure to noise and hypoxia caused an about 40-dB PTS at all frequencies within and above the noise band. Loss of the cochlear amplification was not always related to the CM-suppression. SP was only affected at high frequencies by the combined exposure. Gene expression of β-actin was up-regulated by the noise exposure, which was blocked by hypoxia. Gene expression of SDHa was also up-regulated by the noise and the combined exposure. The data suggest that loss of the cochlear active process, due to damage to the OHC membrane skeleton and to the cellular energy generation system, is related to the noise-induced hearing loss potentiation by hypoxia. Inner hair cell damage may also be involved in the hypoxia potentiation in the basal turn.