Expression of complexes I, II and IV decreased in SGNs of noise-stimulated rats, mediating the damage and degeneration of SGNs

Abstract

Abstract Background: Noise-induced hearing impairment can mediate delayed injury of spiral neurons (SGNs), resulting in degeneration of nerve fibers, synaptic degeneration and even death of SGNs. We believe that delayed injury is related to mitochondrial energy metabolism disorders. Results: We investigated ATP and the electron transport chain (ETC) in rat SGNs after noise injury and found that with prolonged injury time, ATP synthesis and the expression of complexes II and IV decreased, indicating the functional decline of the ETC. The maintenance of ETC function is related to subunit import and assembly of the complex. The disulfide relay mechanism controlled by the apoptosis inducing factor/coiled-coil-helix-coiled-coil-helix domain-containing protein 4（AIF/CHCHD4) pathway can regulate mitochondrial protein import. The results showed that AIF expression in SGNs decreased after noise exposure, indicating that noise damage to SGNs can restoreintramitochondrial protein input by downregulating the AIF/CHCHD4 pathway, hinderingETC function. Conclusion: After noise injury, the mitochondrial function markers, ATP and complexes II/IV down-expressed , indicating insufficiency of ECT function leaded to delay injured SGNs. And the down-regulation of AIF/CHCHD4 function was a possible mechanism that hindered ECT function.