This study aimed to investigate the role of RNF8 (RING finger protein 8) in DNA damage repair in mice of different ages, and to provide new insight into the pathology and treatment of senile deafness. Sixteen C57BL/6J mice aged 8 weeks, 16 weeks and 32 weeks were obtained by paired reproduction. The mice of three age groups were equally divided into two groups, named experimental group (RNF8 gene knockout) and control group (no knockout). The cochlear hair cells, stria vascularis and spiral ganglion cells were observed by HE (hematoxylin-eosin) staining. The degree of DNA damage and the related expressions were observed by immunofluorescence γ-H2AX staining and 8-OH immunohistochemical staining, and the aging of damaged cells was detected by lipofuscin and β-galactosidase staining. HE staining showed that the changes of cochlear hair cells, stria vascularis and spiral ganglion cells were obvious in the same group of mice at different ages. Compared with the control group, the aging changes of cochlear hair cells, stria vascularis and spiral ganglion cells were more significant in the experimental group. Immunofluorescence γ-H2AX staining showed H2AX phosphorylation in injured cells. The aging of cochlea in mice changed, and staining of β-galactosidase in the experimental group suggested that the striae of blood vessels were changed with age at 32 weeks old and staining of lipofuscin showed dark brown staining around the nucleus (P < 0.05). In conclusion, the deletion of RNF8 is an important cause of morphological changes in the cochlea of mice. The deletion of RNF8 accelerates the aging of the cochlea of mice, suggesting that the apoptosis of the cochlea could contribute to aging in RNF8 gene-deficient mice.