Several factors trigger apoptosis in cochlear hair cells. Previous studies have 
shown that mitochondria play key roles in apoptosis, but the role of 
mitochondrial deoxyribonucleic acid (mtDNA) copy number in the pathogenesis of 
hair cell apoptosis remains largely unknown. We used mouse cochlear hair cells 
and House Ear Institute‑Organ of Corti 1 (HEI‑OC1) cells to explore the 
relationship between mtDNA copy number and cell apoptosis. We found that the 
mtDNA copy number of hair cells was reduced relative to mitochondrial mass and 
hypothesized that increasing it might have a protective effect. We then 
increased the mtDNA copy number of the hair and HEI‑OC1 cells by transfecting 
them with an adeno‑associated virus (AAV) vector containing mitochondrial 
transcription factor A (TFAM). We found that the apoptosis rates decreased upon 
inducing apoptosis with neomycin or cisplatin (DDP). To elucidate the 
mechanisms, we analyzed the mitochondrial‑membrane permeability and 
mitochondrial function of HEI‑OC1 cells. Our results suggested that the increase 
in mtDNA copy number could protect hair cells and HEI‑OC1 cells against 
drug‑induced apoptosis by stabilizing the permeability of the mitochondrial 
membrane and mitochondrial function.