Fetal bovine serum inhibits neomycin-induced apoptosis of hair cell-like HEI-OC-1 cells by maintaining mitochondrial function.

Aging and exposure to noise or ototoxic drugs are major causes of hair cell death leading to human hearing loss, and many agents have been developed to protect hair cells from apoptosis. Fetal bovine serum (FBS) is a fundamental ingredient in the culture medium of hair cell-like House Ear Institute Organ of Corti 1 (HEI-OC-1) cells, but there have been no reports about the function of FBS in HEI-OC-1 cell apoptosis. In this study, we found that FBS deprivation alone significantly increased HEI-OC-1 cell apoptosis in the absence of neomycin exposure and that the presence of FBS significantly inhibited HEI-OC-1 cell apoptosis after neomycin exposure compared to FBS-deprived cells. Further, we found that the protective effect of FBS was dose dependent and more effective than the growth factors B27, N2, EGF, bFGF, IGF-1, and heparan sulfate. We also found that FBS deprivation significantly disrupted the expression level of mitochondrial proteins, increased pro-apoptotic gene expression, decreased the mitochondrial membrane potential, and increased reactive oxygen species accumulation in HEI-OC-1 cells after neomycin exposure. These findings indicate that FBS is involved in maintaining the level of mitochondrial proteins, maintaining the balance of oxidant gene expression, and preventing the accumulation of ROS, and thus FBS maintains normal mitochondrial function and inhibits apoptosis in HEI-OC-1 cells after neomycin exposure.