Abstract
Noise exposure causes noise-induced hearing loss (NIHL). NIHL exhibits loss of inner ear sensory hair cells and is often irreparable. Although oxidative stress is involved in hearing loss, the complex mechanisms involved in NIHL are unclear. Hypoxia-inducible factor 1α (HIF-1α) has been suggested to be essential for protecting sensory hair cells. Additionally, it has been shown that ROS is involved in modulating the stability of HIF-1α. To investigate the NIHL pathogenesis, we established a tert-butyl hydroperoxide (t-BHP)-induced oxidative stress damage model in hair-like HEI-OC1 cells and an NIHL model in C57BL/6 mice. Protein and mRNA expression were determined, and biochemical parameters including reactive oxygen species (ROS) accumulation, glucose uptake, adenosine triphosphat (ATP) production, and mitochondrial content were evaluated. In HEI-OC1 cells, t-BHP induced ROS accumulation and reduced mitochondrial content and oxygen consumption, but the ATP level was unaffected. Additionally, there was increased glucose uptake and lactate release along with elevated expression of HIF-1α, glucose transporter 1, and several glycolytic enzymes. Consistently, noise trauma induced oxidative stress and the expression of HIF-1α and glycolytic enzymes in mice. Thus, we concluded that ROS induced HIF-1α expression, which promoted glycolysis, suggesting a metabolic shift maintained the ATP level to attenuate hair cell damage in NIHL.
Highlights
Noise-induced hearing loss (NIHL) is a progressive reduction in hearing ability or even hearing loss caused by noisy environment exposure (Wang and Puel 2018; Chadha et al, 2021)
Based on the current research, we argue that the promotion of glycolysis following reactive oxygen species (ROS)-induced Hypoxia-inducible factor 1α (HIF-1α) activation is an essential metabolic remodeling event in sensory hair cells under oxidative stress, and that increased glycolysis may exert a protective effect on sensory hair cells against noise-induced damage
We demonstrated that noise trauma led to abnormal accumulation of ROS, which induced HIF-1α stabilization in sensory hair cells
Summary
Noise-induced hearing loss (NIHL) is a progressive reduction in hearing ability or even hearing loss caused by noisy environment exposure (Wang and Puel 2018; Chadha et al, 2021). We noticed that several studies about NIHL have reported that ROS-dependent signaling molecules have positive effects on adaptation to stress and cell survival in excessive ROS conditions (Leslie 2006; Collins et al, 2012; Sena and Chandel 2012) The discrepancies between these theories may be explained by the fact that ROS, as a double-edged sword, has dual roles during the initiation, promotion, and progression stages of NIHL. Based on the current research, we argue that the promotion of glycolysis following ROS-induced HIF-1α activation is an essential metabolic remodeling event in sensory hair cells under oxidative stress, and that increased glycolysis may exert a protective effect on sensory hair cells against noise-induced damage
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