Manganese superoxide dismutase influences the extent of noise-induced hearing loss in mice

Tuerdi, Ayinuer; Kinoshita, Makoto; Kamogashira, Teru; Fujimoto, Chisato; Iwasaki, Shinnichi; Shimizu, Takahiko; Yamasoba, Tatsuya

doi:10.1016/j.neulet.2017.02.003

Cited by 26 publications

(31 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, the exogenous activation of SIRT3 through pharmacological means restores partial cochlear function after traumatic noise damage [20] and aminoglycoside damage [38]. In analyses of SIRT3 effector molecules, heterozygous Sod2-KO mice were shown to incur more damage from traumatic noise compared to wild-type controls, including higher ABR thresholds and greater OHC losses [39]. Together, these published data show that in mice, the mitochondrial oxidative stress response is activated after traumatic noise, reduced levels of those effectors worsen trauma outcomes, and increasing the stress response through greater levels of SIRT3 activity improves trauma outcomes.…”

Section: Discussionmentioning

confidence: 99%

Endogenous SIRT3 activity is dispensable for normal hearing recovery after noise exposure in young adult mice

Patel

Shah

Dang

et al. 2020

Preprint

View full text Add to dashboard Cite

18Occupational noise-induced hearing loss (NIHL) affects millions of people worldwide and presents a large 19 social and personal burden. Some genetic variants in the mitochondrial oxidative stress response correlate 20 strongly with susceptibility to NIHL in both humans and mice. Here we test the hypothesis that SIRT3, a 21 regulator of the mitochondrial oxidative stress response, is required in mice for endogenous recovery of 22 auditory thresholds after a sub-traumatic noise exposure. We expose homozygous Sirt3-KO mice and their 23 wild-type littermates to a noise dose that confers a temporary threshold shift, but is not sufficient to 24 permanently reduce cochlear function, compromise cell survival, or damage synaptic structures. We find no 25 difference in hearing function after recovery from noise exposure between the two genotypes, when measured 26 by either auditory brainstem response (ABR) or distortion product otoacoustic emissions (DPOAE). We show 27 that SIRT3-specific immunoreactivity is present in outer hair cells, around the post-synaptic regions of inner 28 hair cells, and faintly within inner hair cells. Nonetheless, outer hair cells and auditory synapses show no 29 increase in loss after noise exposure in the homozygous Sirt3-KO mouse. These data show that SIRT3-30 dependent processes are not necessary for endogenous hearing recovery after a single, sub-traumatic noise 31 exposure. They demonstrate the existence of cellular mechanisms of cochlear homeostasis in addition to the 32 mitochondrial oxidative stress response. We also present a novel statistical analysis for identifying differences 33 between peak 1 amplitude progressions in ABR waveforms. 34

show abstract

Section: Discussionmentioning

confidence: 99%

Endogenous SIRT3 activity is dispensable for normal hearing recovery after noise exposure in young adult mice

Patel

Shah

Dang

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Several KO mouse lines with deficiencies in other major antioxidants or their regulators, such as Sod2 (Tuerdi et al . ), glutathione peroxidase 1 (Ohlemiller et al . ), and nuclear factor erythroid‐2 related factor 2 ( Nrf2 ) (Honkura et al .…”

Section: Discussionmentioning

confidence: 99%

“…For example, mice with deletion of superoxide dismutase 1 (Sod1), a major antioxidant molecule, show increased vulnerability to age-related hearing loss (McFadden et al 1999). Several KO mouse lines with deficiencies in other major antioxidants or their regulators, such as Sod2 (Tuerdi et al 2017), glutathione peroxidase 1 (Ohlemiller et al 2000), and nuclear factor erythroid-2 related factor 2 (Nrf2) (Honkura et al 2016), show vulnerability to NIHL. Moreover, pejvakin KO mice, which have disturbed peroxisome antioxidant activity, show a similar phenotype (Delmaghani et al 2015).…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, NOX4-TG mice show a hearing vulnerability upon NE that is induced by ROS, as confirmed by the compensation observed after the antioxidant treatment. Mouse models with antioxidant-defense failure reportedly have normal hearing (Honkura et al 2016;Tuerdi et al 2017) or only subtle hearing loss (Ohlemiller et al 2000;Delmaghani et al 2015) under baseline conditions, but show exacerbated NIHL and OHC loss after NE. For example, mice lacking Nrf2, which is a transcription factor regulating the major antioxidant response elements (Loboda et al 2016), have normal hearing but increased susceptibility to NE (Honkura et al 2016).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Hearing vulnerability after noise exposure in a mouse model of reactive oxygen species overproduction

Morioka

Sakaguchi

Yamaguchi

et al. 2018

Journal of Neurochemistry

View full text Add to dashboard Cite

Previous studies have convincingly argued that reactive oxygen species (ROS) contribute to the development of several major types of sensorineural hearing loss, such as noise-induced hearing loss (NIHL), drug-induced hearing loss, and age-related hearing loss. However, the underlying molecular mechanisms induced by ROS in these pathologies remain unclear. To resolve this issue, we established an in vivo model of ROS overproduction by generating a transgenic (TG) mouse line expressing the human NADPH oxidase 4 (NOX4, NOX4-TG mice), which is a constitutively active ROS-producing enzyme that does not require stimulation or an activator. Overproduction of ROS was detected at the cochlea of the inner ear in NOX4-TG mice, but they showed normal hearing function under baseline conditions. However, they demonstrated hearing function vulnerability, especially at high-frequency sounds, upon exposure to intense noise, which was accompanied by loss of cochlear outer hair cells (OHCs). The vulnerability to loss of hearing function and OHCs was rescued by treatment with the antioxidant Tempol. Additionally, we found increased protein levels of the heat-shock protein 47 (HSP47) in models using HEK293 cells, including H O treatment and cells with stable and transient expression of NOX4. Furthermore, the up-regulated levels of Hsp47 were observed in both the cochlea and heart of NOX4-TG mice. Thus, antioxidant therapy is a promising approach for the treatment of NIHL. Hsp47 may be an endogenous antioxidant factor, compensating for the chronic ROS overexposure in vivo, and counteracting ROS-related hearing loss.

show abstract

“…In addition, after noise exposure, antioxidant enzymes SOD1 gene and HO-1 gene can transcript and translate in large quantities (Fetoni et al, 2015;Honkura et al, 2016). Tuerdi et al (2017) used Mn-SOD knockout mice to observe the effects of partial deletion of endogenous antioxidants, and found that the knockout mice had more severe hearing loss than wild type mice. Although levels of free radicals still increase substantially after noise exposure, the expression of endogenous antioxidants has a certain protective effect, which suggests that the effect of loud noise can be alleviated by supplementing exogenous antioxidants.…”

Section: Metabolic Damage Oxidative Stress Damagementioning

confidence: 99%

What is noise-induced hearing loss?

2019

View full text Add to dashboard Cite

Noise-induced hearing loss is sensory deafness caused by long-term exposure of the auditory system to a noisy environment. Auditory fatigue is an early symptom of noise-induced hearing loss, and hearing can gradually recover after people leave a noisy environment. However, if people remain in a noisy environment for a prolonged period of time, their hearing will be permanently impaired. Societal changes mean that people are more likely to be exposed to noise. The hearing loss and tinnitus caused by noise seriously affect people's quality of life and lead to huge economic loss. The pathogenesis of noise-induced hearing loss is complex. Various theories try to explain this, such as the oxidative stress theory, but none perfectly explains the occurrence of noise-induced hearing loss. There is no treatment which can completely reverse the damage. More research is required to explore the pathogenesis and to better guide clinical practice. Preventative strategies, such as educating the public about hearing health, should be adopted to reduce the harm of noise-induced hearing loss.

show abstract

Manganese superoxide dismutase influences the extent of noise-induced hearing loss in mice

Cited by 26 publications

References 16 publications

Endogenous SIRT3 activity is dispensable for normal hearing recovery after noise exposure in young adult mice

Endogenous SIRT3 activity is dispensable for normal hearing recovery after noise exposure in young adult mice

Hearing vulnerability after noise exposure in a mouse model of reactive oxygen species overproduction

What is noise-induced hearing loss?

Contact Info

Product

Resources

About