Protective roles of α-lipoic acid in rat model of mitochondrial DNA4834bp deletion in inner ear

Peng, Wei; Hu, Yuxia; Zhong, Yun‐Shi; Chen, Bei; Sun, Yu; Yang, Yang; Kong, Weijia

doi:10.1007/s11596-010-0460-2

Cited by 9 publications

(5 citation statements)

References 26 publications

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“…These characteristics are considered to be associated with an increase in oxidative stress caused by a metabolic disturbance. Previous studies have established a mimetic aging model in the cochleae of rats following 8 weeks of D-gal treatment, and demonstrated that the activity levels of antioxidant enzymes decreased and those of lipid peroxidation increased in this model ( 20 – 22 ). Furthermore, the levels of mitochondrial DNA (mtDNA) common deletion (CD) were significantly increased in the cochleae of the D-gal-treated rats ( 20 – 24 ).…”

Section: Introductionmentioning

confidence: 88%

NADPH oxidase 3-associated oxidative stress and caspase 3-dependent apoptosis in the cochleae of D-galactose-induced aged rats

et al. 2015

Molecular Medicine Reports

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Oxidative damage to mitochondrial DNA (mtDNA) and cell apoptosis are heavily implicated in aging. Our previous study established a mimetic rat model of aging in the cochleae using D-galactose (D-gal), and revealed that chronic injection of D-gal can increase oxidative stress and mtDNA common deletions (CD). The aim of the present study was to investigate the sources of reactive oxygen species and the occurrence of apoptosis in the cochleae of rats following 8 weeks of D-gal exposure. The results of the present study indicated that an elevated accumulation of the mtDNA CD and mitochondrial ultrastructural damage occurred in the cochleae of rats injected with D-gal for 8 weeks. In addition, the levels of 8-hydroxy-2-deoxyguanosine, NADPH oxidase (NOX) 3, P22phox and cleaved caspase 3, and the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end-labelling-positive cells were increased in the cochleae of D-gal-treated rats, compared with the controls. These findings suggested that nitric oxide synthase NOX3-associated oxidative stress may contribute to the accumulation of mtDNA mutations and activate a caspase 3-dependent apoptotic signalling pathway in the cochleae during aging. The present study also provided novel insights into the development of age-associated hearing loss, also termed presbycusis.

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Section: Introductionmentioning

confidence: 88%

NADPH oxidase 3-associated oxidative stress and caspase 3-dependent apoptosis in the cochleae of D-galactose-induced aged rats

et al. 2015

Molecular Medicine Reports

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“…Such damage by ROS is mediated by several oxidative stress-responsive signaling pathways and proinflammatory pathways including NF- κ B, JAK2/STAT3, JNK, IL-16, and IL-1, suggesting that those signaling molecules may be potential targets in protecting cells from noise-induced damage [ 9 – 11 ]. Moreover, ROS is known to deplete the intracochlear antioxidants and inhibit antioxidant enzymes including glutathione peroxidase [ 12 ], superoxide dismutases (SOD) [ 13 , 14 ], NQO1, catalase, and hemeoxygenase-1 (HO-1) [ 15 ]. Such antioxidant enzymes are key players in the defense system that living cells have developed to protect the hair cells against the destructive effects of ROS and have been targets for ototoxic stimuli including noise [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Yang Mi Ryung® Extract on Noise‐Induced Hearing Loss in Mice

Kim

Kwak

Baek

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Noise-induced hearing loss (NIHL) results from the damage of the delicate hair cells inside the ear after excessive stimulation of noise. Unlike certain lower animals such as amphibians, fishes, and birds, in humans, hair cells cannot be regenerated once they are killed or damaged; thus, there are no therapeutic options to cure NIHL. Therefore, it is more important to protect hair cells from the noise before the damage occurs. In this study, we report the protective effect of Yang Mi Ryung extract (YMRE) against NIHL; this novel therapeutic property of YMRE has not been reported previously. Our data demonstrates that the hearing ability damaged by noise is markedly restored in mice preadministrated with YMRE before noise exposure, to the level of normal control group. Our study also provides the molecular mechanism underlying the protective effect of YMRE against NIHL by showing that YMRE significantly blocks noise-induced apoptotic cell death and reduces reactive oxygen species (ROS) production in cochleae. Moreover, quantitative polymerase chain reaction (qPCR) analysis demonstrates that YMRE has anti-inflammatory properties, suppressing the mRNA levels of TNFα and IL-1β induced by noise exposure. In conclusion, YMRE could be a useful preventive intervention to prevent hearing impairment induced by the exposure to excessive noise.

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“…In a study investigating the effects of 17 antioxidant compounds (acetyl-L-carnitine (ALCAR), α-lipoic acid, β-carotene, carnosine, coenzyme Q10 (CoQ10), curcumin, d-α-tocopherol, epigallocatechin-3-gallate (EGCG), gallic acid, lutein, lycopene, melatonin, N-acetyl-L-cysteine (NAC), proanthocyanidin, quercetin, resveratrol and tannic acid) on the prevention of ARHL in mice, ARHL was almost completely prevented by treatment with α-lipoic acid and CoQ10; partially prevented by NAC treatment; and not prevented by the other compounds [43]. Other studies also support the positive preventive effects of α-lipoic acid and CoQ10 on ARHL through research in laboratory animals or human elderly subjects [101,103,104,105]. On the contrary, there are differences in opinion as to whether NAC is effective for the prevention of ARHL in mice [106,107].…”

Section: Mitochondria-targeted Antioxidants For Treatment Of Hearimentioning

confidence: 98%

Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review

Fujimoto

Yamasoba

2019

Antioxidants

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Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.

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Protective roles of α-lipoic acid in rat model of mitochondrial DNA4834bp deletion in inner ear

Cited by 9 publications

References 26 publications

NADPH oxidase 3-associated oxidative stress and caspase 3-dependent apoptosis in the cochleae of D-galactose-induced aged rats

NADPH oxidase 3-associated oxidative stress and caspase 3-dependent apoptosis in the cochleae of D-galactose-induced aged rats

Protective Effect of Yang Mi Ryung® Extract on Noise‐Induced Hearing Loss in Mice

Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review

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