Mitochondrial oxidative damage and apoptosis in age-related hearing loss

Someya, Shinichi; Prolla, Tomas A.

doi:10.1016/j.mad.2010.04.006

Cited by 141 publications

(119 citation statements)

References 84 publications

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“…Experimental evidence suggests that mitochondrial dysfunction associated with reactive oxygen species (ROS) plays a central role in the aging process of cochlear cells. 13 This was evidenced in the present study, in which we observed a significant increase in the level of Glutathione and a slight but significant decline in the SOD activity. A very high increase in the level of one antioxidant might have suppressed the activity of another antioxidant, SOD in the present study.…”

Section: Discussionsupporting

confidence: 73%

Comparative study of oxidative stress in individuals with and without age related hearing loss

Vk¹,

Km²

2015

Int J Res Med Sci

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INTRODUCTIONAge related hearing loss known as Presbycusis is a universal feature of mammalian ageing and refers to sensorineural hearing impairment in elderly individuals. Among community-dwelling elderly people, the prevalence of hearing loss is 24% in those aged 65-74 years and 40% among those who are 75 years of age. The Molecular mechanism underlying Age related hearing loss is about 24%. Along with heart problems, hypertension and arthritis the hearing impairment is one of the four leading chronic health conditions experienced by the elderly people. 1,2 It is characterised by an age dependent decline of auditory function associated with loss of sensory hair cells, spiral ganglion neurons and stria vascularis cells in the cochlea of inner ear.3 It is also associated with difficulty in speech discrimination and central auditory processing of information.Hearing loss occurs when the tiny hairs inside the ear are damaged or die. The hair cells do not re-grow, so most hearing loss is permanent. Stria vascularis is the highly vascular tissue in the lateral wall of the cochlea. The spiral or cochlear ganglion is the group of nerve cells that serve the sense of hearing by sending a representation of ABSTRACT Background: Age related hearing loss is an universal feature of mammalian ageing and refers to sensorineural hearing impairment in elderly individuals. It was reported that increased generation of free radicals during cellular metabolism plays a major role in age related disorders. Therefore, the occurrence of age related hearing loss depends mainly on antioxidant status of the body. Hence, this study was undertaken to investigate the status of Glutathione and Superoxide dismutase in age related hearing loss. Methods: This study was conducted after the approval from institutional ethical committee. The study group included 25 patients diagnosed for age related hearing loss between the age group of 55-80 years of either sex and 25 healthy age and sex matched individuals as controls. Estimation of Glutathione was done by DTNB method and Superoxide Dismutase using standard procedures. The data was analysed using One Way ANOVA. P value less than 0.05 will be considered the level of significance. Results:The results showed that, the Glutathione level in Hearing Loss patients was increased significantly (p=0.0001) as compared to normal controls. The SOD Activity has declined significantly (p=0.001) in Hearing Loss patients as compared to normal controls. Conclusion: We found an association between the level of Glutathione and Super Oxide Dismutase in age related hearing loss. Thus the serum Glutathione and Super Oxide Dismutase level can be used as a biomarker for the assessment of age related hearing loss.

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Section: Discussionsupporting

confidence: 73%

Comparative study of oxidative stress in individuals with and without age related hearing loss

Vk¹,

Km²

2015

Int J Res Med Sci

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“…Furthermore, the finding that shock startle responses of the CoQ-treated mice remained unchanged implies that the deleterious effects are related to the sensory rather than the motor component of the startle reflex. Age-related hearing loss has been associated with increased oxidative damage (Someya and Prolla 2010) and down-regulation of mitochondrial respiratory chain complexes which would lead to an excess production of oxidants (Someya et al 2007) in the cochlea. Previous studies have shown that altering the redox status of the cochlea affects hearing capacity, in particular caloric restriction has been shown to reduce presbycusis and attenuate oxidative damage .…”

Section: Discussionmentioning

confidence: 99%

Coenzyme Q10 supplementation reverses age-related impairments in spatial learning and lowers protein oxidation

Shetty

Forster

Sumien

2012

AGE

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Coenzyme Q10 (CoQ) is widely available as a dietary supplement and remains under consideration as a treatment for age-associated neurodegenerative conditions. However, no studies have determined if supplementation, initiated relatively late in life, could have beneficial effects on mild functional impairments associated with normal brain aging. Accordingly, the current study assessed the effect of CoQ intake in older mice for which cognitive and psychomotor impairments were already evident. Separate groups of young (3.5 months) and relatively old mice (17.5 months) were fed a control diet or a diet supplemented with low (0.72 mg/g) or high (2.81 mg/g) concentrations of CoQ for 15 weeks. After 6 weeks, the mice were given tests for spatial learning (Morris water maze), spontaneous locomotor activity, motor coordination, and startle reflex. Age-related impairments in cognitive and psychomotor functions were evident in the 17.5-month-old mice fed the control diet, and the low-CoQ diet failed to affect any aspect of the impaired performance. However, in the Morris water maze test, old mice on the high-CoQ diet swam to the safe platform with greater efficiency than the mice on the control diet. The old mice supplemented with the highCoQ diet did not show improvement when spatial performance was measured using probe trials and failed to show improvement in other tests of behavioral performance. Protein oxidative damage was decreased in the mitochondria from the heart, liver, and skeletal muscle of the high-CoQ-supplemented mice and, to some extent, in the brain mitochondria. Contrasting with the deleterious effect of long-term CoQ supplementation initiated during young adulthood previously published, this study suggests that CoQ improves spatial learning and attenuates oxidative damage when administered in relatively high doses and delayed until early senescence, after agerelated declines have occurred. Thus, in individuals with age-associated symptoms of cognitive decline, highCoQ intake may be beneficial.

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“…Age-related hearing loss (AHL), characterized by a decline of auditory function with increasing age, is associated with attrition of spiral ganglion neurons and sensory hair cells in the cochlea of the inner ear (90,148). Studies have shown that CR delays the onset of AHL and reduces cochlear pathology (141,150) by reducing oxidative stress (150), which plays a major role in AHL (73,149).…”

Section: Sirt3 Prevents Hearing Loss During Crmentioning

confidence: 99%

Mitochondrial Sirtuins and Their Relationships with Metabolic Disease and Cancer

Kumar

Lombard²

2015

Antioxidants & Redox Signaling

129

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Significance: Maintenance of metabolic homeostasis is critical for cellular and organismal health. Proper regulation of mitochondrial functions represents a crucial element of overall metabolic homeostasis. Mitochondrial sirtuins (SIRT3, SIRT4, and SIRT5) play pivotal roles in promoting this homeostasis by regulating numerous aspects of mitochondrial metabolism in response to environmental stressors. Recent Advances: New work has illuminated multiple links between mitochondrial sirtuins and cancer. SIRT5 has been shown to regulate the recently described post-translational modifications succinyl-lysine, malonyllysine, and glutaryl-lysine. An understanding of these modifications is still in its infancy. Enumeration of SIRT3 and SIRT5 targets via advanced proteomic techniques promises to dramatically enhance insight into functions of these proteins. Critical Issues: In this review, we highlight the roles of mitochondrial sirtuins and their targets in cellular and organismal metabolic homeostasis. Furthermore, we discuss emerging roles for mitochondrial sirtuins in suppressing and/or promoting tumorigenesis, depending on the cellular and molecular context. Future Directions: Currently, hundreds of potential SIRT3 and SIRT5 molecular targets have been identified in proteomic experiments. Future studies will need to validate the major targets of these enzymes, and elucidate how acetylation and/or acylation modulate their functionality. A great deal of interest exists in targeting sirtuins pharmacologically; this endeavor will require development of sirtuin-specific modulators (activators and inhibitors) as potential treatments for cancer and metabolic disease. Antioxid.

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Mitochondrial oxidative damage and apoptosis in age-related hearing loss

Cited by 141 publications

References 84 publications

Comparative study of oxidative stress in individuals with and without age related hearing loss

Comparative study of oxidative stress in individuals with and without age related hearing loss

Coenzyme Q10 supplementation reverses age-related impairments in spatial learning and lowers protein oxidation

Mitochondrial Sirtuins and Their Relationships with Metabolic Disease and Cancer

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