Journal ArticleDOI
Increased mitochondrial DNA damage and decreased base excision repair in the auditory cortex of D-galactose-induced aging rats.
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TLDR
The authors' data showed that mtDNA 4834 bp deletion and TUNEL-positive cells were significantly increased and the expression of pol γ and OGG1 were remarkably down-regulated in the auditory cortex in d-gal-treated rats compared to control rats.Abstract:
Aging has been associated with mitochondrial DNA (mtDNA) common deletion (CD). Age changes in the central auditory system are well known to affect speech perception. Base excision repair (BER) is the major type of DNA repair in mitochondria. The current study was designed to investigate potential causative mechanisms of central presbycusis by using a rat mimetic aging model induced by subcutaneous administration of D-galactose (D-gal). Quantitative real-time PCR and Western blotting analyses were performed to identify the mtDNA 4834 bp deletion and selected mitochondrial DNA repair enzymes, DNA polymerase γ (pol γ) and 8-oxoguanine DNA glycosylase (OGG1). Cell apoptosis in the auditory cortex was detected using terminal deoxynucleotidyltransferase mediated UTP nick-end labeling (TUNEL). Our data showed that mtDNA 4834 bp deletion and TUNEL-positive cells were significantly increased and the expression of pol γ and OGG1 were remarkably down-regulated in the auditory cortex in D-gal-treated rats compared to control rats. During aging, increased mtDNA damage likely results from decreased DNA repair capacity in the auditory cortex. DNA repair enzymes such as pol γ and OGG1 may provide novel pharmacological targets to promote DNA repair and rescue the central auditory system in patients with degenerative diseases.read more
Citations
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Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury
TL;DR: The role of mitochondria in the delayed outcomes of ionization radiation is discussed, and different types of radiation vary in their linear energy transfer (LET) properties, and their effects on various aspects of mitochondrial physiology are discussed.
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D-Galactose-induced accelerated aging model: an overview.
TL;DR: The aim of this article is to comprehensively discuss the use of d-galactose to generate a model of accelerated aging and its possible underlying mechanisms involved in different tissues/organs.
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Role of D-galactose-induced brain aging and its potential used for therapeutic interventions.
TL;DR: The underlying mechanisms involved in D‐galactose‐induced brain aging, particularly as regards alterations in brain mitochondria and cognitive function are discussed, to comprehensively summarize and discuss.
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Role of antioxidants in prevention of age-related hearing loss: a review of literature
TL;DR: It seems that targeting several cell-death pathways is better than targeting the only oxidative stress pathway, and that antioxidant therapy is not a magic elixir that will prevent or treat hearing loss associated with aging completely, but why?
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A long-term high-fat diet increases oxidative stress, mitochondrial damage and apoptosis in the inner ear of d-galactose-induced aging rats
TL;DR: It is demonstrated that HFD may induce oxidative stress, mitochondrial damage and apoptosis in the inner ear, and it provided evidence regarding the link between HFD and an increased risk of age-related hearing loss.
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