ArticleNeurochemical research2016
The Effect of Aging on Mitochondrial Complex I and the Extent of Oxidative Stress in the Rat Brain Cortex.
Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- Mitochondrial Proteome Changes in Rett Syndrome.Biology · 2023Article
- Mitochondrial Dysfunction, Altered Mitochondrial Oxygen, and Energy Metabolism Associated with the Pathogenesis of Schizophrenia.International journal of molecular sciences · 2023Review
- Age-Related Decline in Nrf2/ARE Signaling Is Associated with the Mitochondrial DNA Damage and Cognitive Impairments.International journal of molecular sciences · 2022Article
- Chronic hypoxemia induces mitochondrial respiratory complex gene expression in the fetal sheep brain.JTCVS open · 2022Article
- Alterations in hippocampal mitochondrial dynamics are associated with neurodegeneration and recognition memory decline in old male mice.Biogerontology · 2022Article
- Reduced expression of mitochondrial complex I subunit Ndufs2 does not impact healthspan in mice.Scientific reports · 2022Article
- Article
- Neuroprotection Against NMDA-Induced Retinal Damage by Philanthotoxin-343 Involves Reduced Nitrosative Stress.Frontiers in pharmacology · 2021Article
- β-Carbolines in Experiments on Laboratory Animals.International journal of molecular sciences · 2020Article
- Heterogeneity of GRIM-19 Expression in the Adult Mouse Brain.Cellular and molecular neurobiology · 2019Article
- Gender- and region-specific changes in estrogen signaling in aging rat brain mitochondria.Aging · 2018Article
- Effect of Aging on Mitochondrial Energetics in the Human Atria.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018Article
- Molecular and biochemical evidence on the protective role of ellagic acid and silybin against oxidative stress-induced cellular aging.Molecular and cellular biochemistry · 2018Article
- Fatty Acids, Antioxidants and Physical Activity in Brain Aging.Nutrients · 2017Review
- HIV-1 TAT protein enhances sensitization to methamphetamine by affecting dopaminergic function.Brain, behavior, and immunity · 2017Article
- Pinocembrin Attenuates Mitochondrial Dysfunction in Human Neuroblastoma SH-SY5Y Cells Exposed to Methylglyoxal: Role for the Erk1/2-Nrf2 Signaling Pathway.Neurochemical research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the characteristic features of the aging is dysfunction of mitochondria. Its role in the regulation of metabolism and apoptosis suggests a possible link between these cellular processes. This study investigates the relationship of respiratory complex I with aging-related oxidative stress in the cerebral mitochondria. Deterioration of complex I seen in senescent (26-months old) mitochondria was accompanied by decline in total thiol group content, increase of HNE and HNE-protein adducts as well as decreased content of complex I subunits, GRIM-19 and NDUFV2. On the other hand, decline of complex I might be related with the mitochondrial apoptosis through increased Bax/Bcl-2 cascade in 15-month old animal brains. Higher amount of Bcl-2, Bcl-xL with the lower content of GRIM-19 could maintain to some extent elevated oxidative stress in mitochondria as seen in the senescent group. In the cortical M1 region increased presence of TUNEL+ cells and more than 20-times higher density of Fluoro-Jade C+ cells in 26-months old was observed, suggesting significant neurodegenerative effect of aging in the neuronal cells. Our study supports a scenario in which the age-related decline of complex I might sensitize neurons to the action of death agonists, such as Bax through lipid and protein oxidative stimuli in mitochondria. Although aging is associated with oxidative stress, these changes did not increase progressively with age, as similar extent of lesions was observed in oxidative stress markers of the both aged groups.
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