Increased total DNA damage and oxidative stress in brain are associated with decreased longevity in high sucrose diet fed WNIN/Gr-Ob obese rats

Potukuchi, Aruna; Addepally, Uma; R., Sindhu K.; Raghunath, Manchala

doi:10.1080/1028415x.2017.1332509

Cited by 16 publications

(10 citation statements)

References 41 publications

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“…Indeed, it is well-known that strengthening the antioxidant barrier is the basic protective mechanism against the ROS-mediated injury [106]. However, such changes have not been observed in the cerebral glutathione (GSH) level [55,107,108]. Interestingly, lowered GSH levels (with a simultaneous increase in GSSG (oxidized glutathione) levels) were reported not only in the IR brain, but also in patients with AD, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis and Huntington’s disease [55,107,108,109,110,111,112].…”

Section: Oxidative Stress In the Brain Insulin Resistancementioning

confidence: 99%

“…However, such changes have not been observed in the cerebral glutathione (GSH) level [55,107,108]. Interestingly, lowered GSH levels (with a simultaneous increase in GSSG (oxidized glutathione) levels) were reported not only in the IR brain, but also in patients with AD, Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis and Huntington’s disease [55,107,108,109,110,111,112]. It is postulated that disturbances in glutathione metabolism may result in the impairment of cerebral functioning in both IR and neurodegenerative diseases [110,111].…”

Section: Oxidative Stress In the Brain Insulin Resistancementioning

confidence: 99%

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Insulin Resistance and Oxidative Stress in the Brain: What’s New?

Maciejczyk

Żebrowska

Chabowski

2019

IJMS

168

132

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The latest studies have indicated a strong relationship between systemic insulin resistance (IR) and higher incidence of neurodegeneration, dementia, and mild cognitive impairment. Although some of these abnormalities could be explained by chronic hyperglycaemia, hyperinsulinemia, dyslipidaemia, and/or prolonged whole-body inflammation, the key role is attributed to the neuronal redox imbalance and oxidative damage. In this mini review, we provide a schematic overview of intracellular oxidative stress and mitochondrial abnormalities in the IR brain. We highlight important correlations found so far between brain oxidative stress, ceramide generation, β-amyloid accumulation, as well as neuronal apoptosis in the IR conditions.

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Section: Oxidative Stress In the Brain Insulin Resistancementioning

confidence: 99%

Section: Oxidative Stress In the Brain Insulin Resistancementioning

confidence: 99%

Insulin Resistance and Oxidative Stress in the Brain: What’s New?

Maciejczyk

Żebrowska

Chabowski

2019

IJMS

168

132

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“…Longevity or lifespan of an organism is governed by factors such as oxidative stress, autophagy, dietary restrictions, accumulated DNA damage and disruption in protein homeostasis [16][17][18]. Reactive Oxygen species (ROS) are oxygen molecules containing highly reactive species that can cause genotoxic and physiological damage when produced in excess.…”

Section: Introductionmentioning

confidence: 99%

ROS is the major player in regulating altered autophagy and lifespan insin-3mutants ofC. elegans

2018

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SIN3, a transcriptional corepressor has been implicated in varied functions both as transcription activator and repressor. Recent studies associated Sin3 with the macroautophagic/autophagic process as a negative regulator of Atg8 and Atg32. Though the role of SIN3 in autophagy is being explored, little is known about the overall effect of SIN3 deletion on the survival of an organism. In this study using a Caenorhabditis elegans sin-3(tm1279);him-5(e1490) strain, we demonstrate that under in vivo conditions SIN-3 differentially modulates autophagy and lifespan. We provide evidence that the enhanced autophagy and decreased lifespan observed in sin-3 deletion mutants is dependent on ROS and intracellular oxidative stress. Inability of the mutant worms to maintain redox balance along with dysregulation of enzymatic antioxidants, depletion of GSH and NADP reserves and elevation of ROS markers compromises the longevity of the worms. It is possible that the enhanced autophagic process observed in sin-3 (tm1279);him-5(e1490) worms is required to compensate for oxidative stress generated in these worms.

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“…A series of apoptosis related proteins in terms of Bax, Bcl-2 and caspase-3 are major regulators of cell death and cell survival [32]. In this paper, we conducted if PCB 2 could restrain the apoptotic signalling pathway through H 2 O 2 -induced.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of procyanidin B2 on hydrogen peroxide (H2O2)-induced oxidative damage in MCF-7 cells

Tan

et al. 2020

Appl Biol Chem

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The aim of this study is to assess the cytoprotection and potential molecular mechanisms of procyanidin B2 (PCB2) on hydrogen peroxide (H2O2)-induced oxidative damage in MCF-7 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to determine the viability of MCF-7 cell exposure to H2O2 or PCB2. We measured the antioxidant properties of PCB2 by determining the activities of SOD, GSH-Px, LDH and MDA levels, and evaluated apoptosis and intracellular reactive oxygen species (ROS) levels. The related proteins expression levels were monitored by Western blot. MCF-7 cells induced with H2O2 had a remarkable decrease in cell viability that was suppressed when it was interfered with PCB2 (0.1–10.0 μM). PCB2 interference memorably and dose-dependently inhibited H2O2-induced LDH leakage, ROS and MDA overproduction, while PCB2 markedly increased H2O2-induced the activities of SOD and GSH-Px. Eventually, H2O2 prominently down-regulated the ratio of Bcl-2/Bax and the relative proteins expression levels of Nrf2, GCLC, NQO1 and HO-1, and up-regulated the relative proteins expression levels of cytochrome c, caspase-3 and Keap1. However, the relative expression levels of these proteins were reversed in PCB2-interfered MCF-7 cells. This study implied that protective effect of PCB2 on H2O2-induced oxidative damage in MCF-7 cells might be related to inhibition of mitochondria-dependent apoptosis, activation of Keap1/Nrf2/HO-1 signaling pathway and improvement of the antioxidant enzymes activities.

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Increased total DNA damage and oxidative stress in brain are associated with decreased longevity in high sucrose diet fed WNIN/Gr-Ob obese rats

Cited by 16 publications

References 41 publications

Insulin Resistance and Oxidative Stress in the Brain: What’s New?

Insulin Resistance and Oxidative Stress in the Brain: What’s New?

ROS is the major player in regulating altered autophagy and lifespan insin-3mutants ofC. elegans

Protective effect of procyanidin B2 on hydrogen peroxide (H2O2)-induced oxidative damage in MCF-7 cells

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