Effects of in utero antiretroviral exposure on mitochondrial DNA levels, mitochondrial function and oxidative stress

Hyperbaric oxygen treatment (HBOT)—the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA—increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion—the organelle that consumes most of the oxygen that we breathe—at the epicenter of HBOT’s effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.

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Nicotinamide Riboside Inhibits Alcohol-Induced Inflammation and Oxidative Stress in Macrophages

Current Developments in Nutrition ◽

10.1093/cdn/nzaa045_043 ◽

2020 ◽

Vol 4 (Supplement_2) ◽

pp. 410-410

Author(s):

Hyunju Kang ◽

Young-Ki Park ◽

Ji-Young Lee

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dna ◽

Mitochondrial Respiration ◽

Nuclear Translocation ◽

Antioxidant Properties ◽

Sirtuin 1 ◽

Mouse Bone Marrow ◽

Nicotinamide Riboside ◽

Mitochondrial Dna Copy Number ◽

And Oxidative Stress

Abstract Objectives Macrophages play an essential role in the development of alcohol-induced inflammation. The objective of this study was to investigate whether nicotinamide riboside (NR), a nicotinamide adenine dinucleotide (NAD+) precursor naturally found in milk, can attenuate alcohol-induced inflammation and oxidative stress in macrophages with the elucidation of mechanisms of action. Methods RAW 264.7 macrophages and mouse bone marrow-derived macrophages (BMDMs) were stimulated with 80 mM ethanol with or without 1 mM of NR for 72 h. Expression of genes associated with inflammation and oxidative stress and cellular reactive oxygen species (ROS) accumulation were measured. Also, to evaluate the contribution of sirtuin 1 (SIRT1) to the NR's effect, cellular NAD + level (a cofactor of SIRT1), SIRT1 activity, and mitochondrial DNA copy number were measured. SIRT1 activity was inhibited or activated by sirtinol and resveratrol, respectively, to confirm SIRT1 functions further. Parameters related to mitochondrial respiration were determined using a Seahorse XFe24 Extracellular Flux analyzer. Results NR significantly decreased ethanol-induced inflammatory gene expression, with a concomitant decrease in nuclear translocation of nuclear factor kB p65 in macrophages. Increased cellular ROS levels by ethanol were also attenuated concomitantly with decreased expression of NADPH oxidase 2, a ROS-producing enzyme, by NR in both macrophage cell types. Ethanol decreased SIRT1 mRNA, protein and activity, cellular NAD + level, and mitochondrial DNA, all of which were markedly attenuated by NR. SIRT1 inhibition by sirtinol augmented the inflammatory effects of ethanol, while SIRT1 activation by resveratrol elicited the opposing results. Ethanol increased mitochondrial respiration, ATP production, and proton leak, but decreased maximal respiration and spare respiratory capacity. The ethanol-induced changes in mitochondrial respiration were abolished by NR. Conclusions NR showed anti-inflammatory and antioxidant properties in ethanol-treated macrophages by counteracting the effect of ethanol on lowering SIRT1 expression and cellular NAD+ levels. Therefore, NR may be a potential therapeutic agent for alcohol-induced inflammation and oxidative stress. Funding Sources This work is supported by the NIH 3R01DK108254-04S1.

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Effect of eccentric training on mitochondrial function and oxidative stress in the skeletal muscle of rats

Brazilian Journal of Medical and Biological Research ◽

10.1590/1414-431x20121956 ◽

2013 ◽

Vol 46 (1) ◽

pp. 14-20 ◽

Cited By ~ 9

Author(s):

L.A. Silva ◽

K.F. Bom ◽

C.B. Tromm ◽

G.L. Rosa ◽

I. Mariano ◽

...

Keyword(s):

Oxidative Stress ◽

Skeletal Muscle ◽

Mitochondrial Function ◽

Eccentric Training ◽

And Oxidative Stress

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The Importance of ERα/ERβ Ratio in Breast Cancer: Mitochondrial Function and Oxidative Stress

Breast Cancer - Carcinogenesis, Cell Growth and Signalling Pathways ◽

10.5772/21807 ◽

2011 ◽

Author(s):

Pilar Roca ◽

Jordi Oliver ◽

Jorge Sastre-Serra ◽

Mercedes Nadal-Serrano

Keyword(s):

Breast Cancer ◽

Oxidative Stress ◽

Mitochondrial Function ◽

And Oxidative Stress

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Centella asiatica Attenuates Mitochondrial Dysfunction and Oxidative Stress in Aβ-Exposed Hippocampal Neurons

Oxidative Medicine and Cellular Longevity ◽

10.1155/2017/7023091 ◽

2017 ◽

Vol 2017 ◽

pp. 1-8 ◽

Cited By ~ 12

Author(s):

Nora E. Gray ◽

Jonathan A. Zweig ◽

Donald G. Matthews ◽

Maya Caruso ◽

Joseph F. Quinn ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Mitochondrial Function ◽

Hippocampal Neurons ◽

Neuroblastoma Cells ◽

Water Extract ◽

Centella Asiatica ◽

Antioxidant Response ◽

And Oxidative Stress

Centella asiatica has been used for centuries to enhance memory. We have previously shown that a water extract of Centella asiatica (CAW) protects against the deleterious effects of amyloid-β (Aβ) in neuroblastoma cells and attenuates Aβ-induced cognitive deficits in mice. Yet, the neuroprotective mechanism of CAW has yet to be thoroughly explored in neurons from these animals. This study investigates the effects of CAW on neuronal metabolism and oxidative stress in isolated Aβ-expressing neurons. Hippocampal neurons from amyloid precursor protein overexpressing Tg2576 mice and wild-type (WT) littermates were treated with CAW. In both genotypes, CAW increased the expression of antioxidant response genes which attenuated the Aβ-induced elevations in reactive oxygen species (ROS) and lipid peroxidation in Tg2576 neurons. CAW also improved mitochondrial function in both genotypes and increased the expression of electron transport chain enzymes and mitochondrial labeling, suggesting an increase in mitochondrial content. These data show that CAW protects against mitochondrial dysfunction and oxidative stress in Aβ-exposed hippocampal neurons which could contribute to the beneficial effects of the extract observed in vivo. Since CAW also improved mitochondrial function in the absence of Aβ, these results suggest a broader utility for other conditions where neuronal mitochondrial dysfunction occurs.

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Mitochondrial DNA in liver inflammation and oxidative stress

Life Sciences ◽

10.1016/j.lfs.2019.05.020 ◽

2019 ◽

Vol 236 ◽

pp. 116464 ◽

Cited By ~ 12

Author(s):

Xufei Zhang ◽

Xiuwen Wu ◽

Qiongyuan Hu ◽

Jie Wu ◽

Gefei Wang ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dna ◽

Liver Inflammation ◽

And Oxidative Stress

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MO045MITOCHONDRIAL DYSFUNCTION AND MUSCLE ENERGETICS IN CKD PATIENTS

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfaa140.mo045 ◽

2020 ◽

Vol 35 (Supplement_3) ◽

Author(s):

Jorge Gamboa ◽

Alp Ikizler ◽

Chang Yu ◽

Bruce Damon ◽

Nancy Brown ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Physical Function ◽

Physical Performance ◽

Mitochondrial Function ◽

Resonance Spectroscopy ◽

Muscle Energetics ◽

Intermuscular Adipose Tissue ◽

Markers Of Inflammation ◽

And Oxidative Stress

Abstract Background and Aims Patients with chronic kidney disease (CKD) suffer from frailty and sarcopenia. Skeletal muscle mitochondria are important for physical function and could be a target to prevent frailty and sarcopenia. Method We tested the hypothesis that mitochondrial function worsens with the progression of CKD. We evaluated the interaction between mitochondrial function and co-existing comorbidities such as impaired physical performance, intermuscular adipose tissue (IMAT) infiltration, inflammation, and oxidative stress. We evaluated in-vivo thigh mitochondrial function using 31-phosphorus magnetic resonance spectroscopy to obtain the phosphocreatine (PCr) recovery constant, a measure of mitochondrial function. We measured physical performance using the six-minute walk test, IMAT infiltration and markers of inflammation in plasma. Results Sixty-three participants were studied including controls (n=21), patients with CKD not on maintenance hemodialysis (MHD; n=20), and patients on MHD (n=22). We found a prolonged PCr recovery constant in patients on MHD (53.3 (43.4, 70.1) seconds) and with CKD not on MHD (46.3 (40,0, 49.9) seconds) compared to controls (34.2 (28.8, 43.7) seconds) (p<0.001 between groups), Figure 1A-C. Mitochondrial dysfunction was associated with poor physical performance, greater IMAT, and increased markers of inflammation Figure 2A-C. Conclusion Mitochondrial function worsens with the progression of CKD and correlates with physical function, IMAT, inflammation, and oxidative stress. These data suggest that therapeutic approaches targeted at mitochondrial dysfunction and dynamics could prevent or treat frailty and sarcopenia in patients CKD.

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