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

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

scholarly journals Tamoxifen and oxidative stress: an overlooked connection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nermin S. Ahmed ◽  
Marek Samec ◽  
Alena Liskova ◽  
Peter Kubatka ◽  
Luciano Saso
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Gold Standard ◽  
Pharmacological Activities ◽  
Standard Drug ◽  
Menopausal Women ◽  
Wide Range ◽  
Post Menopausal ◽  
Apoptotic Effects ◽  
And Oxidative Stress

AbstractTamoxifen is the gold standard drug for the treatment of breast cancer in pre and post-menopausal women. Its journey from a failing contraceptive to a blockbuster is an example of pharmaceutical innovation challenges. Tamoxifen has a wide range of pharmacological activities; a drug that was initially thought to work via a simple Estrogen receptor (ER) mechanism was proven to mediate its activity through several non-ER mechanisms. Here in we review the previous literature describing ER and non-ER targets of tamoxifen, we highlighted the overlooked connection between tamoxifen, tamoxifen apoptotic effects and oxidative stress.

scholarly journals Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1827
Author(s):  
Nofar Schottlender ◽  
Irit Gottfried ◽  
Uri Ashery
Keyword(s):  
Oxidative Stress ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Defense Mechanisms ◽  
Term Treatment ◽  
Mitochondrial Activity ◽  
Hyperbaric Oxygen Treatment ◽  
Oxygen Treatment ◽  
Long Term Treatment ◽  
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.

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

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
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.

Antioxidant enzyme activities and oxidative stress in human breast cancer

1994 ◽  
Vol 120 (6) ◽  
pp. 374-377 ◽  
Author(s):  
K. Punnonen ◽  
M. Ahotupa ◽  
K. Asaishi ◽  
M. Hy�ty ◽  
R. Kudo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Human Breast Cancer ◽  
Antioxidant Enzyme Activities ◽  
Human Breast ◽  
And Oxidative Stress

MO045MITOCHONDRIAL DYSFUNCTION AND MUSCLE ENERGETICS IN CKD PATIENTS

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.

Modulation of mitochondrial function and oxidative stress in highly toxic aberrrant-astrocytes

2012 ◽  
Vol 53 ◽  
pp. S178-S179
Author(s):  
L. Martínez-Palma ◽  
A. Cassina ◽  
E. Miquel ◽  
R. Radi ◽  
L. Barbeito ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Function ◽  
And Oxidative Stress
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