Sentences with phrase «mitochondrial reactive oxygen»

We show that increased mitochondrial oxidation of succinate via succinate dehydrogenase (SDH) and an elevation of mitochondrial membrane potential combine to drive mitochondrial reactive oxygen species (ROS) production.»

The expression of micro-RNA miR - 663 was induced by mitochondrial reactive oxygen species production, an apoptotic signal and oxidative stress response, and miR - 663 induced the expression of nuclear - encoded mitochondrial respiratory chain subunits.

Not exact matches

One lit up in the presence of hydrogen peroxide, a prominent reactive oxygen species, whereas the other two acted as mitochondrial injury sensors.

Mitochondrial Complex I: Partial disruption of the function of mitochondrial complex I has been shown to modestly extend life in a number of species, with the dominant theory being that this is a hormetic effect - an increase in the creation of reactive oxygen species prompts cells to react with greater repair and maintenMitochondrial Complex I: Partial disruption of the function of mitochondrial complex I has been shown to modestly extend life in a number of species, with the dominant theory being that this is a hormetic effect - an increase in the creation of reactive oxygen species prompts cells to react with greater repair and maintenmitochondrial complex I has been shown to modestly extend life in a number of species, with the dominant theory being that this is a hormetic effect - an increase in the creation of reactive oxygen species prompts cells to react with greater repair and maintenance efforts.

Reactive Oxygen Species Precede Protein Kinase Cd Activation Independent of Adenosine Triphosphate — sensitive Mitochondrial Channel Opening in Sevoflurane - induced Cardioprotection.

CLK1: Reduced CLK1 activity can extend life in mice due to altered mitochondrial function and consequently lowered generation of reactive oxygen species.

Countering the prevailing theory that cellular hydrogen peroxide signaling is broad and non-specific, Whitehead Institute scientists have discovered that this reactive oxygen species (ROS) in fact triggers a distinct signal transduction cascade under control of the mitochondrial respiratory chain — the Syk pathway — that regulates transcription, translation, metabolism, and the cell cycle in diverse cell types.

The free radical theory hypothesizes that gradual accumulation of mutations in mitochondrial DNA caused by formation of reactive oxygen species (ROS) is a major contributor.

In addition, the loss of Ripk2 has been demonstrated to result in the inability of cells to carry out mitophagy, leading to enhanced mitochondrial production of superoxide / reactive oxygen species and accumulation of damaged mitochondria that will trigger a caspase 1 — dependent inflammasome activation (Lupfer et al., 2014).

Over time however, mutations in these genes occur as a result of constant exposure to reactive oxygen species produced by oxidative phosphorylation, the mitochondrial energy generation process.

Research had shown that increased mitochondrial activity may be at least partly responsible for extending the life span of yeast, roundworms, fruit flies and some mammals — perhaps by reducing the production of disease - causing reactive oxygen species (ROS).

On the other hand, mitochondrial dysfunction, in particular increased formation of mitochondrially derived reactive oxygen species, promote Aß formation.

«Mitochondrial Production of Reactive Oxygen Species and Incidence of Age - Associated Lymphoma in OF1 Mice: Effect of Alternate - Day Fasting,» Mechanisms of Ageing and Development, 126 (11), 1185 - 1191.

In this theory, mitochondrial death from reactive oxygen species leads first to cell death, then organ death and that then kills the whole organism.

«Bioactive compounds reported to stimulate mitochondrial biogenesis are linked to many health benefits such increased longevity, improved energy utilization, and protection from reactive oxygen species.

[1] Ketogenic diet benefits body composition and well - being but not performance in a pilot case study of New Zealand endurance athletes https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5506682 [2] Ketogenic low - carbohydrate diets have no metabolic advantage over nonketogenic low - carbohydrate diets https://academic.oup.com/ajcn/article/83/5/1055/4649481 [3] Energy expenditure and body composition changes after an isocaloric ketogenic diet in overweight and obese men https://academic.oup.com/ajcn/article/104/2/324/456464 [4] Ketones block amyloid https://www.ncbi.nlm.nih.gov/pubmed/26923399 [5] Ketones Inhibit Mitochondrial Production of Reactive Oxygen Species Production Following Glutamate Excitotoxicity by Increasing NADH Oxidation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1865572/ [6] The ketogenic diet may have mood - stabilizing properties https://www.ncbi.nlm.nih.gov/pubmed/11918434 [7] The antidepressant properties of the ketogenic diet http://www.ncbi.nlm.nih.gov/pubmed/15601609

For example, KBs were recently reported to act as neuroprotective agents by raising ATP levels and reducing the production of reactive oxygen species in neurological tissues, 80 together with increased mitochondrial biogenesis, which may help to enhance the regulation of synaptic function.80 Moreover, the increased synthesis of polyunsaturated fatty acids stimulated by a KD may have a role in the regulation of neuronal membrane excitability: it has been demonstrated, for example, that polyunsaturated fatty acids modulate the excitability of neurons by blocking voltage-gated sodium channels.81 Another possibility is that by reducing glucose metabolism, ketogenic diets may activate anticonvulsant mechanisms, as has been reported in a rat model.82 In addition, caloric restriction per se has been suggested to exert neuroprotective effects, including improved mitochondrial function, decreased oxidative stress and apoptosis, and inhibition of proinflammatory mediators, such as the cytokines tumour necrosis factor - α and interleukins.83 Although promising data have been collected (see below), at the present time the real clinical benefits of ketogenic diets in most neurological diseases remain largely speculative and uncertain, with the significant exception of its use in the treatment of convulsion diseases.

Evaluation including total and progressive motility, average path velocity, morphology, membrane lipid peroxidation, presence of sperm reactive oxygen species, sperm chromatin structure, and mitochondrial DNA copy number.