Sentences with phrase «increased reactive oxygen»

Increased reactive oxygen species (ROS) levels have been observed in post-mortem brain tissue from patients with neurodegenerative disorders, including [9]:

«Past studies have shown that having low antioxidant levels and increased reactive oxygen species — chemical products that bind to body cells and cause damage — is related to more severe PAD,» said Matthew Muller, postdoctoral fellow in Larry Sinoway's lab at Penn State College of Medicine, and lead author of the study.

Abstract: Gain - of - function mutations in the presenilin - 1 (PS - 1) promote Alzheimer's disease (AD) by increasing reactive oxygen species, at least part of which is derived by an accompanying increase in generation of amyloid - β (Aβ).

Gain - of - function mutations in the presenilin - 1 (PS - 1) promote Alzheimer's disease (AD) by increasing reactive oxygen species, at least part of which is derived by an accompanying increase in generation of amyloid - β (Aβ).

Anti-cancer drugs often increase reactive oxygen species (ROS) and cause DNA damage.

In particular, our results demonstrate that LA increases reactive oxygen species levels, stimulates the phosphorylation of EGFR, ERK and c - Jun and induces the expression of c - fos.

LTB4 increases edema and chemotaxis, induces release of lysosomal enzymes, increases reactive oxygen species, and enhances production of the cytokines TNF - α, IL - 1, and IL - 6.»

Not exact matches

After 10 days of smoke exposure, the scientists found an overall increase in DNA damage responses to so - called reactive oxygen species within the cells.

Scientists have long assumed that wounded mitochondria release reactive oxygen molecules, which then damage DNA and proteins, increasing disease risk.

At the hearing, Carpenter suggested that cell phones may increase the brain's production of reactive forms of oxygen called free radicals, which can interact with and damage DNA.

One explanation is that the plant sterol diet increased formation of reactive oxygen species in the hippocampus, whereas the Fortasyn diet, which yielded the best results in the spatial memory task, tended to have an opposite effect.

Mitochondria help injured muscle cells (myofibers) repair by soaking up calcium that enters from the site of injury and using it to trigger increased production of reactive oxygen species.

Her research team found that cellular oxidative stress (arising because of reactive oxygen species) increases in mice exposed to THS, damaging proteins, fats and DNA, and leading to hyperglycemia (excess glucose in the blood stream) and insulinemia (excess insulin in the blood)-- a condition also called insulin resistance.

Increased glucose processing has long been thought to inflict damage on the mitochondria (the cell's power generators), which then produce large amounts of reactive oxygen molecules, which in turn leads to kidney disease.

Reactive oxygen species (ROS) induce cellular damages at different levels (proteins, DNA, and lipids) which increase the body susceptibility to noxious injuries with the final result to accelerate aging and decrease lifespan.

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 maintenance efforts.

Specifically, researchers observed a reduction of reactive oxygen species; increase in collagen, which strengthens the fibrous cap; and reduction of the plaque necrotic core, and these changes were not observed in comparison with the free peptide or empty nanoparticles.

The addition of this pendant catalyst created an MnP - PVPON / TA capsule with the following characteristics: 1) the microcapsules synergistically remove reactive oxygen species, including superoxide and hydrogen peroxide, at dramatically increased rates compared to unmodified TA / PVPON microcapsules; 2) the microcapsule does not degrade with long exposure to reactive oxygen species; and 3) the microcapsules are nontoxic to mouse splenocytes.

In the hypothalamus, inhibits leptin - induced reactive oxygen species (ROS) formation and mediates cannabinoid - induced increase in SREBF1 and FASN gene expression (PubMed: 25869131).

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).

THE PEAK OF OXYGEN CONSUMPTION AT THE TIME OF SPERM PENETRATION IS ASSOCIATED WITH AN INCREASE IN REACTIVE OXYGEN SPECIES PRODUCTION IN BOVINE ZYGOTES.

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

For this reason, it is very anti-inflammatory and can reduce reactive oxygen species by increasing oxygen levels.

Specifically, the research demonstrates that grape seed not only damages cancer cells» DNA (by means of an increase of reactive oxygen species), but also prevents the pathways which allow repair (as seen by reduced amounts of the DNA repair molecules Rad51 and Brca1 as well as DNA repair foci).

One eight - month IER trial in obesity - prone rats reported an increase in theproduction of reactive oxygen species (ROS), with no clear mechanistic explanations.26 Another trial, this time over six months, showed that IER - fed rats displayed marked reductions in diastolic compliance and cardiac reserve due to observed reductions in cardiomyocyte size and increased myocardial fibrosis.23 No human trials to date have reported any adverse effects on cardiovascular health during long - term IER.

The resulting drop in glutathione production and intracellular glutathione concentrations compromises the mitochondria's ability to scavenge reactive oxygen species (ROS), producing a vicious cycle that drives the progressive increase in ROS - mediated structural damage and its corollary, the progressive decline in energy production and repair that accompanies aging.

Abnormal Krebs cycle and / or oxidative phosphorylation cause (s) not only glucose hypometabolism but also the increased generation of reactive oxygen species (ROS), oxidative damage, and programmed cell death such as apoptosis.

The other study on simulated digestion was similar: wild raspberries inhibited reactive oxygen species (free radical) generation, stabilised cell membranes, and increased glutathione levels.

Reactive oxygen species (ROS) are not universally bad, and one of their important functions is to signal the body to increase protein synthesis as part of the mTOR pathway.

In vitro, IF pancreatic islets had increased insulin secretion, glucose metabolism and net reactive oxygen species production, while decreased their mass.

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.»

Both factors may elicit a sympathetic and hypothalamic — pituitary — adrenal (HPA) axis response, which drive increased systemic reactive oxygen species production, chronic inflammation, and a metabolic substrate shift toward carbohydrate and away from fat oxidation, manifesting in an array of signs and symptoms often labeled as the overtraining syndrome.16

«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

It has been known for quite some time that intense exercise increases the production of potentially toxic reactive oxygen species (ROS), which have been linked to aging and most chronic diseases, one way or another.

Credit: ZEISS Microscopy Transient, specific bursts of reactive oxygen species can extend lifespan in C. elegans To many people it may sound counter-intuitive to use reactive oxygen species (ROS) as a way to increase lifespan.

So, the thinking is that lower methionine intake leads to less free radical production — the so - called «reactive oxygen species,» which slows the rate of DNA damage, which then would slow the rate of DNA mutation, slowing the rate of aging and disease — thereby potentially increasing our lifespan.

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.

n - 3 fatty acids are polyunsaturated and are very sensitive to reactive oxygen species which in results may increase the risk of CVD or other diseases.

As congestive heart failure progresses, the formation of «free radicals» (reactive molecules created during oxygen metabolism) increases heart cell damage.