Skip to main content

Home/ Dr. Goodyear/ Group items tagged oxidative Stress

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
Nathan Goodyear

Oxidative Stress in Autism - 0 views

www.modernhcp.com/...imcj%208061.pdf

oxidative stress autism ASD oxidative stress selenium detoxification

shared by Nathan Goodyear on 14 Aug 13 - No Cached
  • Nathan Goodyear on 14 Aug 13
     
    high oxidative stress in autism will compromise detoxification. OR is it the other way around? Low Selenium is commonly found in those with autism.
Nathan Goodyear

Role of oxidative stress from mitochondria on agin... [Cornea. 2007] - PubMed result - 0 views

www.ncbi.nlm.nih.gov/...17881913

oxidative mitochondria stress cancer

shared by Nathan Goodyear on 08 Feb 11 - No Cached
  • t is suggested that oxidative stress from mitochondria plays an important role in apoptosis, which leads to precocious aging and cancer.
  • Nathan Goodyear on 08 Feb 11
     
    oxidative stress, mitochondrial death, and cancer 
Nathan Goodyear

Ferrous iron content of intravenous iron formulations - 0 views

www.ncbi.nlm.nih.gov/...PMC4879161

M1 macrophages NK cells FE IRON M1 venofer oxidative stress

shared by Nathan Goodyear on 28 Jun 19 - No Cached
  • Nathan Goodyear on 28 Jun 19
     
    Study finds that IV venofer increases oxidative stress and immune modulation to increase M1 but decreased NK cell expression. The study found that this was related to the effects of the IV Fe2+ (ferrous) form; whereas the oral delivered Fe3+ (ferric) form. More free Fe2+ was released as a result of venofer infusion that was independent of transferrin. This was associated with increased oxidative stress.
Nathan Goodyear

American College of Cardiology Foundation | Journal of the American College of Cardiolo... - 0 views

content.onlinejacc.org/article.aspx

mitochondria oxidative stress heart failure heart

shared by Nathan Goodyear on 19 Mar 13 - No Cached
  • Although currently no drugs that specifically target mitochondrial biogenesis in HF are available, acceleration of this process through adenosine monophosphate–activated kinase (AMPK), endothelial nitric oxide synthase (eNOS), and other pathways may represent a promising therapeutic approach
  • Mitochondrial biogenesis can be enhanced therapeutically with the use of adenosine monophosphate kinase (AMPK) agonists, stimulants of nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway (including phosphodiesteraes type 5 inhibitors), or resveratrol
  • metformin, a commonly used antidiabetic drug that activates AMPK signaling
  • ...10 more annotations...
  • Recent evidence suggests that the eNOS/NO/cGMP pathway is an important activator of mitochondrial biogenesis
  • BH4 (tetrahydrobiopterin) supplementation can prevent eNOS uncoupling and was found to reduce left ventricular hypertrophy
  • folic acid is known to replenish reduced BH4 and has been shown to protect the heart through increased eNOS activity
  • Both folate deficiency and inhibition of BH4 synthesis were associated with reduced mitochondrial number and function
  • Resveratrol, a polyphenol compound responsible for the cardioprotective properties of red wine, was recently identified as a potent stimulator of mitochondrial biogenesis
  • epidemiological studies reveal a reduced risk of cardiovascular disease in premenopausal, but not post-menopausal, women compared with men
  • post-menopausal women
    • Nathan Goodyear
      Nathan Goodyear on 19 Mar 13
       
      I would hypothesis that a change in the predominance of ER expression is one of ER beta to ER alpha: creating a more pro-inflammatory signal.
  • The majority of ROS in the heart appear to come from uncoupling of mitochondrial electron transport chain at the level of complexes I and III
  • Because the majority of ROS in HF comes from mitochondria, these organelles are the primary target of oxidative damage.
  • cardioprotective therapies such as angiotensin-converting enzyme inhibitors and ATII receptor blockers were shown to possess antioxidant properties, although it is not known whether they target mitochondrial ROS directly or indirectly
  • Nathan Goodyear on 19 Mar 13
     
    great review of mitochondrial biogenesis, oxidative stress and heart failure.  
Nathan Goodyear

Obesity - Amelioration of Lipid Abnormalities by [alpha]-Lipoic acid Through Antioxidat... - 0 views

www.nature.com/...oby2011121a.html

ALA alpha-lipoic-acid lipoic acid obesity insulin oxidative stress damage inflammation inflammatory markers cytokine cytokines TNF-alpha IL-6 adiponectin IV intravenous oxidized LDL

shared by Nathan Goodyear on 01 Aug 12 - No Cached
  • Nathan Goodyear on 01 Aug 12
     
    alpha lipoic acid found to improve insulin sensitivity and reduce oxidative stress and inflammatory markers.  In this study, IV ALA was given daily for 2 weeks, and the result was reduced oxidized LDL and all other lipids, improved insulin sensitivity, reduced TNF-alpha, IL-6, and 8-iso-prostaglandin, and increased adiponectin.
Nathan Goodyear

ScienceDirect - Food and Chemical Toxicology : Neuroprotective effect of ginger on anti... - 0 views

www.sciencedirect.com/science

Ginger diabetes oxidative stress

shared by Nathan Goodyear on 27 Apr 11 - No Cached
  • A marked decrease in anti-oxidant marker enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH) and increase in malondialdehyde (MDA) was observed in the diabetic rats
  • inger may be used as therapeutic agent in preventing complications in diabetic patients.
  • These results suggest that ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats
  • Nathan Goodyear on 27 Apr 11
     
    Ginger reduces oxidative stress in diabetic rat model
Nathan Goodyear

Frontiers | Management of Glioblastoma Multiforme in a Patient Treated With Ketogenic M... - 0 views

www.frontiersin.org/...full

press-pulse therapy hyperbaric ketogenic metabolic therapy cancer ketogenic diet Glioblastoma glioblastoma multiforme HBOT nutrition

shared by Nathan Goodyear on 01 Apr 18 - No Cached
  • The SOC for GBM was modified in this patient to initiate KMT prior to surgical resection, to eliminate steroid medication, and to include HBOT as part of the therapy
  • the greatest therapeutic benefit for patients (near 1.0)
  • The observed reduction in blood glucose in our patient would reduce lactic acid fermentation in the tumor cells, while the elevation of ketone bodies would fuel normal cells thus protecting them from hypoglycemia and oxidative stress
  • ...30 more annotations...
  • Previous studies showed that GBM survival and tumor growth was correlated with blood glucose levels
  • Evidence indicates that glioma cells cannot effectively use ketone bodies for energy due to defects in the number, structure, and function of their mitochondria
  • The accuracy of the GKI as a predictor for therapeutic efficacy, however, is better when ketone bodies are measured from the blood than when measured from the urine
  • A reduction of glucose-driven lactic acid fermentation would not only increase tumor cell apoptosis, but would also reduce inflammation and edema in the tumor microenvironment thus reducing tumor cell angiogenesis and invasion
  • Besides serving as a metabolic fuel for GBM, glutamine is also an essential metabolite for normal immune cells
  • therapies that inhibit glutamine availability and utilization must be strategically employed to avoid inadvertent impairment of immune cell functions
  • we used the non-toxic green tea extract, EGCG, and chloroquine in an attempt to limit glutamine availability to the tumor cells
  • EGCG is thought to target the glutamate dehydrogenase activity that facilitates glutamine metabolism in GBM cells
  • Chloroquine, on the other hand, will inhibit lysosomal digestion thus restricting fermentable amino acids and carbohydrates from phagocytosed materials in the tumor microenvironment
  • HBOT to increase oxidative stress in the tumor cells
  • As glucose and glutamine fermentation protect tumor cells from oxidative stress, reduced availability of these metabolites under ketosis could enhance the therapeutic action of HBOT, as we recently described
  • Prior to subtotal tumor resection and standard of care (SOC), the patient conducted a 72-h water-only fast
  • Following the fast, the patient initiated a vitamin/mineral-supplemented ketogenic diet (KD) for 21 days that delivered 900 kcal/day
  • KD (increased to 1,500 kcal/day at day 22
  • the patient received metformin (1,000 mg/day), methylfolate (1,000 mg/day), chloroquine phosphate (150 mg/day), epigallocatechin gallate (400 mg/day), and hyperbaric oxygen therapy (HBOT) (60 min/session, 5 sessions/week at 2.5 ATA)
  • Biomarkers showed reduced blood glucose and elevated levels of urinary ketones with evidence of reduced metabolic activity (choline/N-acetylaspartate ratio) and normalized levels of insulin, triglycerides, and vitamin D
  • This is the first report of confirmed GBM treated with a modified SOC together with KMT and HBOT, and other targeted metabolic therapies
  • Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers
  • less than 20% of younger adults generally survive beyond 24 months
  • glucose and glutamine are the primary fuels that drive the rapid growth of most tumors including GBM
  • Glucose drives tumor growth through aerobic fermentation (Warburg effect), while glutamine drives tumor growth through glutaminolysis
  • The fermentation waste products of these molecules, i.e., lactic acid and succinic acid, respectively, acidify the tumor microenvironment thus contributing further to tumor progression
  • Glucose and glutamine metabolism is also responsible for the high antioxidant capacity of the tumor cells thus making them resistant to chemo- and radiotherapies
  • The reliance on glucose and glutamine for tumor cell malignancy comes largely from the documented defects in the number, structure, and function of mitochondria and mitochondrial-associated membranes
  • These abnormalities cause the neoplastic GBM cells to rely more heavily on substrate level phosphorylation than on oxidative phosphorylation for energy
  • dexamethasone not only increases blood glucose levels but also increases glutamine levels through its induction of glutamine synthetase activity
    • Nathan Goodyear
      Nathan Goodyear on 21 May 18
       
      use mannitol instead
  • Calorie restriction and restricted KD are anti-angiogenic, anti-inflammatory, anti-invasive, and also kill tumor cells through a proapoptotic mechanism
  • Evidence also shows that therapeutic ketosis can act synergistically with several drugs and procedures to enhance cancer management improving both progression free and overall survival
  • hyperbaric oxygen therapy (HBOT) increases oxidative stress on tumor cells especially when used alongside therapies that reduce blood glucose and raise blood ketones
  • The glutamine dehydrogenase inhibitor, epigallocatechin gallate (EGCG) is also proposed to target glutamine metabolism
  • Nathan Goodyear on 01 Apr 18
     
    Case study of Glioblastoma treated with ketogenic metabolic therapy as an adjuct to modified standard therapy.
Nathan Goodyear

Apolipoprotein E allele-dependent antioxidant activity in brains with Alzheimer's disease - 0 views

www.neurology.org/...2319.abstract

antioxidant alzheimer disease brains neurology brain TBARS oxidative stress lipid peroxidation

shared by Nathan Goodyear on 13 Jun 12 - No Cached
  • Nathan Goodyear on 13 Jun 12
     
    TBARS were found elevated in Alzheimer's individuals.  TBARS are the result of oxidative stress.  Thus TBARS can be used to evaluate lipid peroxidation (oxidative damage) in the brain.
Nathan Goodyear

Metabolic biomarkers of increased oxidative stress... [Am J Clin Nutr. 2004] - PubMed r... - 0 views

www.ncbi.nlm.nih.gov/...15585776

ASD autism spectrum disorder detoxification children SAMe SAH homocysteine cystathionine glutathione adenosine

shared by Nathan Goodyear on 05 Jul 11 - No Cached
  • children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione
  • This metabolic profile is consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione) in children with autism
  • increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism.
  • Nathan Goodyear on 05 Jul 11
     
    detoxification impairment and the markers to assess it in children with ASD
Nathan Goodyear

Unveiling the Mechanisms for Decreased Glutathione in Individuals with HIV Infection - 0 views

connection.ebscohost.com/...ione-individuals-hiv-infection

glutathione GSH Nrf2 GSSG HIV inflammation oxidative Stress

shared by Nathan Goodyear on 07 Jan 15 - No Cached
  • Nathan Goodyear on 07 Jan 15
     
    men with HIV have GSH depleted macrophages.  GSH is the reduced, ready to act form of Glutathione.  In contrast, the macrophages were high in the oxidized form of Glutathione--GSSG.  In HIV, the high inflammation increased oxidative stress, likely overwhelmed Nrf2 activation and resulted in decreased GSH synthase transcription and thus decreased Glutathione production balance.
Nathan Goodyear

Oncotarget | NADH autofluorescence, a new metabolic biomarker for cancer stem cells: Id... - 0 views

www.oncotarget.com/index.php

vitamin C IV vitamin C cancer cancer stem cells milk thistle silymarin ascorbic acid bee propolis CAPE glycolytic inhibitor natural

shared by Nathan Goodyear on 08 Dec 17 - No Cached
  • Vitamin C was ~10 times more potent than 2-DG for the targeting of CSCs
  • Cancer stem-like cells (CSCs) are thought to be the root cause of chemotherapy-resistance and radio-resistance
  • ultimately leading to treatment failure in patients with advanced disease [1-3]. They have been directly implicated mechanistically in tumor recurrence and metastasis, resulting in poor patient survival
  • ...26 more annotations...
  • mitochondrial biogenesis may be a key driver of the CSC phenotype
  • Our results indicate that increased mitochondrial oxidative stress and high NADH levels are both key characteristics of the CSC metabolic phenotype
  • high levels of NAD(P)H auto-fluorescence are known to be a surrogate marker for mitochondrial “power”, high OXPHOS capacity and increased ATP production
  • CSCs may be strictly dependent on NAD(P)H to maintain their enhanced mitochondrial function
  • an intact NAD+ salvage pathway is strictly required for mammosphere formation, supporting our results using NAD(P)H auto-fluorescence, which enriched CSC activity by more than 5-fold.
  • Since glycolysis is especially critical for maintaining the TCA cycle, OXPHOS and overall mitochondrial function, we next assessed the effects of known glycolytic inhibitors
  • we show that two other natural products that function as effective glycolysis inhibitors, also inhibited mammosphere formation. More specifically, vitamin C (ascorbic acid), which induces oxidative stress and inhibits the activity of GAPDH (a key glycolytic enzyme) [17], also inhibited mammosphere formation, with an IC-50 of 1 mM (Figure 7B). Therefore, vitamin C was ~10 times more potent than 2-DG at targeting CSC propagation
  • silibinin (the major active constituent of silymarin, an extract of milk thistle seeds) [18], which specifically functions as an inhibitor of glucose uptake, blocked mammosphere formation, with an IC-50 between 200 and 400 µM
  • caffeic acid phenyl ester (CAPE), a key component of honey-bee propolis, has potent anti-cancer properties
  • Propolis has a strong history of medicinal use, dating back more than 2,000 years
  • Because of it aromatic ring structure (Figure 8), we speculated that CAPE might function as a potent inhibitor of oxidative mitochondrial metabolism
  • CAPE quantitatively inhibits the mitochondrial oxygen consumption rate (OCR) and, in turn, induces the onset of aerobic glycolysis (ECAR)
  • CAPE shows a clear selectivity for targeting CSCs and adherent cancer cells, relative to normal fibroblasts.
  • CAPE functions as a “natural” mitochondrial OXPHOS inhibitor, that preferentially targets the CSC sub-population. This could explain CAPE’s known anti-cancer properties
  • Our data directly shows that a small fraction of the total cell population, characterized by increased PGC1α activity, high mitochondrial ROS/H2O2 and high NADH levels, has the ability to survive and grow under anchorage-independent conditions, driving mammosphere formation
  • We highlight the utility of certain natural products, such as Silibinin, Vitamin C and CAPE, that could be used to therapeutically target CSCs. Silibinin is the major active component of silymarin, which is an extract prepared from milk thistle seeds.
  • high NADH is a property that is conserved between normal and cancerous stem cells
  • Previous studies have also shown that when non-CSCs and CSCs are both fed mitochondrial fuels (such as L-lactate or ketone bodies), that CSCs quantitatively produce more NADH in response to this stimulus
  • CSCs may be strictly dependent on NADH to maintain their enhanced mitochondrial function
  • The Noble Prize winner, Linus Pauling, was among the first to describe and clinically test the efficacy of Vitamin C, as a relatively non-toxic anti-cancer agent
  • Vitamin C has two mechanisms of action. First, it is a potent pro-oxidant, that actively depletes the reduced glutathione pool, leading to cellular oxidative stress and apoptosis in cancer cells. Moreover, it also behaves as an inhibitor of glycolysis, by targeting the activity of GAPDH, a key glycolytic enzyme.
  • Here, we show that Vitamin C can also be used to target the CSC population, as it is an inhibitor of energy metabolism that feeds into the mitochondrial TCA cycle and OXPHOS
  • Vitamin C may prove to be promising agent for new clinical trials, aimed at testing its ability to reduce CSC activity in cancer patients, as an add-on to more conventional therapies, to prevent tumor recurrence, further disease progression and metastasis
  • Interestingly, a breast cancer based clinical study has already shown that the use of Vitamin C, concurrent with or within 6 months of chemotherapy, significantly reduces both tumor recurrence and patient mortality
  • CAPE quantitatively reduces mitochondrial oxygen consumption (OCR), while inducing a reactive increase in glycolysis (ECAR). As such, it potently inhibits mammosphere formation with an IC-50 of ~2.5 µM. Similarly, it also significantly inhibits cell migration
  • we also demonstrate that 7 different inhibitors of key energetic pathways can be used to effectively block CSC propagation, including three natural products (silibinin, ascorbic acid and CAPE). Future studies will be necessary to test their potential for clinical benefit in cancer patients.
  • Nathan Goodyear on 08 Dec 17
     
    The future of cancer therapy is cancer stem cells.  Study finds that Vitamin C, silymarin, and bee propolis blocks mitochondrial energy pathways in cancer stem cells.  Vitamin C is a known glycolytic inhbitor. Vitamin C was found to inhibit glycolysis via GAPDH targeting to inhibit the energy pathways of the mitochondria in CSCs.  The authors propse that Vitamin C can be used as add on therapies for conventional therapies to specifically attack the CSCs and their contribution to recrurence, treatment resistance, and metastasis potential all in addition to the ability of vitamin C to reduce the side effects of chemotherapy.
Nathan Goodyear

Type 1 5'-deiodinase activity is inhibited by oxidative stress and restored by alpha-li... - 0 views

www.ncbi.nlm.nih.gov/...26947333

thyroid T3 oxidative stress alpha lipoic acid deiodinase rT3 reverse T3 thyroid metabolites thyroid metabolism hormones

shared by Nathan Goodyear on 28 Sep 16 - No Cached
  • Nathan Goodyear on 28 Sep 16
     
    oxidative stress decreased type 1 deiodinase activity and thus T4 to T3 conversion, resulting in increased rT3 production.  Of interesting note, Alpha lipoic acid increased type I deiodinase activity and T4 to T3 conversion.
Nathan Goodyear

Chronic antioxidant treatment improves arterial renovascular hypertension and oxidative... - 0 views

www.ncbi.nlm.nih.gov/...20186128

blood pressure hypertension vitamin C oxidative stress

shared by Nathan Goodyear on 16 Jan 17 - No Cached
  • Nathan Goodyear on 16 Jan 17
     
    animal study finds vitamin C improves hypertension via renovascular source and oxidative stress.  The dosage was 150 mg/kg/day.  This would be equivalent to 10,800 grams daily for a 72 human.  But what about a 200 lb male or female?  That would be 13,650 grams of vitamin C daily.
Nathan Goodyear

Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in... - 0 views

www.ncbi.nlm.nih.gov/...PMC2845588

astaxanthin inflammation oxidative stress CRP antioxidants

shared by Nathan Goodyear on 31 May 16 - No Cached
  • Nathan Goodyear on 31 May 16
     
    astaxanthin reduced oxidative stress biomarker and inflammation in human study.
Nathan Goodyear

Omega-3 LCPUFA supplement: a nutritional strategy to prevent maternal and neonatal oxid... - 0 views

www.ncbi.nlm.nih.gov/...27072591

omega 3 omega-3 oxidative stress pregnancy

shared by Nathan Goodyear on 25 Apr 16 - No Cached
  • Nathan Goodyear on 25 Apr 16
     
    Omega 3 supplementation prevented oxidative stress in pregnancy.
Nathan Goodyear

DASH Diet Lowers Blood Pressure and Lipid-Induced Oxidative Stress in Obesity - 0 views

hyper.ahajournals.org/...422.full

DASH diet dietary lifestyle changes oxidative stress inflammation IR insulin resistance obesity overweight HTN hypertension blood pressure

shared by Nathan Goodyear on 14 Jan 12 - No Cached
  • Nathan Goodyear on 14 Jan 12
     
    DASH diet shown to lower oxidative stress, inflammation, improve insulin resistance, lower inflammation, and aid weight loss.
Nathan Goodyear

RB&E | Abstract | Levothyroxine and lung cancer in females: the importance of oxidative... - 0 views

www.rbej.com/...abstract

levothyroxine T4 lung cancer hypothyroid oxidative stress

shared by Nathan Goodyear on 22 Dec 13 - No Cached
  • Nathan Goodyear on 22 Dec 13
     
    Interesting study finds T4 therapy, levothyroxine,  linked to increased lung cancer.  The link could be through oxidative stress.
Nathan Goodyear

Effects of astaxanthin on oxidative stress in overweight and obese adults. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...21480416

oxidative stress astaxanthin malondialdehyde superoxide disumutase isoprostane

shared by Nathan Goodyear on 14 Jul 15 - No Cached
  • Nathan Goodyear on 14 Jul 15
     
    short study found that astaxanthin at 5 and 20 mg was associated with a reduction in oxidative stress biomarkers.
Nathan Goodyear

Glucose Fluctuations in Association With Oxidative Stress Among Children With T1DM: Com... - 0 views

press.endocrine.org/...jc.2014-2879

diabetes oxidative stress

shared by Nathan Goodyear on 20 May 15 - No Cached
  • Nathan Goodyear on 20 May 15
     
    glucose fluctuations in type I diabetic children associated with oxidative stress.
Nathan Goodyear

Increased oxidative stress in obesity: Implications for metabolic syndrome, diabetes, h... - 0 views

www.sciencedirect.com/...S1871403X13000434

oxidative stress obesity hypertension dyslipidemia atherosclerosis cancer metabolic syndrome

shared by Nathan Goodyear on 11 Nov 13 - No Cached
  • Nathan Goodyear on 11 Nov 13
     
    increased oxidative stress, from obesity, linked to most diseases of aging.
‹ Previous 21 - 40 of 221 Next › Last »
Showing 20▼ items per page