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Nathan Goodyear

Anticonvulsant Mechanisms of the Ketogenic Diet - Bough - 2007 - Epilepsia - Wiley Onli... - 0 views

onlinelibrary.wiley.com/...full

ketogenic ketogenic diet seizures nutrition diet glucose mitochondria insulin ROS oxidative stress

shared by Nathan Goodyear on 16 Nov 16 - No Cached
  • The ketogenic diet (KD) is a high-fat, low-protein, low-carbohydrate diet that has been employed as a treatment for medically refractory epilepsy for 86 years
  • The hallmark feature of KD treatment is the production of ketone bodies by the liver
  • almost any diet that produces ketonemia and/or diminished blood glucose levels can induce an anticonvulsant effect.
  • Nathan Goodyear on 16 Nov 16
     
    ketogenic diet reduces seizures.  Proposed mechanisms: reduced insulin, reduced ROS, reduces oxidative stress, reduced inflammation, increased GABA/Gluatamate ratio.  In the end, it reduces inflammation and increases mitochondrial efficiency.
Nathan Goodyear

ESTROGEN SIGNALING AND NEUROPROTECTION IN CEREBRAL ISCHEMIA - 0 views

www.ncbi.nlm.nih.gov/...PMC3324183

estrogen estradiol cerebral ischemia neuordegeneration brain protection ROS oxidative stress

shared by Nathan Goodyear on 10 Mar 14 - No Cached
  • Nathan Goodyear on 10 Mar 14
     
    estradiol plays an important role in neuropreservation following cerebral ischemia.  The mechanism is through ER alpha stimulation.  The result is a reduction of ROS and oxidative stress.  This occurs through the classic intranuclear and the rapid membrane receptors as well.
Nathan Goodyear

Radical changes in multiple sclerosis pathogenesis - 0 views

www.sciencedirect.com/...S0925443910001213

ROS reactive oxygen species MS multiple sclerosis

shared by Nathan Goodyear on 19 Mar 14 - No Cached
  • Nathan Goodyear on 19 Mar 14
     
    good discussion on ROS and MS.
Nathan Goodyear

Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress - 0 views

www.ncbi.nlm.nih.gov/...PMC3107571

ER endoplasmic reticulum Neurodegeneration ROS apoptosis stress ER stress

shared by Nathan Goodyear on 09 Jul 13 - No Cached
  • Nathan Goodyear on 09 Jul 13
     
    Endoplasmic reticulum stress and the implications in neurodegenerative disease through ROS and cell death.
Nathan Goodyear

Levothyroxine and lung cancer in females: the importance of oxidative stress - 0 views

www.rbej.com/...1477-7827-11-75.pdf

T4 synthroid lung cancer oxidative stress ROS reactive oxygenation species

shared by Nathan Goodyear on 13 Aug 13 - No Cached
  • Nathan Goodyear on 13 Aug 13
     
    Study links synthetic T4, synthroid, to increased risk of Lung cancer. The authors acknowledge that the limitations of this study are large. Yet, the association is evident. The proposed mechanism is likely the overdosing and the resultant ROS as a result.
Nathan Goodyear

Aging and Luteinizing Hormone Effects on Reactive Oxygen Species Production and DNA Dam... - 0 views

www.biolreprod.org/...100.full

LH ROS reactive oxygen species oxidative stress testicles Testosterone male hormone hormones

shared by Nathan Goodyear on 04 Dec 13 - No Cached
  • Nathan Goodyear on 04 Dec 13
     
    Interesting rat model finds that stimulation of the leydig cells of the testis by LH induces ROS.  May be one of the mechanisms by which androgen therapy will induce long-term requirement for replacement.
Nathan Goodyear

PLOS ONE: Low Mercury Concentration Produces Vasoconstriction, Decreases Nitric Oxide B... - 0 views

www.plosone.org/...10.1371%2Fjournal.pone.0049005

Hg mercury NO RAS renin angiotensin system ROS hypertension oxidative stress vasoconstriction

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    Animal model found that low Hg decreased NO availability.  The result is vasoconstriction induced by ROS and hypertension. The hypertension is the result of an activation of the renin angiotensin system.  The importance here is that low Hg levels induced this change.
Nathan Goodyear

Endothelial dysfunction of rat coronary arteries after exposure to low concentrations o... - 0 views

www.ncbi.nlm.nih.gov/...PMC3081124

Hg mercury NO cardiovascular disease heart health ROS reactive oxygen species oxidative stress

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    low dose, chronic exposure induces ROS and decreased NO availability.  This decrease in NO will result in increase vasoconstriction.  This will have localized effects and will result in increased central pressure as a result of the increased peripheral pressure.  In addition, inhibition of COMT will result in increase in catecholeamines.
Nathan Goodyear

ScienceDirect - 0 views

www.sciencedirect.com/...S2213231717309424

Cancer redox ROS reactive oxygen species RNS "reactive nitrogen species" NO eNOS iNOS nNOS catalase SOD

shared by Nathan Goodyear on 04 Dec 18 - No Cached
  • Nathan Goodyear on 04 Dec 18
     
    Great review of the redox system in cancer cells. Everybody focus' on the ROS, but forget about the RNS from NO. The current marketing pushes NO for CVD.
Nathan Goodyear

Contribution of Reactive Oxygen Species to Ovarian Cancer Cell Growth Arrest and Killin... - 0 views

cancer artesunate ROS

shared by Nathan Goodyear on 06 Jun 19 - No Cached
  • Nathan Goodyear on 06 Jun 19
     
    Artesunate increased ROS in ovarian cancer cells that lead to G1 cell cycle arrest and halt in proliferation.
Nathan Goodyear

Vitamin C preferentially kills cancer stem cells in hepatocellular carcinoma via SVCT-2... - 0 views

www.nature.com/...s41698-017-0044-8

cancer cancer stem cells liver cancer vitamin C IV vitamin C oncology

shared by Nathan Goodyear on 30 Jan 18 - No Cached
  • Chen et al. have revealed that ascorbate at pharmacologic concentrations (0.3–20 mM) achieved only by intravenously (i.v.) administration selectively kills a variety of cancer cell lines in vitro, but has little cytotoxic effect on normal cells.
  • Ascorbic acid (the reduced form of vitamin C) is specifically transported into cells by sodium-dependent vitamin C transporters (SVCTs)
  • SVCT-1 is predominantly expressed in epithelial tissues
  • ...41 more annotations...
  • whereas the expression of SVCT-2 is ubiquitous
  • differential sensitivity to VC may result from variations in VC flow into cells, which is dependent on SVCT-2 expression.
  • high-dose VC significantly impaired both the tumorspheres initiation (Fig. 4d, e) and the growth of established tumorspheres derived from HCC cells (Fig. 4f, g) in a time-dependent and dose-dependent manner.
  • Hepatocellular carcinoma (HCC)
  • The antioxidant, N-acetyl-L-cysteine (NAC), preventing VC-induced ROS production (a ROS scavenger), completely restored the viability and colony formation among VC-treated cells
  • DNA double-strand damage was found following VC treatment
  • DNA damage was prevented by NAC
  • Interestingly, the combination of VC and cisplatin was even more effective in reducing tumor growth and weight
  • Consistent with the in vitro results, stemness-related genes expressions in tumor xenograft were remarkably reduced after VC or VC+cisplatin treatment, whereas conventional cisplatin therapy alone led to the increase of CSCs
  • VC is one of the numerous common hepatoprotectants.
  • Interestingly, at extracellular concentrations greater than 1 mM, VC induces strong cytotoxicity to cancer cells including liver cancer cells
  • we hypothesized that intravenous VC might reduce the risk of recurrence in HCC patients after curative liver resection.
  • Intriguingly, the 5-year disease-free survival (DFS) for patients who received intravenous VC was 24%, as opposed to 15% for no intravenous VC-treated patients
  • Median DFS time for VC users was 25.2 vs. 18 months for VC non-users
  • intravenous VC use is linked to improved DFS in HCC patients.
  • In this study, based on the elevated expression of SVCT-2, which is responsible for VC uptake, in liver CSCs, we revealed that clinically achievable concentrations of VC preferentially eradicated liver CSCs in vitro and in vivo
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      the authors here made similar mistakes to the Mayo authors i.e. under doses here in this study.  They dosed at only 2 grams IVC.  A woefully low dose of IVC.
  • Additionally, we found that intravenous VC reduced the risk of post-surgical HCC progression in a retrospective cohort study.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      positive results despite a low dose used.
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Their comfort zone was 1mM.  They should have targeted 20-40 mM.
  • Three hundred thirty-nine participants (55.3%) received 2 g intravenous VC for 4 or more days after initial hepatectomy
  • As the key protein responsible for VC uptake in the liver, SVCT-2 played crucial roles in regulating the sensitivity to ascorbate-induced cytotoxicity
  • we also observed that SVCT-2 was highly expressed in human HCC samples and preferentially elevated in liver CSCs
  • SVCT-2 might serve as a potential CSC marker and therapeutic target in HCC
  • CSCs play critical roles in regulating tumor initiation, relapse, and chemoresistance
  • we revealed that VC treatment dramatically reduced the self-renewal ability, expression levels of CSC-associated genes, and percentages of CSCs in HCC, indicating that CSCs were more susceptible to VC-induced cell death
  • as a drug for eradicating CSCs, VC may represent a promising strategy for treatment of HCC, alone or particularly in combination with chemotherapeutic drugs
  • In HCC, we found that VC-generated ROS caused genotoxic stress (DNA damage) and metabolic stress (ATP depletion), which further activated the cyclin-dependent kinase inhibitor p21, leading to G2/M phase cell cycle arrest and caspase-dependent apoptosis in HCC cells
  • we demonstrated a synergistic effect of VC and chemotherapeutic drug cisplatin on killing HCC both in vitro and in vivo
  • Intravenous VC has also been reported to reduce chemotherapy-associated toxicity of carboplatin and paclitaxel in patients,38 but the specific mechanism needs further investigation
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      so, exclude the benefit to patients until the exact mechanism of action, which will never be fully elicited?!?!?
  • Our retrospective cohort study also showed that intravenous VC use (2 g) was related to the improved DFS in HCC patients after initial hepatectomy
    • Nathan Goodyear
      Nathan Goodyear on 31 Jan 18
       
      Terribly inadequate dose.  Target is 20-40 mM which other studies have found occur with 50-75 grams of IVC.
  • several clinical trials of high-dose intravenous VC have been conducted in patients with advanced cancer and have revealed improved quality of life and prolonged OS
  • high-dose VC was not toxic to immune cells and major immune cell subpopulations in vivo
  • high recurrence rate and heterogeneity
  • tumor progression, metastasis, and chemotherapy-resistance
  • SVCT-2 was highly expressed in HCC samples in comparison to peri-tumor tissues
  • high expression (grade 2+/3+) of SVCT-2 was in agreement with poorer overall survival (OS) of HCC patients (Fig. 1c) and more aggressive tumor behavior
  • SVCT-2 is enriched in liver CSCs
  • these data suggest that SVCT-2 is preferentially expressed in liver CSCs and is required for the maintenance of liver CSCs.
  • pharmacologic concentrations of plasma VC higher than 0.3 mM are achievable only from i.v. administration
  • The viabilities of HCC cells were dramatically decreased after exposure to VC in dose-dependent manner
  • VC and cisplatin combination further caused cell apoptosis in tumor xenograft
  • These results verify that VC inhibits tumor growth in HCC PDX models and SVCT-2 expression level is associated with VC response
  • qPCR and IHC analysis demonstrated that expression levels of CSC-associated genes and percentages of CSCs in PDXs dramatically declined after VC treatment, confirming the inhibitory role of VC in liver CSCs
  • Nathan Goodyear on 30 Jan 18
     
    IV vitamin C in vitro and in vivo found to "preferentially" eradicate cancer stem cells.  In addition, IV vitamin C was found to be adjunctive to chemotherapy, found to be hepatoprotectant.  This study also looked at SVCT-2, which is the transport protein important in liver C uptake.
Nathan Goodyear

Vitamin C Mitigates Oxidative Stress and Tumor Necrosis Factor-Alpha in Severe Communit... - 0 views

www.hindawi.com/...426740

LPS lipopolysaccharides ROS TNF-alpha TNF tumor necrosis factor IL-6 inflammation pneumonia vitamin C

shared by Nathan Goodyear on 06 Dec 17 - No Cached
  • Nathan Goodyear on 06 Dec 17
     
    Cell culture study found that vitamin C inhibited LPS mediated increase in ROS, TNF-alpha, IL-6... The cells were taken from adults with pneumonia
Nathan Goodyear

Curcumin decreases malignant characteristics of glioblastoma stem cells via induction o... - 0 views

bmccancer.biomedcentral.com/...s12885-017-3058-2

STAT3 ROS MAPK curcumin glioblastoma multiforme

shared by Nathan Goodyear on 17 Apr 21 - No Cached
  • Nathan Goodyear on 17 Apr 21
     
    Curcumin increases ROS in glioblastoma.
Nathan Goodyear

Redox regulation in cancer - 0 views

www.ncbi.nlm.nih.gov/...PMC2835886

estrogen cancer stem cells reaction" CSC hormones cancer Redox

shared by Nathan Goodyear on 08 Nov 18 - No Cached
  • Mitochondrial electron-transport chain and other oxidizing agents are the prime pathways that generate excess ROS in vivo
  • Permanent modification of genetic material resulting from the oxidative damage is one of the vital steps involved in mutagenesis that leads to carcinogenesi
  • The most frequent DNA mutations caused during oxidative stress, initiated by ionizing radiation and other environmental carcinogens are 7,8-dihydro-8-oxoguanine (8-Oxo-G) and Thymine Glycol (TG)
  • ...3 more annotations...
  • catalase and SOD, GPx, GST
  • insulin like growth factor I, or fibroblast growth factor 2 generates ROS
  • Depletion of GSH increases the sensitivity of cells to ROS
  • Nathan Goodyear on 08 Nov 18
     
    The redox reaction in cancer: great read!
Nathan Goodyear

Ferritin induction protects cortical astrocytes from heme-mediated oxidative injury - S... - 0 views

www.sciencedirect.com/...S0306452202002439

ROS ferritin HO-1 heme-oxygenase-1

shared by Nathan Goodyear on 24 May 20 - No Cached
  • Nathan Goodyear on 24 May 20
     
    HO-1 induces increase in ferritin to reduce ROS
Nathan Goodyear

Molecular mechanism and functional consequences of lansoprazole-mediated heme oxygenase... - 0 views

www.ncbi.nlm.nih.gov/...PMC2747059

ferritin heme-oxygenase-1 HO-1 ROS

shared by Nathan Goodyear on 24 May 20 - No Cached
  • Nathan Goodyear on 24 May 20
     
    HO-1 and thus increase in ferritin induction by lansoprozole reduces ROS.
Nathan Goodyear

L-ascorbate Attenuates Methamphetamine Neurotoxicity Through Enhancing the Induction of... - 0 views

pubmed.ncbi.nlm.nih.gov/23022510

heme-oxygenase-1 vitamin C oxidative stress ROS reactive oxygen species

shared by Nathan Goodyear on 24 May 20 - No Cached
  • Nathan Goodyear on 24 May 20
     
    vitamin C reduces methamphetamine induced ROS view upregulation of heme-oxygenase-1 expression.
Nathan Goodyear

Nutrition Journal | Full text | Homocysteine and reactive oxygen species in metabolic s... - 0 views

www.nutritionj.com/4

homocysteine atherogenesis CVD metabolic syndrome metabolic syndrome

shared by Nathan Goodyear on 23 Jul 12 - No Cached
  • Nathan Goodyear on 23 Jul 12
     
    homocysteine contributes to atherogenesis and CVD via: increased ROS, induces endothelial dysfunction, increases platelete adhesion and thrombosis, increases smooth muscle cell proliferation, endothelial cell cytotoxicity, increases LDL oxidation, vasoconstriction, increased MCP-1 and IL-8, and induces endothelial HMG CoA reductase.
Nathan Goodyear

Clinical and Pathological Roles of Ro/SSA Autoantibody System - 0 views

www.hindawi.com/...606195

Anti-SSA antibodies Anti-Ro Lupus Sjogren's syndrome autoimmune disease

shared by Nathan Goodyear on 12 Aug 13 - No Cached
  • Nathan Goodyear on 12 Aug 13
     
    Clinical use of anti-SSA antibodies.  Most commonly linked with Lupus and Sjogren's syndrome.  
Nathan Goodyear

Urinary Estrogens and Estrogen Metabolites and Subsequent Risk of Breast Cancer among P... - 0 views

cancerres.aacrjournals.org/...696.full

estrogen metabolites estrogen metabolism ER estrogen receptors ROS hormones cancer breast cancer

shared by Nathan Goodyear on 07 Oct 15 - No Cached
  • both 2- and 4-catechol estrogen metabolites bind to the ER with affinities comparable with estradiol, 4-catechol estrogen metabolites have lower dissociation rates than estradiol and an enhanced ability to upregulate ER-dependent processes
  • 2-catechol estrogen metabolites act as either weak mitogens (39) or weak inhibitors of cell proliferation
  • While 16α-hydroxyestrone binds to the ER with lower affinity than estradiol, it binds covalently (41) and leads to a constitutively activated ER
  • ...15 more annotations...
  • 4-hydroxyestradiol and 16α-hydroxyestrone increasing proliferation and decreasing apoptosis in a manner similar to estradiol; however, these effects were achieved only at concentrations 10-fold higher than estradiol (39). In contrast, 2-hydroxyestradiol did not have substantial proliferative or antiapoptotic effects
  • In our study, the associations with both 2-hydroxyestrone and 16α-hydroxyestrone were nonsignificantly inverse and we did not observe a consistent trend or significant associations between the 2-hydroxyestrone:16α-hydroxyestrone ratio and breast cancer risk
  • Ratios of the 3 hydroxylation pathways were not significantly associated with risk although the 2:16-pathway and 4:16-pathway ratios were suggestively inversely associated
  • a significant inverse association with the ratio of parent estrogens to estrogen metabolites
  • several potentially estrogenic and genotoxic mechanisms
  • Estrogen metabolites also can be genotoxic
  • Catechol estrogens can be oxidized into quinones and induce DNA damage directly through the formation of DNA adducts, or indirectly via redox cycling and generation of reactive oxygen species
  • the oxidized forms of the catechol estrogens differ in their ability to damage DNA through adducts, with oxidized 2-catechols forming stable and reversible DNA adducts and oxidized 4-catechols forming unstable adducts, which lead to depurination and mutations
  • 2- and 4-catechols have been shown to produce reactive oxygen species and induce oxidative DNA damage
  • act independently from the ER
  • 16α-Hydroxyestrone also may be genotoxic
  • While the catechol estrogens have estrogenic and genotoxic potential, the methylated catechol estrogens, which are catechol estrogens with one hydroxyl group methylated, have been hypothesized to lower the risk of breast cancer
  • The suggested mechanisms are indirect, by decreasing circulating levels of catechol estrogens and thereby the opportunity for catechols to exert genotoxic or proliferative effects, or direct, by inhibiting tumor growth and inducing apoptosis
  • the balance between phase I (oxidation) and phase II (methylation) metabolism of estrogen may be important in hormonally related cancer development.
  • Despite the estrogenic and genotoxic potential of many of the estrogen metabolites, we only observed a significantly increased breast cancer risk with one estrogen metabolite, 17-epiestriol, which has particularly strong estrogenic activity and binds to both ERα and ERβ with an affinity comparable with estradiol
  • Nathan Goodyear on 07 Oct 15
     
    review of estrogen metabolites and breast cancer risk in premenopausal women.
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