Skip to main content

Home/ Dr. Goodyear/ Group items tagged N-acetylcysteine

Rss Feed Group items tagged

Filter: All | Bookmarks | Topics Simple Middle
Nathan Goodyear

Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity ... - 0 views

erj.ersjournals.com/...1535.full.pdf+html

flu influenza NAC N-acetylcysteine immunity

shared by Nathan Goodyear on 18 Jan 13 - No Cached
  • Nathan Goodyear on 18 Jan 13
     
    N-acetylcysteine, also known as NAC, a precursor to glutathione, is shown to significantly reduce the incidence of flu symptoms.  NAC should be taken through out the winter months as a flu prevention?  Well, this study does not support that, but if one gets the flu, NAC will significantly reduce the flu symptoms.
Nathan Goodyear

Controlled trial of N-acetylcysteine for patients with probable Alzheimer's disease - 0 views

www.medicinalnutraceutics.com/...AC%20Alzheimer's%20Disease.pdf

NAC N-acetylcysteine AD Alzheimer's disease Alzheimers inflammation AGE advanced glycation end products

shared by Nathan Goodyear on 11 Jun 12 - No Cached
  • Nathan Goodyear on 11 Jun 12
     
    NAC shown to improve secondary measures of cognitive function in small study in those with Alzheimer's disease. NAC proves to be a reliable means to reduce free radical induced advanced glycation end productions and resultant inflammation. Also was shown to be well tolerated.
Nathan Goodyear

N-acetylcysteine (NAC) in neurological disorders: mechanisms of action and therapeutic ... - 0 views

www.ncbi.nlm.nih.gov/...PMC3967529

NAC N-acetylcysteine MS multiple sclerosis

shared by Nathan Goodyear on 30 Oct 16 - No Cached
  • There is a marked increase in expression of TNF in active multiple sclerosis (MS)
  • a correlation exists between cerebrospinal fluid levels of TNF and the severity and progression of disease
  • With cytokine activation, free-radical production increases and this has been demonstrated in MS
  • ...1 more annotation...
  • NAC inhibits the toxicity of TNF and in an animal model of MS
  • Nathan Goodyear on 30 Oct 16
     
    Good discussion of NAC and neurodegenerative diseases.
Nathan Goodyear

N-Acetylcysteine: Multiple Clinical Applications - August 1, 2009 - American Family Phy... - 0 views

www.aafp.org/...p265.html

NAC N-acetylcysteine detoxification

shared by Nathan Goodyear on 02 Mar 12 - No Cached
  • Nathan Goodyear on 02 Mar 12
     
    use of NAC provides many health benefits above and beyond tylenol overdose.
Nathan Goodyear

A Randomized Controlled Pilot Trial of Oral N-Acetylcysteine in Children with Autism - 0 views

www.biologicalpsychiatryjournal.com/...fulltext

autism ASD glutathione NAC N-acetylcysteine children

shared by Nathan Goodyear on 04 Mar 14 - No Cached
  • Nathan Goodyear on 04 Mar 14
     
    900 mg of NAC over short 4 week course provided significant improvement in behavior of children with autism.  No pre treatment evaluation was performed.  One wonders if therapeutic therapy was actually undertaken if the results would have been better.  NAC is a precursor to Glutathione production and detoxification compromise is common place in autism.
Nathan Goodyear

N-Acetylcysteine for Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis o... - 0 views

www.ncbi.nlm.nih.gov/...PMC4306416

NAC N-acetylcysteine PCOS infertility women women's health female hormone hormones

shared by Nathan Goodyear on 23 Feb 15 - No Cached
  • compared effects of NAC with placebo or metformin in women with PCOS
  • NAC significantly improved rates of live births and spontaneous ovulation compared to placebo in women with PCOS
  • we found no evidence of effects of NAC on improving menstrual regularity, acne, hirsutism, BMI, fasting insulin, fasting glucose, or HOMA-IR
  • ...3 more annotations...
  • NAC was not associated with greater benefits to metformin for improving pregnancy rate, spontaneous ovulations, and menstrual regularity
  • Metformin also improved the BMI, total testosterone, insulin level, and lipid levels compared to NAC
  • All the studies were of short duration (three months)
  • Nathan Goodyear on 23 Feb 15
     
    Data review finds NAC improves pregnancy rates and ovulation rates in women with PCOS against placebo.  Meta-analysis revealed limited studies on the topic.  When compared to metformin, there was no difference found.  Though, one wonders if attacking insulin resistance through proper diet and additional neutraceutical approach would negate that.  The reason?  NAC and metformin are working in different biochemical pathways.  The authors here seem to not realize this. It appears that they think NAC and metormin are both working in the same manner, but they don't.  The fact that there is still benefit found compared to placebo, despited the authors lack of understanding of what NAC is and does is a positive.
Nathan Goodyear

N-Acetylcysteine Improves Liver Function in Patients with Non-Alcoholic Fatty Liver Dis... - 0 views

www.ncbi.nlm.nih.gov/...PMC3270338

NAC N-acetylcysteine NAFLD non-alcoholic fatty liver fatty liver liver enzymes

shared by Nathan Goodyear on 17 Jul 18 - No Cached
  • Nathan Goodyear on 17 Jul 18
     
    Oral NAC useful for elevated liver enzymes in NAFLD
Nathan Goodyear

Glucocorticoids plus N-Acetylcysteine in Severe Alcoholic Hepatitis | NEJM - 0 views

www.nejm.org/...NEJMoa1101214

NAC N-acetylcysteine bilirubin liver hepatitis alcoholic hepatitis

shared by Nathan Goodyear on 20 Aug 18 - No Cached
  • Nathan Goodyear on 20 Aug 18
     
    NAC benefits short-term survival in alcoholic hepatitis, including a drop in bilirubin.
Nathan Goodyear

[A clinical study of N-acetylcysteine treatment in chronic hepatitis B patients]. - Pub... - 0 views

www.ncbi.nlm.nih.gov/...18647523

NAC N-acetylcysteine hepatitis liver bilirubin glutathione

shared by Nathan Goodyear on 20 Aug 18 - No Cached
  • Nathan Goodyear on 20 Aug 18
     
    NAC more beneficial in lowering Total bilirubin compared to glutathione in patients with chronic hepatitis B.
Nathan Goodyear

N-acetylcysteine improves antitumoural response of Interferon alpha by NF-kB downregula... - 0 views

www.ncbi.nlm.nih.gov/...PMC3539937

IFN-alpha N-acetylcysteine hepatocellular cancer liver cancer NAC hepatocellular carcinoma

shared by Nathan Goodyear on 03 Mar 21 - No Cached
  • Nathan Goodyear on 03 Mar 21
     
    NAC for treatment of hepatocellular cancer.
Nathan Goodyear

PLOS ONE: N-Acetyl Cysteine May Support Dopamine Neurons in Parkinson's Disease: Prelim... - 0 views

journals.plos.org/...article

Parkinsons Parkinson's disease NAC N-acetylcysteine brain

shared by Nathan Goodyear on 17 Jun 16 - No Cached
  • Nathan Goodyear on 17 Jun 16
     
    pilot study finds that NAC protects the dopaminergic neurons in the brains in cell line stud.  Clinical found increased dopamine binding in the brain compared to placebo in individuals with Parkinson's disease.
Nathan Goodyear

Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer... - 0 views

www.ncbi.nlm.nih.gov/...PMC5282724

EMT TME metastasis cancer stem cells cancer MMP2 Notch MMP-9 MMP-2 radioresistance Hedgehog CSC MMP9 Snail HIF-1alpha tumor microenvironment epithelial to mesenchymal transition TGF-beta radiation

shared by Nathan Goodyear on 09 Feb 21 - No Cached
  • More than half of cancer patients are treated with IR at some point during their treatment
  • fractionation schedule is the delivery of 1.8–2.0 Gy per day, five days per week
  • Nuclear DNA is the primary target of IR; it causes DNA damage (genotoxic stress) by direct DNA ionization
  • ...121 more annotations...
  • IR also indirectly induces DNA damage by stimulating reactive oxygen species (ROS) production
  • IR is known to induce EMT in vitro
  • p53 is activated in response to IR-induced DNA damage
  • IR paradoxically also promotes tumour recurrence and metastasis
  • DNA double-strand breaks (DSBs)
  • cancer cells undergoing EMT acquire invasive and metastatic properties
  • changes in the tumour microenvironment (TME)
  • IR seems to induce EMT and CSC phenotypes by regulating cellular metabolism
  • EMT, stemness, and oncogenic metabolism are known to be associated with resistance to radiotherapy and chemotherapy
  • Hanahan and Weinberg proposed ten hallmarks of cancer that alter cell physiology to enhance malignant growth: 1) sustained proliferation, 2) evasion of growth suppression, 3) cell death resistance, 4) replicative immortality, 5) evasion of immune destruction, 6) tumour-promoting inflammation, 7) activation of invasion and metastasis, 8) induction of angiogenesis, 9) genome instability, and 10) alteration of metabolism
  • EMT is a developmental process that plays critical roles in embryogenesis, wound healing, and organ fibrosis
  • IR is known to induce stemness and metabolic alterations in cancer cells
  • transforming growth factor-β [TGF-β], epidermal growth factor [EGF]) and their associated signalling proteins (Wnt, Notch, Hedgehog, nuclear-factor kappa B [NF-κB], extracellular signal-regulated kinase [ERK], and phosphatidylinositol 3-kinase [PI3K]/Akt
  • activate EMT-inducing transcription factors, including Snail/Slug, ZEB1/δEF1, ZEB2/SIP1, Twist1/2, and E12/E47
  • Loss of E-cadherin is considered a hallmark of EMT
  • IR has been shown to induce EMT to enhance the motility and invasiveness of several cancer cells, including those of breast, lung, and liver cancer, and glioma cells
  • IR may increase metastasis in both the primary tumour site and in normal tissues under some circumstance
  • sublethal doses of IR have been shown to enhance the migratory and invasive behaviours of glioma cells
  • ROS are known to play an important role in IR-induced EMT
  • High levels of ROS trigger cell death by causing irreversible damage to cellular components such as proteins, nucleic acids, and lipids, whereas low levels of ROS have been shown to promote tumour progression—including tumour growth, invasion, and metastasis
  • hypoxia-inducible factor-1 (HIF-1) is involved in IR-induced EMT
  • Treatment with the N-acetylcysteine (NAC), a general ROS scavenger, prevents IR-induced EMT, adhesive affinity, and invasion of breast cancer cells
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      NAC for all patients receiving radiation therapy
  • Snail has been shown to play a crucial role in IR-induced EMT, migration, and invasion
  • IR activates the p38 MAPK pathway, which contributes to the induction of Snail expression to promote EMT and invasion
  • NF-κB signalling that promotes cell migration
  • ROS promote EMT to allow cancer cells to avoid hostile environments
  • HIF-1 is a heterodimer composed of an oxygen-sensitive α subunit and a constitutively expressed β subunit.
  • Under normoxia, HIF-1α is rapidly degraded, whereas hypoxia induces stabilisation and accumulation of HIF-1α
  • levels of HIF-1α mRNA are enhanced by activation of the PI3K/Akt/mammalian target of rapamycin (mTOR)
  • IR is known to increase stabilisation and nuclear accumulation of HIF-1α, since hypoxia is a major condition for HIF-1 activation
  • IR induces vascular damage that causes hypoxia
  • ROS is implicated in IR-induced HIF-1 activation
  • IR causes the reoxygenation of hypoxic cancer cells to increase ROS production, which leads to the stabilisation and nuclear accumulation of HIF-1
  • IR increases glucose availability under reoxygenated conditions that promote HIF-1α translation by activating the Akt/mTOR pathway
  • The stabilised HIF-1α then translocates to the nucleus, dimerizes with HIF-1β, and increases gene expression— including the expression of essential EMT regulators such as Snail—to induce EMT, migration, and invasion
  • TGF-β signalling has been shown to play a crucial role in IR-induced EMT
  • AP-1 transcription factor is involved in IR-induced TGF-β1 expression
  • Wnt/β-catenin signalling is also implicated in IR-induced EMT
  • Notch signalling is known to be involved in IR-induced EMT
  • IR also increases Notch-1 expression [99]. Notch-1 is known to induce EMT by upregulating Snail
  • PAI-1 signalling is also implicated in IR-induced Akt activation that increases Snail levels to induce EMT
  • EGFR activation is known to be associated with IR-induced EMT, cell migration, and invasion by activating two downstream pathways: PI3K/Akt and Raf/MEK/ERK
  • ROS and RNS are also implicated in IR-induced EGFR activation
  • IR has also been shown to activate Hedgehog (Hh) signalling to induce EMT
  • IR has been shown to induce Akt activation through several signalling pathways (EGFR, C-X-C chemokine receptor type 4 [CXCR4]/C-X-C motif chemokine 12 [CXCL12], plasminogen activator inhibitor 1 [PAI-1]) and upstream regulators (Bmi1, PTEN) that promote EMT and invasion
  • CSCs possess a capacity for self-renewal, and they can persistently proliferate to initiate tumours upon serial transplantation, thus enabling them to maintain the whole tumour
  • Conventional cancer treatments kill most cancer cells, but CSCs survive due to their resistance to therapy, eventually leading to tumour relapse and metastasis
  • identification of CSCs, three types of markers are utilised: cell surface molecules, transcription factors, and signalling pathway molecules
  • CSCs express distinct and specific surface markers; commonly used ones are CD24, CD34, CD38, CD44, CD90, CD133, and ALDH
  • Transcription factors, including Oct4, Sox2, Nanog, c-Myc, and Klf4,
  • signalling pathways, including those of TGF-β, Wnt, Hedgehog, Notch, platelet-derived growth factor receptor (PDGFR), and JAK/STAT
  • microRNAs (miRNAs), including let-7, miR-22, miR-34a, miR-128, the miR-200 family, and miR-451
  • Non-CSCs can be reprogrammed to become CSCs by epigenetic and genetic changes
  • EMT-inducing transcription factors, such as Snail, ZEB1, and Twist1, are known to confer CSC properties
  • Signalling pathways involved in EMT, including those of TGF-β, Wnt, and Notch, have been shown to play important roles in inducing the CSC phenotype
  • TGF-β1 not only increases EMT markers (Slug, Twist1, β-catenin, N-cadherin), but also upregulates CSC markers (Oct4, Sox2, Nanog, Klf4) in breast and lung cancer cells
  • some CSC subpopulations arise independently of EMT
  • IR has been shown to induce the CSC phenotype in many cancers, including breast, lung, and prostate cancers, as well as melanoma
  • Genotoxic stress due to IR or chemotherapy promotes a CSC-like phenotype by increasing ROS production
  • IR has been shown to induce reprogramming of differentiated cancer cells into CSCs
  • In prostate cancer patients, radiotherapy increases the CD44+ cell population that exhibit CSC properties
  • IR also induces the re-expression of stem cell regulators, such as Sox2, Oct4, Nanog, and Klf4, to promote stemness in cancer cells
  • EMT-inducing transcription factors and signalling pathways, including Snail, STAT3, Notch signalling, the PI3K/Akt pathway, and the MAPK cascade, have been shown to play important roles in IR-induced CSC properties
  • STAT3 directly binds to the Snail promoter and increases Snail transcription, which induces the EMT and CSC phenotypes, in cisplatin-selected resistant cells
  • Other oncogenic metabolic pathways, including glutamine metabolism, the pentose phosphate pathway (PPP), and synthesis of fatty acids and cholesterol, are also enhanced in many cancers
  • metabolic reprogramming
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • metabolic reprogramming
  • tumour cells exhibit high mitochondrial metabolism as well as aerobic glycolysis
  • occurring within the same tumour
  • CSCs can be highly glycolytic-dependent or oxidative phosphorylation (OXPHOS)-dependen
  • mitochondrial function is crucial for maintaining CSC functionality
  • cancer cells depend on mitochondrial metabolism and increase mitochondrial production of ROS that cause pseudo-hypoxia
  • HIF-1 then enhances glycolysis
  • CAFs have defective mitochondria that lead to the cells exhibiting the Warburg effect; the cells take up glucose, and then secrete lactate to 'feed' adjacent cancer cells
  • lactate transporter, monocarboxylate transporter (MCT)
  • nutrient microenvironment
  • Epithelial cancer cells express MCT1, while CAFs express MCT4. MCT4-positive, hypoxic CAFs secrete lactate by aerobic glycolysis, and MCT1-expressing epithelial cancer cells then uptake and use that lactate as a substrate for the tricarboxylic acid (TCA) cycle
  • MCT4-positive cancer cells depend on glycolysis and then efflux lactate, while MCT1-positive cells uptake lactate and rely on OXPHOS
  • metabolic heterogeneity induces a lactate shuttle between hypoxic/glycolytic cells and oxidative/aerobic tumour cells
  • bulk tumour cells exhibit a glycolytic phenotype, with increased conversion of glucose to lactate (and enhanced lactate efflux through MCT4), CSC subsets depend on oxidative phosphorylation; most of the glucose entering the cells is converted to pyruvate to fuel the TCA cycle and the electron transport chain (ETC), thereby increasing mitochondrial ROS production
  • the major fraction of glucose is directed into the pentose phosphate pathway, to produce redox power through the generation of NADPH and ROS scavengers
  • HIF-1α, p53, and c-Myc, are known to contribute to oncogenic metabolism
  • regulatory molecules involved in EMT and CSCs, including Snail, Dlx-2, HIF-1, STAT3, TGF-β, Wnt, and Akt, are implicated in the metabolic reprogramming of cancer cells
  • HIF-1 induces the expression of glycolytic enzymes, including the glucose transporter GLUT, hexokinase, lactate dehydrogenase (LDH), and MCT, resulting in the glycolytic switch
  • HIF-1 represses the expression of pyruvate dehydrogenase kinase (PDK), which inhibits pyruvate dehydrogenase (PDH), thereby inhibiting mitochondrial activity
  • STAT3 has been implicated in EMT-induced metabolic changes as well
  • TGF-β and Wnt play important roles in the metabolic alteration of cancer cells
  • Akt is also implicated in the glycolytic switch and in promoting cancer cell invasiveness
  • EMT, invasion, metastasis, and stemness
  • pyruvate kinase M2 (PKM2), LDH, and pyruvate carboxylase (PC), are implicated in the induction of the EMT and CSC phenotypes
  • decreased activity of PKM2 is known to promote an overall shift in metabolism to aerobic glycolysis
  • LDH catalyses the bidirectional conversion of lactate to pyruvate
  • High levels of LDHA are positively correlated with the expression of EMT and CSC markers
  • IR has been shown to induce metabolic changes in cancer cells
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR enhances glycolysis by upregulating GAPDH (a glycolysis enzyme), and it increases lactate production by activating LDHA, which converts pyruvate to lactate
  • IR also elevates MCT1 expression that exports lactate into the extracellular environment, leading to acidification of the tumour microenvironment
  • IR increases intracellular glucose, glucose 6-phosphate, fructose, and products of pyruvate (lactate and alanine), suggesting a role for IR in the upregulation of cytosolic aerobic glycolysis
  • Lactate can activate latent TGF-
  • lactate stimulates cell migration and enhances secretion of hyaluronan from CAF that promote tumour metastasis
  • promote tumour survival, growth, invasion, and metastasis; enhance the stiffness of the ECM; contribute to angiogenesis; and induce inflammation by releasing several growth factors and cytokines (TGF-β, VEGF, hepatocyte growth factor [HGF], PDGF, and stromal cell-derived factor 1 [SDF1]), as well as MMP
  • tumours recruit the host tissue’s blood vessel network to perform four mechanisms: angiogenesis (formation of new vessels), vasculogenesis (de novo formation of blood vessels from endothelial precursor cells), co-option, and modification of existing vessels within tissues.
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • immunosuppressive cells such as tumour-associated macrophages (TAM), MDSCs, and regulatory T cells, and the immunosuppressive cytokines, TGF-β and interleukin-10 (IL-10)
  • intrinsic immunogenicity or induce tolerance
  • cancer immunoediting’
  • three phases: 1) elimination, 2) equilibrium, and 3) escape.
  • The third phase, tumour escape, is mediated by antigen loss, immunosuppressive cells (TAM, MDSCs, and regulatory T cells), and immunosuppressive cytokines (TGF-β and IL-10).
  • IR can elicit various changes in the TME, such as CAF activity-mediated ECM remodelling and fibrosis, cycling hypoxia, and an inflammatory response
  • IR activates CAFs to promote the release of growth factors and ECM modulators, including TGF-β and MMP
  • TGF-β directly influences tumour cells and CAFs, promotes tumour immune escape, and activates HIF-1 signalling
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      And now the receipts
  • MMPs degrade ECM that facilitates angiogenesis, tumour cell invasion, and metastasis
    • Nathan Goodyear
      Nathan Goodyear on 09 Feb 21
       
      Receipts and mechanisms
  • IR also promotes MMP-2/9 activation in cancer cells to promote EMT, invasion, and metastasis
  • IR-induced Snail increases MMP-2 expression to promote EMT
  • Radiotherapy has the paradoxical side-effect of increasing tumour aggressiveness
  • IR promotes ROS production in cancer cells, which may induce the activation of oncogenes and the inactivation of tumour suppressors, which further promote oncogenic metabolism
  • Metabolic alterations
  • oncogenic metabolism
  • elicit various changes in the TME
  • Although IR activates an antitumour immune response, this signalling is frequently suppressed by tumour escape mechanisms
  • Nathan Goodyear on 09 Feb 21
     
    Important review article.
Nathan Goodyear

Acetaminophen Overdose with Altered Acetaminophen Pharmacokinetics and Hepatotoxicity A... - 0 views

www.theannals.com/...1333.short

Glutathione NAC IV therapy tylenol acetaminophen toxicity

shared by Nathan Goodyear on 10 Nov 11 - No Cached
  • Nathan Goodyear on 10 Nov 11
     
    IV NAC therapy treatment for tylenol toxicity.  NAC is the precursor to glutathione
Nathan Goodyear

The Effect of Glutathione and N-Acetylcysteine on Lipoperoxidative Damage in Patients w... - 0 views

171.66.122.149/...1907

IV glutathione NAC therapy treatment septic shock oxidative stress

shared by Nathan Goodyear on 10 Nov 11 - No Cached
  • Nathan Goodyear on 10 Nov 11
     
    IV glutathione and NAC shown to reduce oxidative stress markers associated with septic shock
1 - 20 of 28 Next ›
Showing 20▼ items per page