scholarly journals Novel Redox Tests for Maillard Abuse-Induced Redox Imbalance: a Pilot Single Case Paradigm Analyzing Dietary Oxidized-Browned Foods and Their Instant-Influence on Oral-Intestinal, Extracellular, and Intracellular Systemic Oxidative and Reductive Stress and Eventual Association with COVID-19 Sepsis and Other Leading Causes of Morbidity and Mortality Globally

2021 ◽  
pp. 1-6
Author(s):  
James A Cocores
Keyword(s):  
Oxidative Stress ◽  
Single Case ◽  
Cell Receptor ◽  
Morbidity And Mortality ◽  
Urine Ph ◽  
Systemic Oxidative Stress ◽  
Lipid Panel ◽  
End Products ◽  
Intracellular Redox

The public health hazards associated with Maillard end-products such as melanoidins and advanced lipoxidation end-products (ALEs) and advanced glycation end-products (AGEs), intermediary Maillard reaction creations, include most of the leading causes of morbidity and mortality globally. At the same time, only a few clinicians understand the intricacies linking redox biophysics and disease to humans and animals, explained here and in companion articles in simple to conceptualize terms. Maillard abuse causes increased systemic oxidative stress (SOS: pE-> pH+), an accelerant to the fatal vascular complications of type 1 diabetes. Maillard abuse-induced SOS (pE-> pH+) is also linked to type 2 diabetes, thyroid disorders, polycystic ovary syndrome, low testosterone, and osteoporosis. Many studies have shed light on exotic, intricate, and pricey markers to test extracellular and intracellular Maillard reaction-induced redox imbalance. And their corresponding influence on soluble and cell receptor signaling and the Maillard-induced redox-based diseases and deaths they cause. Inconclusive and pricey new markers for measuring extracellular and intracellular redox balance and imbalance cost thousands of US Dollars (USD) per in vivo assay. The author presents seven extracellular and intracellular redox markers costing less than 150 USD per in vivo assay, using standard laboratory tests available to medical centers worldwide. A PubMed search revealed no studies testing colas, pizza, burgers, and wings-specific intra-day Maillard-rich food binges on TSH, TG/HDL ratio (THR), VLDL/HDL ratio (VHR), LDL/HDL ratio (LHR), and urine pH+ extracellular redox markers, and neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) intracellular redox indicators. The objective of this pilot single case study is to test the feasibility of replication on a much larger scale. The second objective is to analyze the potential influence or lack of impact of Maillard intermediate and end-products on oral-intestine, corporal extracellular, and intracellular redox biophysics, soluble and cell receptor signaling, immunosuppression, inflammation, and risk for developing one or more of the leading causes of morbidity and mortality worldwide at three targeted intraday-pH+ points. The participant met inclusion criteria and drank acidic tide-inducing Maillard-rich colas to prompt an intra-oral-intestinal and the body’s extracellular systemic oxidative stress (SOS: pE-> pH+)-associated plasma acidic-tide. And had blood drawn for CBC with differential and platelet count, comprehensive metabolic panel, lipid panel, and TSH, and provided a sample for a routine urinalysis after an at-home confirmation of extracellular acidic-tide using ‘Just Fitter pH Test Strips pH 4.5 – pH 9.0.’ In a concerted attempt to reach an at-home urine pH+ strip value of 5.5, the top of the 4.5 to 5.5 urine and 7.35 to 7.38 blood systemic oxidative stress range (SOS: pE-> pH+). Before driving to the lab to give blood and urine samples for CBC with differential, comprehensive metabolic panel, lipid panel, TSH, and routine urinalysis. A similar procedure occurred to consuming mainly alkaline-botanical pizza, peanut butter shake, stronger alkaline tide-inducing acidic bacon double cheeseburgers and twelve fried chicken wings. The move from cola-associated urine pH+ 6 to pizza-associated pH+ 6.5 within the prime systemic energy PSE (pE- = pH+) urine pH+ range increased oral-intestinal, extracellular, and intracellular SOS by a factor of 50. The move from pizza-associated urine pH+ 6.5 to burgers and wings-associated pH+ 7.0 within the systemic reductive stress (SRS: pE-< pH+) urine pH+ range of 6.7 to 7.7, increased oral-intestinal, extracellular, and intracellular SOS (SOS: pE- > pH+) by a massive score of 556. This pilot study warrants reproduction on a larger scale with similarly healthy participants with elevated antioxidant tone. Such Maillard-intense trials require safe inclusionary criteria that limit initial subject sample pools to the equivalent of less than 25% of healthy females and males 8 to 80 years of age within or close to their ideal body mass indices and waist-to-height ratios.

scholarly journals Novel Redox Tests for Maillard Abuse-Induced Redox Imbalance: a Pilot Single Case Paradigm Analyzing Dietary Oxidized-Browned Foods and Their Instant-Influence on Oral-Intestinal, Extracellular, and Intracellular Systemic Oxidative and Reductive Stress and Eventual Association with COVID-19 Sepsis and Other Leading Causes of Morbidity and Mortality Globally

2021 ◽  
pp. 1-6 ◽  
Author(s):  
James A Cocores
Keyword(s):  
Oxidative Stress ◽  
Single Case ◽  
Cell Receptor ◽  
Morbidity And Mortality ◽  
Urine Ph ◽  
Systemic Oxidative Stress ◽  
Lipid Panel ◽  
End Products ◽  
Intracellular Redox

The public health hazards associated with Maillard end-products such as melanoidins and advanced lipoxidation end-products (ALEs) and advanced glycation end-products (AGEs), intermediary Maillard reaction creations, include most of the leading causes of morbidity and mortality globally. At the same time, only a few clinicians understand the intricacies linking redox biophysics and disease to humans and animals, explained here and in companion articles in simple to conceptualize terms. Maillard abuse causes increased systemic oxidative stress (SOS: pE-> pH+), an accelerant to the fatal vascular complications of type 1 diabetes. Maillard abuse-induced SOS (pE-> pH+) is also linked to type 2 diabetes, thyroid disorders, polycystic ovary syndrome, low testosterone, and osteoporosis. Many studies have shed light on exotic, intricate, and pricey markers to test extracellular and intracellular Maillard reaction-induced redox imbalance. And their corresponding influence on soluble and cell receptor signaling and the Maillard-induced redox-based diseases and deaths they cause. Inconclusive and pricey new markers for measuring extracellular and intracellular redox balance and imbalance cost thousands of US Dollars (USD) per in vivo assay. The author presents seven extracellular and intracellular redox markers costing less than 150 USD per in vivo assay, using standard laboratory tests available to medical centers worldwide. A PubMed search revealed no studies testing colas, pizza, burgers, and wings-specific intra-day Maillard-rich food binges on TSH, TG/HDL ratio (THR), VLDL/HDL ratio (VHR), LDL/HDL ratio (LHR), and urine pH+ extracellular redox markers, and neutrophil/lymphocyte ratio (NLR) and platelet/lymphocyte ratio (PLR) intracellular redox indicators. The objective of this pilot single case study is to test the feasibility of replication on a much larger scale. The second objective is to analyze the potential influence or lack of impact of Maillard intermediate and end-products on oral-intestine, corporal extracellular, and intracellular redox biophysics, soluble and cell receptor signaling, immunosuppression, inflammation, and risk for developing one or more of the leading causes of morbidity and mortality worldwide at three targeted intraday-pH+ points. The participant met inclusion criteria and drank acidic tide-inducing Maillard-rich colas to prompt an intra-oral-intestinal and the body’s extracellular systemic oxidative stress (SOS: pE-> pH+)-associated plasma acidic-tide. And had blood drawn for CBC with differential and platelet count, comprehensive metabolic panel, lipid panel, and TSH, and provided a sample for a routine urinalysis after an at-home confirmation of extracellular acidic-tide using ‘Just Fitter pH Test Strips pH 4.5 – pH 9.0.’ In a concerted attempt to reach an at-home urine pH+ strip value of 5.5, the top of the 4.5 to 5.5 urine and 7.35 to 7.38 blood systemic oxidative stress range (SOS: pE-> pH+). Before driving to the lab to give blood and urine samples for CBC with differential, comprehensive metabolic panel, lipid panel, TSH, and routine urinalysis. A similar procedure occurred to consuming mainly alkaline-botanical pizza, peanut butter shake, stronger alkaline tide-inducing acidic bacon double cheeseburgers and twelve fried chicken wings. The move from cola-associated urine pH+ 6 to pizza-associated pH+ 6.5 within the prime systemic energy PSE (pE- = pH+) urine pH+ range increased oral-intestinal, extracellular, and intracellular SOS by a factor of 50. The move from pizza-associated urine pH+ 6.5 to burgers and wings-associated pH+ 7.0 within the systemic reductive stress (SRS: pE-< pH+) urine pH+ range of 6.7 to 7.7, increased oral-intestinal, extracellular, and intracellular SOS (SOS: pE- > pH+) by a massive score of 556. This pilot study warrants reproduction on a larger scale with similarly healthy participants with elevated antioxidant tone. Such Maillard-intense trials require safe inclusionary criteria that limit initial subject sample pools to the equivalent of less than 25% of healthy females and males 8 to 80 years of age within or close to their ideal body mass indices and waist-to-height ratios.

Pyocyanin induces systemic oxidative stress, inflammation and behavioral changes in vivo

2018 ◽  
Vol 28 (6) ◽  
pp. 410-414 ◽  
Author(s):  
Devinder Arora ◽  
Susan Hall ◽  
Shailendra Anoopkumar-Dukie ◽  
Rachel Morrison ◽  
Amelia McFarland ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Behavioral Changes ◽  
Systemic Oxidative Stress

scholarly journals Circulating uromodulin inhibits systemic oxidative stress by inactivating the TRPM2 channel

2019 ◽  
Vol 11 (512) ◽  
pp. eaaw3639 ◽  
Author(s):  
Kaice A. LaFavers ◽  
Etienne Macedo ◽  
Pranav S. Garimella ◽  
Camila Lima ◽  
Shehnaz Khan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transient Receptor Potential ◽  
Kidney Injury ◽  
Receptor Potential ◽  
Underlying Mechanism ◽  
High Serum ◽  
Systemic Oxidative Stress ◽  
Trpm2 Channel ◽  
Poor Outcomes

High serum concentrations of kidney-derived protein uromodulin [Tamm-Horsfall protein (THP)] have recently been shown to be independently associated with low mortality in both older adults and cardiac patients, but the underlying mechanism remains unclear. Here, we show that THP inhibits the generation of reactive oxygen species (ROS) both in the kidney and systemically. Consistent with this experimental data, the concentration of circulating THP in patients with surgery-induced acute kidney injury (AKI) correlated with systemic oxidative damage. THP in the serum dropped after AKI and was associated with an increase in systemic ROS. The increase in oxidant injury correlated with postsurgical mortality and need for dialysis. Mechanistically, THP inhibited the activation of the transient receptor potential cation channel, subfamily M, member 2 (TRPM2) channel. Furthermore, inhibition of TRPM2 in vivo in a mouse model mitigated the systemic increase in ROS during AKI and THP deficiency. Our results suggest that THP is a key regulator of systemic oxidative stress by suppressing TRPM2 activity, and our findings might help explain how circulating THP deficiency is linked with poor outcomes and increased mortality.

scholarly journals Cystine/glutamate antiporter xCT (SLC7A11) facilitates oncogenic RAS transformation by preserving intracellular redox balance

2019 ◽  
Vol 116 (19) ◽  
pp. 9433-9442 ◽  
Author(s):  
Jonathan K. M. Lim ◽  
Alberto Delaidelli ◽  
Sean W. Minaker ◽  
Hai-Feng Zhang ◽  
Milena Colovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Redox Balance ◽  
Gene Encoding ◽  
Oncogenic Ras ◽  
Opposing Effects ◽  
Whole Transcriptome ◽  
Intracellular Redox

The RAS family of proto-oncogenes are among the most commonly mutated genes in human cancers and predict poor clinical outcome. Several mechanisms underlying oncogenic RAS transformation are well documented, including constitutive signaling through the RAF-MEK-ERK proproliferative pathway as well as the PI3K-AKT prosurvival pathway. Notably, control of redox balance has also been proposed to contribute to RAS transformation. However, how homeostasis between reactive oxygen species (ROS) and antioxidants, which have opposing effects in the cell, ultimately influence RAS-mediated transformation and tumor progression is still a matter of debate and the mechanisms involved have not been fully elucidated. Here, we show that oncogenic KRAS protects fibroblasts from oxidative stress by enhancing intracellular GSH levels. Using a whole transcriptome approach, we discovered that this is attributable to transcriptional up-regulation of xCT, the gene encoding the cystine/glutamate antiporter. This is in line with the function of xCT, which mediates the uptake of cystine, a precursor for GSH biosynthesis. Moreover, our results reveal that the ETS-1 transcription factor downstream of the RAS-RAF-MEK-ERK signaling cascade directly transactivates the xCT promoter in synergy with the ATF4 endoplasmic reticulum stress-associated transcription factor. Strikingly, xCT was found to be essential for oncogenic KRAS-mediated transformation in vitro and in vivo by mitigating oxidative stress, as knockdown of xCT strongly impaired growth of tumor xenografts established from KRAS-transformed cells. Overall, this study uncovers a mechanism by which oncogenic RAS preserves intracellular redox balance and identifies an unexpected role for xCT in supporting RAS-induced transformation and tumorigenicity.

scholarly journals Lipid Peroxidation: A Signaling Mechanism in Diagnosis of Diseases

2021 ◽  
Author(s):  
Kalpana Sabanna Patil ◽  
Raju Ratan Wadekar
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Clinical Practice ◽  
Oxidation Products ◽  
Signaling Mechanism ◽  
Unsaturated Lipids ◽  
End Products ◽  
Lipid Radicals

Quantification of reactive oxygen species, is perplexing either in vivo or in vitro due to their short half-lives. Consequently, to define the magnitude of oxidative stress, the more stable oxidation products can be measured in biological samples. The oxidative stress leads to the lipid peroxidation that involves the initiation, termination and propagation of lipid radicals, wherein, the process involves the oxygen uptake, rearrangement of the double bonds in unsaturated lipids, that leads to polyunsaturated fatty acid deterioration. Subsequently, the toxic signaling end products are considered as biomarkers of free radicals that act both as signaling molecules and as cytotoxic products cause covalent alteration of lipid peroxidation products. The use of validated signaling mechanism (s) of Lipid peroxidation and products derived thereof exhibits its use clinical practice and basic clinical research as well as in clinical practice has become common place, and their presence as endpoints in clinical trials is now broadly accepted. This knowledge can be used to diagnose disease earlier, or to prevent it before it starts. The signaling markers can be used to excel the effectiveness of the prevailing medicines and to improve the new medicines.

scholarly journals Effects of Pirfenidone and Nintedanib on Markers of Systemic Oxidative Stress and Inflammation in Patients with Idiopathic Pulmonary Fibrosis: A Preliminary Report

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1064
Author(s):  
Alessandro G. Fois ◽  
Elisabetta Sotgiu ◽  
Valentina Scano ◽  
Silvia Negri ◽  
Sabrina Mellino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Thiobarbituric Acid ◽  
Related Factor ◽  
Beneficial Effects ◽  
Systemic Oxidative Stress ◽  
Markers Of Oxidative Stress

Introduction: In vitro evidence suggests that pirfenidone and nintedanib, approved agents for the treatment of idiopathic pulmonary fibrosis (IPF), exert anti-inflammatory and anti-oxidant effects. We aimed to investigate such effects in vivo in IPF patients. Methods: Systemic circulating markers of oxidative stress [nuclear factor erythroid 2–related factor 2 (Nrf2), thiobarbituric acid- reactive substances (TBARS), homocysteine (Hcy), cysteine (Cys), asymmetric dimethylarginine (ADMA) and ADMA/Arginine ratio, glutathione (GSH), plasma protein –SH (PSH), and taurine (Tau)] and inflammation [Kynurenine (Kyn), Tryptophan (Trp) and Kyn/Trp ratio] were measured at baseline and after 24-week treatment in 18 IPF patients (10 treated with pirfenidone and 8 with nintedanib) and in 18 age- and sex-matched healthy controls. Results: Compared to controls, IPF patients had significantly lower concentrations of reduced blood GSH (457 ± 73 µmol/L vs 880 ± 212 µmol/L, p < 0.001) and plasma PSH (4.24 ± 0.95 µmol/g prot vs 5.28 ± 1.35 µmol/g prot, p = 0.012). Pirfenidone treatment significantly decreased the Kyn/Trp ratio (0.030 ± 0.011 baseline vs 0.025 ± 0.010 post-treatment, p = 0.048) whilst nintedanib treatment significantly increased blood GSH (486 ± 70 μmol/L vs 723 ± 194 μmol/L, p = 0.006) and reduced ADMA concentrations (0.501 ± 0.094 vs. 0.468 ± 0.071 μmol/L, p = 0.024). Conclusion: pirfenidone and nintedanib exert beneficial effects on specific markers of oxidative stress and inflammation in IPF patients.

scholarly journals Protective Effects of the MushroomLactarius deterrimusExtract on Systemic Oxidative Stress and Pancreatic Islets in Streptozotocin-Induced Diabetic Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Mirjana Mihailović ◽  
Jelena Arambašić Јovanović ◽  
Aleksandra Uskoković ◽  
Nevena Grdović ◽  
Svetlana Dinić ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pancreatic Islets ◽  
Diabetes Management ◽  
Therapeutic Potential ◽  
Cell Mass ◽  
Diabetic Rats ◽  
Nuclear Antigen ◽  
Protective Effects ◽  
Systemic Oxidative Stress

The aim of this study was to assess thein vivoeffects of the extract of the medicinal mushroom,Lactarius deterrimus, when administered (60 mg/kg, i.p.) daily for four weeks to streptozotocin- (STZ-) induced diabetic rats. Diabetic rats treated with theL. deterrimusextract displayed several improved biochemical parameters in the circulation: reduced hyperglycemia, lower triglyceride concentration and reduced glycated hemoglobin, glycated serum protein, and advanced glycation end product (AGE) levels. This treatment also adjusted the diabetes-induced redox imbalance. Thus, higher activities of the antioxidative enzymes, superoxide dismutase, and catalase in the circulation were accompanied by increased levels of free intracellular thiols and glutathionylated proteins after treatment with theL. deterrimusextract. In addition to a systemic antioxidant effect, the administration of the extract to diabetic rats also had a positive localized effect on pancreatic islets where it decreased AGE formation, and increased the expression of chemokine CXCL12 protein that mediates the restoration ofβ-cell population through the activation of the serine/threonine-specific Akt protein kinase prosurvival pathway. As a result, the numbers of proliferating cell nuclear antigen- (PCNA-) and insulin-positiveβ-cells were increased. These results show that the ability of theL. deterrimusextract to alleviate oxidative stress and increaseβ-cell mass represents a therapeutic potential for diabetes management.

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