Abstract P198: Redox Monitoring Reveals Increased Susceptibility of Whole Blood to Oxidative Stress During Hemorrhagic Shock

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Nathan J White ◽  
Maryanne M Collinson ◽  
Richard A Boe ◽  
Kevin R Ward
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Redox Potential ◽  
Stress Responses ◽  
Whole Blood ◽  
P Value ◽  
Redox Potentials ◽  
Redox Stress ◽  
Voltage Potential ◽  
Severe Shock

Introduction: The oxidation/reduction (redox) chemistry of blood during resuscitation is not well defined. Improved understanding of whole blood redox behavior would assist in developing better resuscitation monitoring and possibly reducing free radical injury both of which are PULSE initiative priorities. We use direct electrochemical measurement of equilibrium redox potential to assess the hypothesis that the overall response of blood to strong oxidant/reductant challenge is altered during shock. Methods: Five swine underwent hemorrhage to an oxygen debt (OD) of 80 cc/kg. Arterial blood was tested at baseline (BL) and after hemorrhage when OD equaled 40 and 80 cc/kg. Native redox potential was measured as the equilibrium voltage potential recorded between a freshly polished 2mm Au and standard Ag/AgCl electrode submerged in whole blood (n=34). The oxidative and reductive stress responses at each level of OD were defined as the change from native voltage potential induced by the addition of a strong oxidant (KMnO4) (n=18) or reductant (Dithiotreitol) (n=18). Mean native redox potentials and mean redox stress responses were compared for differences at increasing levels of OD using repeated measures ANCOVA. Results: Lactate increased significantly with OD (mean diff BL vs. OD=80, +4.7 mmol/L [1.3, 8.1]). No effect of OD was found on native redox potential (p value =0.233). A significant effect of OD was found on redox stress response (p value =0.0276). The redox response to oxidative stress increased from BL with increasing oxygen debt, and became significantly greater at OD=80 cc/kg (mean diff =+31.9 Rmv [3.9, 59.9]). Conclusions: Whole-blood redox potential did not change significantly even with severe shock, suggesting active redox buffering. However, our results suggest that the oxidative buffering capacity of blood may become impaired during severe shock as demonstrated by the significantly more positive redox potentials elicited by oxidative stress when OD was elevated. Impaired redox buffering during shock may exacerbate free radical injury induced by the oxidative stress of resuscitation. Monitoring the response of blood to oxidative stress may be a useful way to determine susceptibility to oxidative damage during resuscitation.

scholarly journals Correlation between plasma 5-aminolevulinic acid concentrations and indicators of oxidative stress in lead-exposed workers

1997 ◽  
Vol 43 (7) ◽  
pp. 1196-1202 ◽  
Author(s):  
Cristine A Costa ◽  
Gilmar C Trivelato ◽  
Adriana M P Pinto ◽  
Etelvino J H Bechara
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Lead Poisoning ◽  
Stress Responses ◽  
Aminolevulinic Acid ◽  
Aerobic Oxidation ◽  
Protoporphyrin Ix ◽  
Acute Intermittent Porphyria ◽  
Blood Concentrations ◽  
Exposed Workers

Abstract 5-Aminolevulinic acid (ALA), a heme precursor accumulated in acute intermittent porphyria and lead poisoning, undergoes metal-catalyzed aerobic oxidation at physiological pH to yield reactive free radical species (O2−·>, HO·, and ALA·). We analyzed the relationships between plasma ALA concentrations, blood concentrations of lead, protoporphyrin IX (PP-IX), superoxide dismutase (SOD), and methemoglobin (metHb), and urine chemiluminescence (CL) in samples collected from lead-exposed workers. All variables measured were substantially (P <0.01) higher (2–8-fold) in the lead-exposed workers (n = 60). Plasma ALA concentrations were, on average, 6-fold higher in lead-exposed workers. We observed positive linear relationships between ALA and lead (r = 0.992), ALA and PP-IX (r = 0.891), ALA and metHb (r = 0.984), lead and SOD (r = 0.948), ALA and urine CL (r = 0.987), and lead and PP-IX (r = 0.993). These data are consistent with our free radical hypothesis for lead poisoning, where ALA distribution to and accumulation in several organs may trigger oxidative stress responses.

scholarly journals Augmentation of Glucotoxicity, Oxidative Stress, Apoptosis and Mitochondrial Dysfunction in HepG2 Cells by Palmitic Acid

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1979 ◽  
Author(s):  
Arwa Alnahdi ◽  
Annie John ◽  
Haider Raza
Keyword(s):  
Oxidative Stress ◽  
Cell Signaling ◽  
Palmitic Acid ◽  
Mitochondrial Dysfunction ◽  
Stress Responses ◽  
High Glucose ◽  
Hepg2 Cells ◽  
High Energy ◽  
Redox Stress ◽  
Energy Metabolites

Hyperglycemia and hyperlipidemia are the hallmarks of diabetes and obesity. Experimental and epidemiological studies have suggested that dietary management and caloric restriction are beneficial in reducing the complications of diabesity. Studies have suggested that increased availability of energy metabolites like glucose and saturated fatty acids induces metabolic, oxidative, and mitochondrial stress, accompanied by inflammation that may lead to chronic complications in diabetes. In the present study, we used human hepatoma HepG2 cells to investigate the effects of high glucose (25 mM) and high palmitic acid (up to 0.3 mM) on metabolic-, inflammatory-, and redox-stress-associated alterations in these cells. Our results showed increased lipid, protein, and DNA damage, leading to caspase-dependent apoptosis and mitochondrial dysfunction. Glucolipotoxicity increased ROS production and redox stress appeared to alter mitochondrial membrane potential and bioenergetics. Our results also demonstrate the enhanced ability of cytochrome P450s-dependent drug metabolism and antioxidant adaptation in HepG2 cells treated with palmitic acid, which was further augmented with high glucose. Altered NF-kB/AMPK/mTOR-dependent cell signaling and inflammatory (IL6/TNF-α) responses were also observed. Our results suggest that the presence of high-energy metabolites enhances apoptosis while suppressing autophagy by inducing inflammatory and oxidative stress responses that may be responsible for alterations in cell signaling and metabolism.

scholarly journals Redox stress reshapes carbon fluxes of Pseudomonas putida for cytosolic glucose oxidation and NADPH generation

2020 ◽  
Author(s):  
Pablo I. Nikel ◽  
Tobias Fuhrer ◽  
Max Chavarría ◽  
Alberto Sánchez-Pascuala ◽  
Uwe Sauer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pseudomonas Putida ◽  
Stress Responses ◽  
Pentose Phosphate ◽  
Flux Analysis ◽  
Glutathione System ◽  
Redox Stress ◽  
Cyclic Operation ◽  
Shed Light ◽  
Tracer Experiments

AbstractThe soil bacterium and metabolic engineering platform Pseudomonas putida tolerates high levels of endogenous and exogenous oxidative stress, yet the ultimate reason of such property remains unknown. To shed light on this question, NADPH generation routes—the metabolic currency that fuels redox stress responses—were assessed when P. putida KT2440 was challenged with H2O2 as proxy of oxidative conditions. 13C-tracer experiments, metabolomics and flux analysis, together with inspection of physiological parameters and measurement of enzymatic activities, revealed a substantial flux reconfiguration under oxidative stress. In particular, periplasmic glucose processing was rerouted to cytoplasmic oxidation, and cyclic operation of the pentose phosphate pathway led to significant NADPH fluxes, exceeding biosynthetic demands by ~50%. This NADPH surplus, in turn, fuelled the glutathione system for H2O2 reduction. These properties not only contribute to the tolerance of P. putida to environmental stresses, but they also highlight the value of this host for harsh biotransformations.

scholarly journals 1492: REDOX POTENTIAL IN SWINE SHOCK CORRELATES TO METABOLITE CHANGES ACTIVE IN OXIDATIVE STRESS RESPONSES

2021 ◽  
Vol 50 (1) ◽  
pp. 750-750
Author(s):  
Rodney Daniels ◽  
Mohamad Tiba ◽  
Brandon Cummings ◽  
Yan Rou Yap ◽  
Sardar Ansari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox Potential ◽  
Stress Responses ◽  
Oxidative Stress Responses

scholarly journals Periodic Exposure of Keratinocytes to Cold Physical Plasma: AnIn VitroModel for Redox-Related Diseases of the Skin

2016 ◽  
Vol 2016 ◽  
pp. 1-17 ◽  
Author(s):  
Anke Schmidt ◽  
Thomas von Woedtke ◽  
Sander Bekeschus
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Stress Responses ◽  
Redox Regulation ◽  
Chronic Wounds ◽  
Inflammatory Responses ◽  
Redox Homeostasis ◽  
Redox Stress ◽  
Hacat Keratinocyte ◽  
Physical Plasma

Oxidative stress illustrates an imbalance between radical formation and removal. Frequent redox stress is critically involved in many human pathologies including cancer, psoriasis, and chronic wounds. However, reactive species pursue a dual role being involved in signaling on the one hand and oxidative damage on the other. Using a HaCaT keratinocyte cell culture model, we investigated redox regulation and inflammation to periodic, low-dose oxidative stress after two, six, eight, ten, and twelve weeks. Chronic redox stress was generated by recurrent incubation with cold physical plasma-treated cell culture medium. Using transcriptome microarray technology, we identified both acute ROS-stress responses as well as numerous adaptions after several weeks of redox challenge. We determined a differential expression (2-fold, FDR < 0.01,p<0.05) of 260 genes that function in inflammation and redox homeostasis, such as cytokines (e.g., IL-6, IL-8, and IL-10), growth factors (e.g., CSF2, FGF, and IGF-2), and antioxidant enzymes (e.g., HMOX, NQO1, GPX, and PRDX). Apoptotic signaling was affected rather modestly, especially in p53 downstream targets (e.g., BCL2, BBC3, and GADD45). Strikingly, the cell-protective heat shock protein HSP27 was strongly upregulated (p<0.001). These results suggested cellular adaptions to frequent redox stress and may help to better understand the inflammatory responses in redox-related diseases.

State of the enzyme link of antioxidant protection in boys with hypoandrogenism

2020 ◽  
Vol 40 (4) ◽  
pp. 32-36
Author(s):  
L. K. Parkhomenko ◽  
◽  
L. A. Strashok ◽  
S. I. Turchina ◽  
G. V. Kosovtsova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Free Radical ◽  
Glutathione Peroxidase ◽  
Free Radical Oxidation ◽  
Conjugated Dienes ◽  
Delayed Puberty ◽  
Control Group ◽  
Antioxidant Protection ◽  
Radical Oxidation

Recently, interest in the problem of free radical oxidation in biological membranes, which is directly related to both the normal functioning of cells and the occurrence, course and outcome of many pathological conditions, has increased again in clinical medicine. The aim was to determine the role and impact of antioxidant defense in boys with hypoandrogenism. The study involved 75 adolescents with hypoandrogenism aged 13–18 years, who underwent a complex of clinical and laboratory examinations. All patients were conducted complex of anthropometric research and determination of the degree of delayed puberty, laboratory and instrumental examination. Free radical oxidation was determined by the levels of malondialdehyde, conjugated dienes, carbonated proteins, superoxide dismutase and catalase in the serum, and restored glutathione and glutathione peroxidase in whole blood. Based on their determination, the coefficient of oxidative stress was calculated. Statistical processing of results was performed using parametric and nonparametric methods. The study of indicators of the free radical oxidation process found that adolescents with hypoandrogenism have multidirectional changes in the oxidation of proteins and lipids, namely: the level of conjugated dienes increases, the concentration of malondialdehyde remains at the level of the control group, and the level of carbonated proteins tends to decrease. As for the activity of antioxidant protection enzymes, a significant decrease in the level of glutathione peroxidase was detected, while the level of superoxide dismutase and catalase remained at the level of normative indicators. Oxidative stress accompanies and is one of the pathogenetic links in the formation or maintenance of the state of hypoandrogenism in boys. This requires the use of antioxidants, the complex of which must be selected individually.

Gender differences in biochemical measurement reflecting the state of free-radical oxidation and antioxidant protection among workers in metallurgical production

2019 ◽  
Vol 1 (10) ◽  
pp. 877-881
Author(s):  
I. A. Umnyagina ◽  
L. A. Strakhova ◽  
T. V. Blinova
Keyword(s):  
Oxidative Stress ◽  
Gender Differences ◽  
Free Radical ◽  
Biochemical Parameters ◽  
Free Radical Oxidation ◽  
The Body ◽  
Antioxidant Protection ◽  
Radical Oxidation ◽  
Metallurgical Production ◽  
Production Factors

Introduction. To date, age and sex differences have been established for many biochemical parameters. Gender differences in indicators for systems such as antioxidant, thiol-disulfide, oxidative stress and inflammation systems are absent or under study.The aim of the study was to identify gender differences in biochemical parameters reflecting the functioning of antioxidant systems of the body and free radical oxidation in workers of metallurgical production, in contact with harmful production factors.Materials and methods. The blood of men and women working at the metallurgical enterprise of the Nizhny Novgorod region (n=80) under the influence of a complex of physical and chemical production factors was studied. Total oxidative stress, total antioxidant capacity of serum, glutathione levels were studied by photometric biochemical methods. Levels of C-reactive protein and 8-hydroxy–2-deoxyguanosine were studied by ELISA.Results. The average amount of peroxides in the serum of women exceeded 1.6 times this figure in men. In the group of men, the content of 8-Ondg was higher by 26% (p=0.012), the level of GS-by 12% (p=0.019), the activity of SOD — by 1.5–2 times (p=0.0001), the level of CRP — by 2 times (p=0.008) compared to similar indicators in women.Conclusions. Studies of gender differences in workers under the influence of harmful production factors will allow more effective approach to the etiology, treatment and prognosis of production-related diseases. Indicators of oxidative stress and antioxidant protection can be indicators of the health of workers under the influence of harmful industrial factors and be important in the prevention of diseases associated with oxidative stress.

Features of the oxidative status in patients with lupus nephritis

2020 ◽  
Vol 24 (1) ◽  
pp. 39-44
Author(s):  
E. V. Smirnova ◽  
E. V. Proskurnina ◽  
T. N. Krasnova
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Lupus Nephritis ◽  
Blood Plasma ◽  
Respiratory Burst ◽  
Oxidative Status ◽  
Free Radical Production ◽  
Radical Production ◽  
Neutrophil Activity ◽  
Kidney Involvement

BACKGROUND. Oxidative status impairment plays a significant role in the pathogenesis of SLE and lupus nephritis (LN). The data about oxidative status in this disease are incomplete, that’s why it’s necessary to use a new approach to study it. THE AIM: To study oxidative status in SLE patients with kidney involvement. PATIENTS AND METHODS:53 patients with SLE were included in this prospective study, among them 40 patients with different severity of kidney involvement, control group were 87 healthy donors. Oxidative stress parameters were measured: antioxidant activity (AOA) of blood plasma and parameters, characterizing the state of the main source of reactive oxygen species (ROS) – neutrophils, more specifically: specific spontaneous neutrophil activity, specific stimulated activity (peak and integral), coefficient of respiratory burst attenuation, representing the rate of free radical production decrease after stimulation, the higher the value of this parameter, the slower is free radical production decrease. RESULTS. It was shown elevation of neutrophil free radical-producing activity parameters and elevation of blood plasma AOA in patients with LN, comparing to healthy controls. Immunosuppressive therapy with glucocorticosteroids (GCS) and cytostatics (CS) increased blood plasma AOA comparing to monotherapy with GCS. A correlation between oxidative status impairment and intensity of inflammatory reactions was found: correlation of respiratory burst attenuation coefficient with blood sedimentation rate was shown. Reduction of spontaneous free radical-producing neutrophil activity was found in LN patients with NS, which might be the result of neutrophil functional activity attenuation in high disease activity. CONCLUSION. The increased free radical-producing neutrophil activity was shown, which might be the cause of oxidative stress in SLE with LN. It seems warranted investigation of these parameters in samples of larger volume to search targets aimed at neutrophils. The necessity of antioxidant therapy in patients with SLE seems doubtful, as they show significant increase of blood plasma AOA, which might result from compensatory reaction of human organism to oxidative stress and therapy with GCS and CS.

Protective Activity of Fucoidan and Alginic Acid against Free Radical-Induced Oxidative Stress under in Vitro and Cellular System

2007 ◽  
Vol 12 (4) ◽  
pp. 191-196 ◽  
Author(s):  
Mi-Jung So ◽  
Boh-Kyung Kim ◽  
Mi-Jin Choi ◽  
Kun-Young Park ◽  
Sook-Hee Rhee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Alginic Acid ◽  
Cellular System ◽  
Protective Activity

scholarly journals Metabolic Changes and Oxidative Stress in Diabetic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1143
Author(s):  
Midori Sakashita ◽  
Tetsuhiro Tanaka ◽  
Reiko Inagi
Keyword(s):  
Oxidative Stress ◽  
Kidney Disease ◽  
Stress Responses ◽  
Diabetic Kidney Disease ◽  
Renin Angiotensin System ◽  
Therapeutic Agents ◽  
Metabolic Changes ◽  
Diabetic Kidney ◽  
Glucose Levels ◽  
Patients With Diabetes

Diabetic kidney disease (DKD) is a major cause of end-stage kidney disease, and it is crucial to understand the pathophysiology of DKD. The control of blood glucose levels by various glucose-lowering drugs, the common use of inhibitors of the renin–angiotensin system, and the aging of patients with diabetes can alter the disease course of DKD. Moreover, metabolic changes and associated atherosclerosis play a major role in the etiology of DKD. The pathophysiology of DKD is largely attributed to the disruption of various cellular stress responses due to metabolic changes, especially an increase in oxidative stress. Therefore, many antioxidants have been studied as therapeutic agents. Recently, it has been found that NRF2, a master regulator of oxidative stress, plays a major role in the pathogenesis of DKD and bardoxolone methyl, an activator of NRF2, has attracted attention as a drug that increases the estimated glomerular filtration rate in patients with DKD. This review outlines the altered stress responses of cellular organelles in DKD, their involvement in the pathogenesis of DKD, and discusses strategies for developing therapeutic agents, especially bardoxolone methyl.

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