scholarly journals Lipoperoxidation and Protein Oxidative Damage Exhibit Different Kinetics During Septic Shock

2008 ◽  
Vol 2008 ◽  
pp. 1-8 ◽  
Author(s):  
Max Andresen ◽  
Tomas Regueira ◽  
Alejandro Bruhn ◽  
Druso Perez ◽  
Pablo Strobel ◽  
...  
Keyword(s):  
Septic Shock ◽  
Vitamin E ◽  
Vitamin C ◽  
Oxidative Damage ◽  
Plasma Protein ◽  
Thiobarbituric Acid ◽  
Methionine Sulfoxide ◽  
Protein Carbonyls ◽  
Antioxidant Power ◽  
Radical Trapping

Septic shock (SS)-related multiorgan dysfunction has been associated with oxidative damage, but little is known about the temporal damage profile and its relationship to severity. The present work investigated prospectively 21 SS patients. Blood samples were obtained at diagnosis, 24, 72 hours, day 7, and at 3 months. At admission, thiobarbituric acid reactive substances (TBARSs), plasma protein carbonyls, plasma protein methionine sulfoxide (MS), ferric/reducing antioxidant power (FRAP), total red blood cell glutathione (RBCG), uric acid (UA), and bilirrubin levels were increased (P<.05). Total radical—trapping antioxidant potential (TRAP) and vitamin-E were similar to controls, and vitamin-C was decreased (P<.05). During evolution, TBARS and RBCG increased (P<.001), vitamin-E levels remained stable, whereas plasma protein carbonyls and MS, TRAP, vitamin-C, reduced glutathione, and UA levels decreased (P<.006). After 3 months, plasma protein carbonyls and MS persisted elevated. More severe patients exhibited higher TBARS, TRAP, FRAP, vitamin-C, UA, and bilirrubin levels. Our results suggest early and persistent oxidative stress during septic shock and a correlation between increasing levels of lipoperoxidation and sepsis severity.

scholarly journals Variegate porphyria induces plasma and neutrophil oxidative stress: effects of dietary supplementation with vitamins E and C

2009 ◽  
Vol 103 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Miguel D. Ferrer ◽  
Pedro Tauler ◽  
Antoni Sureda ◽  
Clara Palacín ◽  
Josep A. Tur ◽  
...  
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Oxidative Damage ◽  
Antioxidant Activities ◽  
Dietary Supplementation ◽  
Antioxidant Defenses ◽  
Ros Production ◽  
Double Blind ◽  
Variegate Porphyria ◽  
Vitamins E And C

Our aim was to analyse the influence of variegate porphyria (VP) on the antioxidant defenses and markers of oxidative damage and inflammation in plasma and neutrophils and the effects of dietary supplementation with vitamins E and C on these parameters in plasma, neutrophils and erythrocytes. Twelve women affected by VP and twelve pair-matched healthy control women participated in a double-blind crossover study. Each participant took 50 mg/d of vitamin E and 150 mg/d of vitamin C, or a placebo, for 6 months, by consuming an almond-based beverage as the vehicle. Women affected by VP presented higher C-reactive protein and malondialdehyde (MDA) circulating levels. Plasma antioxidant defenses were not different between porphyric and control women. Neutrophils from VP women presented decreased catalase (CAT) and glutathione reductase (GR) activities together with increased protein carbonyl levels. Reactive oxygen species (ROS) production from stimulated neutrophils was also higher in porphyric women than their controls. Dietary supplementation was effective in increasing α-tocopherol levels in neutrophils and in reducing MDA levels in plasma. Erythrocyte CAT and GR activities were enhanced by the enriched beverage only in the control subjects. In conclusion, women affected by VP present a situation of inflammation, plasma oxidative damage and neutrophils more primed to the oxidative burst, with decreased antioxidant activities and increased ROS production capabilities and protein oxidative damage. Dietary supplementation with vitamin E (50 mg/d) and vitamin C (150 mg/d) for 6 months decreased plasma oxidative damage and enhanced the erythrocyte activities of CAT and GR.

scholarly journals Plasma Protein Carbonyls as Biomarkers of Oxidative Stress in Chronic Kidney Disease, Dialysis, and Transplantation

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Graziano Colombo ◽  
Francesco Reggiani ◽  
Claudio Angelini ◽  
Silvia Finazzi ◽  
Emanuela Astori ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Peritoneal Dialysis ◽  
Kidney Transplantation ◽  
Renal Replacement Therapy ◽  
Oxidative Damage ◽  
Plasma Protein ◽  
Protein Carbonyls ◽  
Ckd Progression ◽  
Biomarkers Of Oxidative Stress

Accumulating evidence indicates that oxidative stress plays a role in the pathophysiology of chronic kidney disease (CKD) and its progression; during renal replacement therapy, oxidative stress-derived oxidative damage also contributes to the development of CKD systemic complications, such as cardiovascular disease, hypertension, atherosclerosis, inflammation, anaemia, and impaired host defence. The main mechanism underlying these events is the retention of uremic toxins, which act as a substrate for oxidative processes and elicit the activation of inflammatory pathways targeting endothelial and immune cells. Due to the growing worldwide spread of CKD, there is an overwhelming need to find oxidative damage biomarkers that are easy to measure in biological fluids of subjects with CKD and patients undergoing renal replacement therapy (haemodialysis, peritoneal dialysis, and kidney transplantation), in order to overcome limitations of invasive monitoring of CKD progression. Several studies investigated biomarkers of protein oxidative damage in CKD, including plasma protein carbonyls (PCO), the most frequently used biomarker of protein damage. This review provides an up-to-date overview on advances concerning the correlation between plasma protein carbonylation in CKD progression (from stage 1 to stage 5) and the possibility that haemodialysis, peritoneal dialysis, and kidney transplantation improve plasma PCO levels. Despite the fact that the role of plasma PCO in CKD is often underestimated in clinical practice, emerging evidence highlights that plasma PCO can serve as good biomarkers of oxidative stress in CKD and substitutive therapies. Whether plasma PCO levels merely serve as biomarkers of CKD-related oxidative stress or whether they are associated with the pathogenesis of CKD complications deserves further evaluation.

scholarly journals Effect of Different Stages of Chronic Kidney Disease and Renal Replacement Therapies on Oxidant-Antioxidant Balance in Uremic Patients

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Hadja Fatima Tbahriti ◽  
Abbou Kaddous ◽  
Malika Bouchenak ◽  
Khedidja Mekki
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Antioxidant Enzymes ◽  
Vitamin E ◽  
Kidney Disease ◽  
Thiobarbituric Acid ◽  
Study Groups ◽  
Cardiovascular Complications ◽  
Protein Carbonyls ◽  
Severe Stage

Oxidative stress seems to be involved in the path physiology of cardiovascular complications of chronic kidney disease (CKD). In this study, we determined the effect of different stages of CKD and substitutive therapies on oxidative stress. One hundred sixty-seven patients (age:44±06years; male/female: 76/91) with CKD were divided into 6 groups according to the National Kidney Foundation classification. Prooxidant status was assessed by assaying thiobarbituric acid reactive substances, hydroperoxides, and protein carbonyls. Antioxidant defence was performed by analysis of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, vitamin E, Iron, and bilirubin. TBARS and LPO were higher in HD patients compared to other groups (P<0.001), while protein carbonyls were more increased in PD patients. The antioxidant enzymes were declined already at severe stage of CKD and they were declined notably in HD patients (P<0.001). Similar observation was found for vitamin E, Fe, and bilirubin where we observed a significant decrease in the majority of study groups, especially in HD patients (P<0.001). The evolution of CKD was associated with elevated OS. HD accentuates lipid, while PD aggravates protein oxidation. However, the activity of antioxidant enzymes was altered by impaired renal function and by both dialysis treatments.

ANTIOXIDANT EFFECTS OF TAURINE, VITAMIN C, AND VITAMIN E ON OXIDATIVE DAMAGE IN HIPPOCAMPUS CAUSED BY THE ADMINISTRATION OF 3-NITROPROPIONIC ACID IN RATS

2004 ◽  
Vol 114 (9) ◽  
pp. 1133-1145 ◽  
Author(s):  
ERIKA RODRÍGUEZ-MARTÍNEZ ◽  
CONCEPCIÓN RUGERIO-VARGAS ◽  
ALBA I. RODRÍGUEZ ◽  
GABINO BORGONIO-PÉREZ ◽  
SELVA RIVAS-ARANCIBIA
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Oxidative Damage ◽  
Nitropropionic Acid ◽  
Antioxidant Effects ◽  
3 Nitropropionic Acid

Hippocampal mitochondrial dysfunction in rat aging

2008 ◽  
Vol 294 (2) ◽  
pp. R501-R509 ◽  
Author(s):  
Ana Navarro ◽  
José M. López-Cepero ◽  
Manuel J. Bández ◽  
María-Jesús Sánchez-Pino ◽  
Carmen Gómez ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Enzymatic Activity ◽  
Mitochondrial Dysfunction ◽  
Thiobarbituric Acid ◽  
Statistical Correlation ◽  
Protein Carbonyls ◽  
Complex Iv ◽  
Mitochondrial Nitric Oxide Synthase ◽  
Mitochondrial Oxidative Damage ◽  
Oxide Synthase

Hippocampus mitochondrial dysfunction with impaired electron transfer and increased oxidative damage was observed upon rat aging. Hippocampal mitochondria of aged (12 mo) and senescent (20 mo) rats showed, compared with young (4 mo) rats, marked decreases in the rate of state 3 respiration with NAD-dependent substrates (32–51%) and in the activities of mitochondrial complexes I (57–73%) and IV (33–54%). The activity of mitochondrial nitric oxide synthase was also decreased, 53–66%, with age. These losses in enzymatic activity were more marked in the hippocampus than in brain cortex or in whole brain. The histochemical assay of mitochondrial complex IV in the hippocampus showed decreased staining upon aging. Oxidative damage, determined as the mitochondrial content of thiobarbituric-acid reactive substances (TBARS) and protein carbonyls, increased in aged and senescent hippocampus (66–74% in TBARS and 48–96% in carbonyls). A significant statistical correlation was observed between mitochondrial oxidative damage and enzymatic activity. Mitochondrial dysfunction with shortage of energy supply is considered a likely cause of dysfunction in aged hippocampus.

Effect of supplementation with vitamins E, C and β-carotene on antioxidative/oxidative status parameters in sows during the postpartum period

2015 ◽  
Vol 18 (2) ◽  
pp. 299-305 ◽  
Author(s):  
M. Szczubiał
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Postpartum Period ◽  
Thiobarbituric Acid ◽  
Oxidative Status ◽  
Control Group ◽  
Sh Groups ◽  
Spectrophotometric Methods ◽  
Oxidative Balance ◽  
Β Carotene

Abstract The effect of vitamins E, C and β-carotene supplementation in sows on the parameters of antioxidative/oxidative status during the postpartum period was investigated. Twenty four primiparous sows, divided into two groups (experimental and control), were included in the study. After the half-way point of pregnancy until farrowing, each experimental sow received feed supplemented twice a week with 200 mg of vitamin E and 1000 mg of vitamin C, and additionally, 70 mg of β-carotene were administered via intramuscular injection, on day 14 and day 7 before farrowing. The control group was not supplemented. Blood samples were collected before supplementation (gestational day 57-58), 48 hours and 7 days after parturition. The following antioxidative and oxidative parameters were measured using spectrophotometric methods: glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), vitamin C, vitamin E, thiobarbituric acid reactive substances (TBARS), and sulfhydryl groups (SH groups). In supplemented sows the erythrocyte activity of GSH-Px and CAT was found to be significantly higher on day 7 after farrowing and the activity of SOD was significantly higher at 48 hours postpartum, compared to the control group. The concentration of vitamins C and E in plasma of the supplemented group was found to be significantly higher and the content of TBARS was found significantly lower at both postpartum measurement points, compared to the control group. The content of SH groups was significantly higher on day 7 postpartum, compared to the control group. The study findings indicate that supplementation of pregnant sows with vitamins E, C and β-carotene in the second half of pregnancy has beneficial effects on the antioxidative/oxidative balance in the postpartum period by increasing the antioxidative potential and reducing lipid and protein peroxidation.

scholarly journals Influence of lycopene and vitamin C from tomato juice on biomarkers of oxidative stress and inflammation

2007 ◽  
Vol 99 (1) ◽  
pp. 137-146 ◽  
Author(s):  
Karin Jacob ◽  
María J. Periago ◽  
Volker Böhm ◽  
Gaspar Ros Berruezo
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Antioxidant Capacity ◽  
Human Study ◽  
Thiobarbituric Acid ◽  
Tomato Juice ◽  
Protein Carbonyls ◽  
Beneficial Effects ◽  
Lipid Status ◽  
Biomarkers Of Oxidative Stress

A human study was carried out to investigate whether tomato juice, rich in natural lycopene and fortified with vitamin C, is able to reduce several biomarkers of oxidative stress and inflammation and whether the effect can be attributed to lycopene, vitamin C or any other micronutrient. Following a 2-week depletion phase, volunteers were assigned randomly to ingest either tomato juice with (LC) or without (L) vitamin C fortification for 2 weeks (daily dose 20·6 mg lycopene and 45·5/435 mg vitamin C). Plasma and urine were analysed for carotenoids and vitamin C, lipid status, antioxidant capacity, thiobarbituric acid reactive substances (TBARS) and 8-epi-PGF2α, protein carbonyls, cytokines IL-1β and TNFα and C-reactive protein (CRP). The consumption of tomato juice led to a reduction in total cholesterol levels (L: 157·6v. 153·2 mg/dl,P = 0·008; LC: 153·4v. 147·4 mg/dl,P = 0·002) and that of CRP (L: 315·6v. 262·3 μg/l,P = 0·017; LC: 319·2v. 247·1 μg/l,P = 0·001) in both groups. The vitamin C-fortified juice slightly raised the antioxidant capacity in urine and decreased TBARS in plasma and urine. All other markers were affected to a lesser extent or remained unchanged. Cholesterol reduction was correlated with lycopene uptake (P = 0·003), whereas the other effects could not be related with particular micronutrients. Any beneficial effects of tomato consumption for human health cannot be attributed only to lycopene and, as the additional supplementation with ascorbic acid indicates, a variety of antioxidants might be needed to optimize protection against chronic diseases.

scholarly journals The role of redox signaling in cardiac hypertrophy induced by experimental hyperthyroidism

2008 ◽  
Vol 41 (6) ◽  
pp. 423-430 ◽  
Author(s):  
A S R Araujo ◽  
P Schenkel ◽  
A T Enzveiler ◽  
T R G Fernandes ◽  
W A Partata ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin E ◽  
Vitamin C ◽  
Cardiac Hypertrophy ◽  
Protein Oxidation ◽  
Diastolic Pressure ◽  
Glycogen Synthase ◽  
Left Ventricular ◽  
Experimental Hyperthyroidism ◽  
Radical Trapping

This study was conducted to test whether oxidative stress activates the intracellular protein kinase B (AKT1) signaling pathway, which culminates with cardiac hypertrophy in experimental hyperthyroidism. Male Wistar rats were divided into four groups: control, vitamin E, thyroxine (T4), and T4+vitamin E. Hyperthyroidism was induced by T4 administration (12 mg/l in drinking water for 28 days). Vitamin E treatment was given during the same period via s.c. injections (20 mg/kg per day). Morphometric and hemodynamic parameters were evaluated at the end of the 4-week treatment period. Protein oxidation, redox state (reduced glutathione, GSH/glutathione dissulfide, GSSG), vitamin C, total radical-trapping antioxidant potential (TRAP), hydrogen peroxide (H2O2), and nitric oxide metabolites (NOX) were measured in heart homogenates. The p-AKT1/AKT1 ratio, p-glycogen-synthase kinase (GSK)3B/GSK3B ratio, FOS, and JUN myocardial protein expression were also quantified by western blot after 4 weeks. Increases in biochemical parameters, such as protein oxidation (41%), H2O2 (62%), and NOX (218%), and increase in the left ventricular end-diastolic pressure were observed in the T4 group. T4 treatment also caused a decrease in GSH/GSSG ratio (83%), vitamin C (34%), and TRAP (55%). These alterations were attenuated by vitamin E administration to the hyperthyroid rats. Expression of p-AKT1/AKT1, p-GSK3B/GSK3B, FOS, and JUN were elevated in the T4 group (by 69, 37, 130, and 33% respectively), whereas vitamin E administration promoted a significant reduction in their expression. These results indicate that oxidative stress plays an important role in cardiac hypertrophy, and suggest redox activation of AKT1 and JUN/FOS signaling pathways with H2O2 acting as a possible intracellular mediator in this adaptive response to experimental hyperthyroidism.

Nephrotoxicity in rats induced by chlorpryfos-ethyl and ameliorating effects of antioxidantsy

2002 ◽  
Vol 21 (4) ◽  
pp. 223-230 ◽  
Author(s):  
M Oncu ◽  
F Gultekin ◽  
E Karaöz ◽  
I Altuntas ◽  
N Delibas
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Mononuclear Cells ◽  
Kidney Tissue ◽  
Thiobarbituric Acid ◽  
Glomerular Sclerosis ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
High Doses ◽  
Chlorpyrifos Ethyl

Nephrotoxicity induced by chlorpyrifos-ethyl (CE) and ameliorating effects of melatonin and vitamin E plus vitamin C were evaluated in rats exposed to CE. Experimental groups were as follows: control (C), CE treated (CE), vitamin E plus vitamin C treated (Vit), melatonin treated (Mel), vitamin E plus vitamin C plus CE treated (Vit+CE), and melatonin plus CE treated (Mel+CE). The rats in the CE, Vit+CE and Mel+CE groups were administered orally with CE in two equal doses of 41 mg/kg body weight (0.25 LD50). Melatonin and vitamins E and C were administrated intramuscularly at the doses of 10, 150 and 200 mg/kg, respectively. The levels of thiobarbituric acid reactive substance (TBARS) and antioxidant potential (AOP), and the activities of glutathione peroxidase (GSHPx), catalase (CAT) and superoxide dismutase (SOD) were studied in the homogenates of kidney tissue. There were no significant differences in the activities of SOD and CAT between the experimental groups. The level of TBARS increased significantly (P<0.05) while AOP decreased significantly (P<0.05) in the CE group compared with the C group. GSH-Px activity was significantly (P<0.05) lower in the CE group and higher in the melatonin group than the control group. Histopathological changes were found in the kidney tissue of rats treated with CE. These were infiltration in mononuclear cells at perivascular and peritubular areas, hydropic degenerations in tubule epithelium and glomerular sclerosis. The severity of the lesions was reduced by administration of vitamins and melatonin. These results suggest that CE increases lipid peroxidation and decreases AOP by increasing oxidative stress, and that high doses of melatonin and a combination of vitamin E plus vitamin C considerably reduce the toxic effect of CE on kidney tissue of rats.

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