scholarly journals Oxidative Damage, Inflammation, and Toll-Like Receptor 4 Pathway Are Increased in Preeclamptic Patients: A Case-Control Study

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Fabiana C. B. Bernardi ◽  
Francine Felisberto ◽  
Francieli Vuolo ◽  
Fabricia Petronilho ◽  
Daniela R. Souza ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Protein Carbonyls ◽  
Myeloperoxidase Activity ◽  
Toll Like Receptor 4 ◽  
Protein Levels ◽  
Pathway Activation ◽  
Control Study

Problem.There was no direct correlation between plasma and placental oxidative damage parameters and inflammation and evidence of TLR4 pathway activation in the placenta in preeclamptic (PE) patients.Method of Study.33 PE patients and 33 normotensive pregnant women were included. The maternal section of the placenta and blood were collected to the determination of oxidative damage markers (thiobarbituric acid reactive species and protein carbonyls), inflammatory response (interleukin-6 and myeloperoxidase activity), and activation of the TLR-4-NF-kB pathway.Results.An increase of IL-6 levels in both plasma and placenta was observed, but myeloperoxidase activity was not significantly different comparing the groups. Oxidative damage parameters were increased in plasma and placenta in PE patients. A significant increase of the protein levels of TLR-4 and NF-kB was observed in the placenta.Conclusion.The TLR4-NF-kB pathway is upregulated in PE, probably generating local and systemic inflammatory response that is followed by local and systemic oxidative damage.

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.

scholarly journals AÇÃO PROTETORA DO TROLOX FRENTE AO DANO OXIDATIVO INDUZIDO PELO GLIFOSATO E TROP® EM MODELO ANIMAL

2019 ◽  
Vol 8 (1) ◽  
pp. 56-70
Author(s):  
Vilmair Zancanaro ◽  
Camila Katerin Perondi ◽  
Aline Conte ◽  
Claudriana Locatelli
Keyword(s):  
Vitamin E ◽  
Oxidative Damage ◽  
Renal Damage ◽  
Protective Action ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Mechanisms Of Toxicity ◽  
Genotoxic Potential ◽  
Low Toxicity

O glifosato é um herbicida utilizado em vários tipos de culturas e é considerado de baixa toxicidade, no entanto, os mecanismos de toxicidade das formulações ainda não estão bem esclarecidos. O objetivo do estudo foi avaliar os efeitos do Trop® e do glifosato sobre os parâmetros oxidativos, potencial genotóxico, função renal e  hepática, em animais submetidos ou não ao tratamento com vitamina E. Utilizou-se camundongos Swiss machos albinos, divididos em nove grupos (n=8): Controle (salina); glifosato (50 e 500 mg/kg); Trop® (50 e 500 mg/kg); Glifosato e vitamina E (20 e 200 mg/kg); Trop® e vitamina E (20 e 200 mg/kg). O tratamento foi realizado em dose única via oral. Após 48 horas, os animais foram sacrificados o sangue e o fígado coletados. O potencial genotóxico foi avaliado pela técnica de micronúcleos, a peroxidação lipídica através das espécies reativas ao ácido tiobarbitúrico (TBARS); a capacidade antioxidante pela concentração de glutationa reduzida (GSH) e catalase (CAT); a função renal através das dosagens de uréia e creatinina e a função hepática através das dosagens da Alanina-amino-transferase (ALT) e Aspartato-amino-transferase (AST). Os resultados mostram que não houve um aumento no número de micronúcleos nos eritrócitos demonstrando assim que não houve danos no DNA. Os níveis de TBARS e atividade da CAT teve aumento significativo em comparação aos animais controle e redução da GSH. Os valores de uréia e creatinina tiveram um aumento significativo quando os animais foram tratados com as doses de 500mg/Kg, no entanto, estes efeitos foram revertidos quando os animais foram tratados com combinação de vitamina E 200 mg/Kg. As dosagens de AST e ALT não evidenciaram alterações entre os grupos tratados. Os resultados mostram que uma exposição única ao glifosato pode causar dano oxidativo hepático e alteração na função renal que pode ser revertido pela administração de anti-oxidantes em particular a vitamina E.Palavras-chave: Glifosato. Dano Oxidativo. Potencial Genotóxico. TROLOX OF PROTECTIVE ACTION FRONT OXIDATIVE DAMAGE INDUCED BY GLYPHOSATE AND TROP® IN ANIMAL MODELABSTRACT: Glyphosate is an herbicide used in various types of cultures, considered to have low toxicity, however, the mechanisms of toxicity of the formulations are not wellunderstood. Theaim of the study was to evaluate the effects of Glyphosate on Trop® and oxidative parameters, potential genotoxic an drenal function in animals submitted or not to treatment with vitamin E. Male albino Swiss mice were used divided into nine groups (n=8). The control group (saline); Glyphosate (50 and 500mg/kg); Trop® (50 and 500mg/kg); Glyphosate + Vitamin E (20 and 200 mg/kg); Trop® + Vitamin E (20 and 200 mg/kg). Treatment was performed in a single oral dose, 48 hours after treatment the animals were sacrificed the blood and liver were collected. The genotoxic potential was assessed by micronucleus technique. The evaluation of lipid peroxidation was accomplished by determination of thiobarbituric acid reactive species (TBARS). The antioxidant status was evaluated by concentration of reduced glutathione (GSH) and the catalase (CAT) activity. The renal function was evaluated through the urea and creatinine dosages. The results show that there was not increase in the number of micronuclei in erythrocytes of the peripheral blood of animals treated with Glyphosate or Trop® thus demonstrating that DNA damage has not occurred when animals were treated with the herbicide. However, the oxidative parameters were altered, the levels of TBARS and CAT activity had a significant increase compared to control animals and significantly reduced GSH. The values of urea and creatinine were significantly higher when animals were treated with doses of 500mg/Kg, however, these effects were reversed when the animals were treated with combination of vitamin E 200mg/Kg. The results show that even a single exposure to Glyphosate may cause hepatic oxidative and renal damage which can be reversed by the administration of antioxidants in particular vitamin E.Keywords: Glyphosate. Oxidative damage. Genotoxic potential.

scholarly journals Ginsenoside-Rg1 Protects the Liver against Exhaustive Exercise-Induced Oxidative Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Mallikarjuna Korivi ◽  
Chien-Wen Hou ◽  
Chih-Yang Huang ◽  
Shin-Da Lee ◽  
Ming-Fen Hsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Thiobarbituric Acid ◽  
Exhaustive Exercise ◽  
Protein Carbonyls ◽  
Regular Exercise ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ginsenoside Rg1 ◽  
Exercise Induced ◽  
First Time

Despite regular exercise benefits, acute exhaustive exercise elicits oxidative damage in liver. The present study determined the hepatoprotective properties of ginsenoside-Rg1 against exhaustive exercise-induced oxidative stress in rats. Forty rats were assigned into vehicle and ginsenoside-Rg1 groups (0.1 mg/kg bodyweight). After 10-week treatment, ten rats from each group performed exhaustive swimming. Estimated oxidative damage markers, including thiobarbituric acid reactive substance (TBARS) (67%) and protein carbonyls (56%), were significantly (P<0.01) elevated after exhaustive exercise but alleviated in ginsenoside-Rg1 pretreated rats. Furthermore, exhaustive exercise drastically decreased glutathione (GSH) content (∼79%) with concurrent decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities. However, these changes were attenuated in Rg1 group. Additionally, increased xanthine oxidase (XO) activity and nitric oxide (NO) levels after exercise were also inhibited by Rg1 pretreatment. For the first time, our findings provide strong evidence that ginsenoside-Rg1 can protect the liver against exhaustive exercise-induced oxidative damage.

scholarly journals Cardiopulmonary Bypass Induces Acute Lung Injury via the High-Mobility Group Box 1/Toll-Like Receptor 4 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Yuxiao Deng ◽  
Lei Hou ◽  
Qiaoyi Xu ◽  
Qi Liu ◽  
Su Pan ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Cardiopulmonary Bypass ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
High Mobility Group ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Protein Levels

During cardiopulmonary bypass (CPB), pulmonary ischemia/reperfusion (I/R) injury can cause acute lung injury (ALI). Our previous research confirmed that abnormal high-mobility group box 1 (HMGB1) release after CPB was closely related to ALI. However, the mechanism underlying the HMGB1-mediated induction of ALI after CPB is unclear. Our previous study found that HMGB1 binds Toll-like receptor 4 (TLR4), leading to lung injury, but direct evidence of a role for these proteins in the mechanism of CPB-induced lung injury has not been shown. We examined the effects of inhibiting HMGB1 or reducing TLR4 expression on CPB-induced lung injury in rats administered anti-HMBG1 antibody or TLR4 short-hairpin RNA (shTLR4), respectively. In these rat lungs, we studied the histologic changes and levels of interleukin- (IL-) 1β, tumour necrosis factor- (TNF-) α, HMGB1, and TLR4 after CPB. After CPB, the lung tissues from untreated rats showed histologic features of injury and significantly elevated levels of IL-1β, TNF-α, HMGB1, and TLR4. Treatment with anti-HMGB1 attenuated the CPB-induced morphological inflammatory response and protein levels of IL-1β, TNF-α, HMGB1, and TLR4 in the lung tissues and eventually alleviated the ALI after CPB. Treatment with shTLR4 attenuated the CPB-induced morphological inflammatory response and protein levels of IL-1β, TNF-α, and TLR4 in the lung tissues and eventually alleviated the ALI after CPB, but could not alleviate the HMGB1 protein levels induced by CPB. In summary, the present study demonstrated that the HMGB1/TLR4 pathway mediated the development of ALI induced by CPB.

scholarly journals Effects of Resistance Training on the Redox Status of Skeletal Muscle in Older Adults

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 350
Author(s):  
Paulo H. C. Mesquita ◽  
Donald A. Lamb ◽  
Joshua S. Godwin ◽  
Shelby C. Osburn ◽  
Bradley A. Ruple ◽  
...  
Keyword(s):  
Older Adults ◽  
Skeletal Muscle ◽  
Resistance Training ◽  
Oxidative Damage ◽  
Redox Status ◽  
Protein Carbonyls ◽  
Antioxidant Enzyme Activities ◽  
Mrna Levels ◽  
Antioxidant Genes ◽  
Protein Levels

The aim of this study was to investigate the effects of resistance training (RT) on the redox status of skeletal muscle in older adults. Thirteen males aged 64 ± 9 years performed full-body RT 2x/week for 6 weeks. Muscle biopsies were obtained from the vastus lateralis prior to and following RT. The mRNA, protein, and enzymatic activity levels of various endogenous antioxidants were determined. In addition, skeletal muscle 4-hydroxynonenal and protein carbonyls were determined as markers of oxidative damage. Protein levels of heat shock proteins (HSPs) were also quantified. RT increased mRNA levels of all assayed antioxidant genes, albeit protein levels either did not change or decreased. RT increased total antioxidant capacity, catalase, and glutathione reductase activities, and decreased glutathione peroxidase activity. Lipid peroxidation also decreased and HSP60 protein increased following RT. In summary, 6 weeks of RT decreased oxidative damage and increased antioxidant enzyme activities. Our results suggest the older adult responses to RT involve multi-level (transcriptional, post-transcriptional, and post-translational) control of the redox status of skeletal muscle.

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.

Glycosylated Plasma Protein Measurement by a Semi-Automated Method

1986 ◽  
Vol 23 (2) ◽  
pp. 198-203 ◽  
Author(s):  
J C Moore ◽  
M C Outlaw ◽  
A J Barnes ◽  
R C Turner
Keyword(s):  
Plasma Proteins ◽  
Thiobarbituric Acid ◽  
Plasma Samples ◽  
Protein Levels ◽  
Hydroxymethyl Furfural ◽  
Automated Method ◽  
Coefficients Of Variation ◽  
The Mean ◽  
Protein Measurement

A semi-automated method for determination of glycosylation of plasma proteins using the thiobarbituric acid method is described. Plasma samples (100 μL) and a plasma pool used as a secondary standard were incubated in 0·3 M oxalic acid at 100°C for exactly 2 h. The hydroxymethyl furfural released and the total protein were measured concurrently on a Technicon AAII Autoanalyzer. Addition of 10 or 20 mmol glucose to plasma samples caused a minimal increase in the measured glycosylated protein. Within-batch and between-batch coefficients of variation were 3·1% and 4·9% respectively. The mean glycosylated protein levels for 52 normals and 48 maturity-onset diabetics were (±1SD) 0·96±0·13 and 1·75±0·32 nmol HMF/mg protein/2 h incubation.

Conjugated Linoleic Acid Causes a Marked Increase in Liver α-Tocopherol and Liver α-Tocopherol Transfer Protein in C57BL/6 J Mice

2010 ◽  
Vol 80 (1) ◽  
pp. 65-73 ◽  
Author(s):  
Pei-Min Chao ◽  
Wan-Hsuan Chen ◽  
Chun-Huei Liao ◽  
Huey-Mei Shaw
Keyword(s):  
Antioxidant Enzymes ◽  
Linoleic Acid ◽  
Conjugated Linoleic Acid ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substances ◽  
Control Groups ◽  
Protein Levels ◽  
Transfer Protein ◽  
And Control

Conjugated linoleic acid (CLA) is a collective term for the positional and geometric isomers of a conjugated diene of linoleic acid (C18:2, n-6). The aims of the present study were to evaluate whether levels of hepatic α-tocopherol, α-tocopherol transfer protein (α-TTP), and antioxidant enzymes in mice were affected by a CLA-supplemented diet. C57BL/6 J mice were divided into the CLA and control groups, which were fed, respectively, a 5 % fat diet with or without 1 g/100 g of CLA (1:1 mixture of cis-9, trans-11 and trans-10, cis-12) for four weeks. α-Tocopherol levels in plasma and liver were significantly higher in the CLA group than in the control group. Liver α-TTP levels were also significantly increased in the CLA group, the α-TTP/β-actin ratio being 2.5-fold higher than that in control mice (p<0.01). Thiobarbituric acid-reactive substances were significantly decreased in the CLA group (p<0.01). There were no significant differences between the two groups in levels of three antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and catalase). The accumulation of liver α-tocopherol seen with the CLA diet can be attributed to the antioxidant potential of CLA and the ability of α-TTP induction. The lack of changes in antioxidant enzyme protein levels and the reduced lipid peroxidation in the liver of CLA mice are due to α-tocopherol accumulation.

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