scholarly journals α-Tocopherol Protects the Heart, Muscles, and Testes from Lipid Peroxidation in Growing Male Rats Subjected to Physical Efforts

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Magdalena Górnicka ◽  
Anna Ciecierska ◽  
Jadwiga Hamulka ◽  
Małgorzata E. Drywień ◽  
Joanna Frackiewicz ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Experimental Period ◽  
Treadmill Running ◽  
Male Rats ◽  
Rat Tissues ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Tocopherol Concentration

The effect of α-tocopherol supplementation on adaptation to training is still equivocal. The aim of the study was to determine the effect of training and α-tocopherol supplementation on α-tocopherol and thiobarbituric acid reactive substance (TBARS) concentration in the rat liver, heart, muscles, and testes. Male Wistar rats (n=32) were divided into four groups (nonsupplemented, not trained—C; nonsupplemented, trained—CT; supplemented, not trained—E; supplemented and trained—ET). During the 14-day experimental period, 2 mg/d of vitamin E as α-tocopherol acetate was administered to the animals (groups E and ET). Rats in the training group (CT and ET) were subjected to 15 minutes of treadmill running each day. The α-tocopherol levels in rat tissues were assessed using high-performance liquid chromatography (HPLC). Lipid peroxides were determined by TBARS spectrophotometric method. α-Tocopherol had a significant impact on α-tocopherol concentration in all tissues. Training increased the α-tocopherol concentration in the heart and muscles but reduced it in the liver. Training also caused increased lipid peroxidation in the muscles, heart, and testes; but a higher α-tocopherol content in tissues reduced the TBARS level. The main finding of the study is that impaired α-tocopherol status and its adequate intake is needed to maintain optimal status to prevent damage to the skeletal and cardiac muscles as well as the testes in growing individuals.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

Skeletal muscle lipid peroxidation in exercised and food-restricted rats during aging

1989 ◽  
Vol 67 (1) ◽  
pp. 69-75 ◽  
Author(s):  
J. W. Starnes ◽  
G. Cantu ◽  
R. P. Farrar ◽  
J. P. Kehrer
Keyword(s):  
Lipid Peroxidation ◽  
Gastrocnemius Muscle ◽  
Thiobarbituric Acid ◽  
Exercise Group ◽  
Alpha Tocopherol ◽  
Treadmill Running ◽  
Control Group ◽  
Muscle Lipid ◽  
Fischer 344 ◽  
Skeletal Muscle Lipid

The effects of chronic endurance exercise and food restriction on nonenzymatic lipid peroxidation (LP) of gastrocnemius muscle during aging were studied in male, Fischer 344 rats. One set of rats aged 6 and 18 mo were assigned to an exercise group (treadmill running) or an age-matched sedentary control group. After 6 mo (at the ages of 12 and 24 mo), LP and levels of alpha-tocopherol and its oxidized form, alpha-tocopheryl quinone, were measured. The extent of LP was determined in homogenates by measuring the content of thiobarbituric acid-reactive substances. After homogenization, the muscles were immediately evaluated for basal LP and also incubated in the presence of oxidant stressors for 2 h to assess antioxidant capacity (AOC) and for 24 h to estimate total peroxidizable lipid (TPL). Basal LP was not affected by age or exercise. AOC was not affected by exercise at either age. However aging significantly decreased AOC and increased alpha-tocopheryl quinone in both sedentary and exercised groups. TPL was not affected by age, but was increased by exercise training (P less than 0.05). Another set of rats was divided into the following three groups at 3 mo of age: sedentary, fed ad libitum (S); sedentary, caloric restricted by alternate day feeding (R); and exercised by forced treadmill running (E). Two years later, when the rats were 27 mo of age, the extent of LP was assessed.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Organ-Specific Oxidative Events under Restrictive Versus Full Reperfusion Following Hemorrhagic Traumatic Shock in Rats

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2195
Author(s):  
Carina Penzenstadler ◽  
Anna Zifko ◽  
Mohammad Jafarmadar ◽  
Janin Schulte ◽  
Joachim Struck ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Electron Paramagnetic Resonance Spectroscopy ◽  
Thiobarbituric Acid ◽  
Traumatic Shock ◽  
Male Rats ◽  
Resonance Spectroscopy ◽  
Stress Reactions ◽  
Paramagnetic Resonance ◽  
Early Reperfusion ◽  
Ros Formation

Background aim: Reperfusion after hemorrhagic traumatic shock (HTS) is often associated with complications that are partly ascribed to the formation of reactive oxygen species (ROS). The aim of our study was to compare the effects of restrictive reperfusion (RR) to rapid full reperfusion (FR) on ROS formation and/or oxidative events. Materials and methods: Anesthetized male rats were randomly subjected to HTS followed by FR (75 mL/kg/h) or RR (30 mL/kg/h for 40 min, followed by 75 mL/kg/h) with Ringer’s solution (n = 8/group). Compartment-specific ROS formation was determined by infusion of ROS scavenger 1-hydroxy-3-carboxy-2,2,5,5-tetramethyl-pyrrolidine hydrochloride (CP-H) during resuscitation, followed by electron paramagnetic resonance spectroscopy. Sham-operated animals (n = 8) served as controls. The experiment was terminated 100 min post-shock. Results: Mean arterial pressure was significantly higher in the FR compared to the RR group during early reperfusion. Only RR animals, not FR animals, showed significantly higher ROS concentrations in erythrocytes (1951 ± 420 vs. 724 ± 75 AU) and in liver (474 ± 57 vs. 261 ± 21 AU) compared to sham controls. This was accompanied by elevated alanine aminotransferase and creatinine levels in RR animals compared to both shams and FR animals, while lipid peroxidation products (thiobarbituric acid reactive substances) were significantly increased only in the kidney in the FR group (p < 0.05). RR animals showed significantly higher plasma peroxiredoxin-4 values when compared to the FR group (20 ± 2 vs. 14 ± 0.5 RLU). Conclusion: Restrictive reperfusion after HTS is associated with increased ROS formation in erythrocytes and liver compared to sham controls. Moreover, the restrictive reperfusion is associated with a more pronounced injury to the liver and kidney, which is likely mediated by other than lipid peroxidation process and/or oxidative stress reactions.

scholarly journals Blood Oxidative Stress Modulates Alveolar Bone Loss in Chronically Stressed Rats

2020 ◽  
Vol 21 (10) ◽  
pp. 3728 ◽  
Author(s):  
Micaele Maria Lopes Castro ◽  
Priscila Cunha Nascimento ◽  
Deiweson Souza-Monteiro ◽  
Sávio Monteiro Santos ◽  
Mayra Barros Arouck ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Alveolar Bone ◽  
Physical Restraint ◽  
Thiobarbituric Acid ◽  
Experimental Period ◽  
Thiobarbituric Acid Reactive Substance ◽  
Micro Ct ◽  
Plus Maze ◽  
Behavioral Parameters ◽  
Experimental Periodontitis

We aimed to investigate the effects of chronic stress (CS) on experimental periodontitis (EP) in rats. For this, 28 Wistar rats were divided into four groups: control, ligature-induced experimental periodontitis (EP), chronic stress (CS; by physical restraint model) and CS+EP (association of chronic stress and ligature-induced periodontitis). The experimental period lasted 30 days, including exposure to CS every day and ligature was performed on the 15th experimental day. After 30 days, the animals were submitted to the behavioral test of the elevated plus maze (EPM). Next, rats were euthanized for blood and mandible collection in order to evaluate the oxidative biochemistry (by nitric oxide (NO), reduced-glutathione activity (GSH), and thiobarbituric acid reactive substance levels (TBARS)) and alveolar bone characterization (by morphometric, micro-CT, and immunohistochemistry), respectively. The behavioral parameters evaluated in EPM indicated higher anxiogenic activity in the CS and CS+EP, groups, which is a behavioral reflex of CS. The results showed that CS was able to change the blood oxidative biochemistry in CS and CS+EP groups, decrease GSH activity in the blood, and increase the NO and TBARS concentrations. Thus, CS induces oxidative blood imbalance, which can potentialize or generate morphological, structural, and metabolic damages to the alveolar bone.

Changes in lipid peroxidation and free radical scavengers in the brain of hyper- and hypothyroid aged rats

1995 ◽  
Vol 147 (2) ◽  
pp. 361-365 ◽  
Author(s):  
T Mano ◽  
R Sinohara ◽  
Y Sawai ◽  
N Oda ◽  
Y Nishida ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Lipid Peroxide ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Free Radical Scavengers ◽  
Aged Rats ◽  
Radical Scavengers ◽  
Old Rats ◽  
The Brain

Abstract To determine how lipid peroxides and free radical scavengers are changed in the brain of hyper- or hypothyroid rats, we examined the behavior of lipid peroxide and free radical scavengers in the cerebral cortex of aged (1·5 years old) rats that had been made hyper- or hypothyroid by the administration of thyroxine or methimazol for 4 weeks. Concentrations of catalase, Mn-superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were increased in hyperthyroid rats compared with euthyroid rats. Concentrations of total SOD, Cu,Zn-SOD and GSH-PX were increased but that of Mn-SOD was decreased in hypothyroid animals. There were no differences among hyperthyroid, hypothyroid and euthyroid rats in the levels of coenzymes 9 or 10. The concentration of lipid peroxides, determined indirectly by the measurement of thiobarbituric acid reactants, was decreased in hyperthyroid rats but not in hypothyroid rats when compared with euthyroid animals. These findings suggest that free radicals and lipid peroxides are scavenged to compensate for the changes induced by hyper- or hypothyroidism. Journal of Endocrinology (1995) 147, 361–365

scholarly journals Changes of Prooxidant-Antioxidant Systems in Experimental Acute Pancreatitis

2017 ◽  
Vol 24 (3) ◽  
Author(s):  
Viktoria Cherkasova ◽  
Luibomyr Zaiats
Keyword(s):  
Lipid Peroxidation ◽  
Acute Pancreatitis ◽  
White Male ◽  
Thiobarbituric Acid ◽  
Activity Level ◽  
Male Rats ◽  
Antioxidant Systems ◽  
Diene Conjugates ◽  
Pronounced Increase ◽  
Oxidation Rates

Mortality in acute destructive pancreatitis, despite the development and introduction of new methods of treatment, remains stable high and in severe forms reaches 25-85%. Activation of neutrophils and macrophages in acute pancreatitis leads to an "oxygen burst", which is closely linked with the activation of lipid peroxidation.Goals. The purpose is to establish dynamic changes in the indexes of prooxidant-antioxidant systems in acute L-arginine-induced pancreatitis.Materials and methods. The study was performed on 62 white male rats of Wistar line weighing 180-220g, with modeled acute pancreatitis. Blood for analysis have been taken: the blood serum on 12, 24, 48 and 72 hours of experiment to determine the activity level of thiobarbituric acid products, diene conjugates, catalase and lactate for assessment of the intensity of oxidative stress and antioxidant systems.Results. The obtained results of the study showed that acute L-arginine-induced pancreatitis is accompanied by an intensification of lipid peroxidation processes (LPO). Revealed that the most pronounced increase in all blood parameters is observed 24 hours after the beginning of the study. A significant increase in the active products of tiobarbituric acid (TBA-AP) and diene conjugates (DC) was detected - 1.98 and 2.7 times, respectively, and 2.2 times the growth of catalase (CT). At the next stage of the experiment there is a slowdown in the rate of LPO, as evidenced by the following values. Thus, for 48 years in the 3rd group: TBA-AP - they increased by 5.1% (p> 0.05), DC - by 3.3% (p> 0.05), and the level of CT - by 43.4% (P <0.05), compared with data for 24 hours. It is important to note that at 72 hours, the CT level decreased by 23.3% (p> 0.05), which may indicate an exhaustion of antioxidant systems. Indicators of LPO on 72 hours compared with 48 hours in group III: TBA-AP - increased by 1.7% (p> 0.05), DC - by 5.7% (p> 0.05).Conclusions. Acute L-arginine-induced pancreatitis is accompanied by an intensification of lipid peroxidation-oxidation processes that can potentiate the development of multiple organ failure in pancreatic inflammation. The most pronounced changes in lipid peroxidation-oxidation rates are observed for 24 hours of study.

scholarly journals Exposure of precision-cut rat liver slices to ethanol accelerates fibrogenesis

2010 ◽  
Vol 299 (3) ◽  
pp. G661-G668 ◽  
Author(s):  
Courtney S. Schaffert ◽  
Michael J. Duryee ◽  
Robert G. Bennett ◽  
Amy L. DeVeney ◽  
Dean J. Tuma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cytokine Production ◽  
Smooth Muscle Actin ◽  
Thiobarbituric Acid ◽  
Ethanol Metabolism ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ethanol Treatment ◽  
Liver Slices

Ethanol metabolism in the liver induces oxidative stress and altered cytokine production preceding myofibroblast activation and fibrogenic responses. The purpose of this study was to determine how ethanol affects the fibrogenic response in precision-cut liver slices (PCLS). PCLS were obtained from chow-fed male Wistar rats (200–300 g) and were cultured up to 96 h in medium, 25 mM ethanol, or 25 mM ethanol and 0.5 mM 4-methylpyrazole (4-MP), an inhibitor of ethanol metabolism. Slices from every time point (24, 48, 72, and 96 h) were examined for glutathione (GSH) levels, lipid peroxidation [thiobarbituric acid-reactive substance (TBARS) assay], cytokine production (ELISA and RT-PCR), and myofibroblast activation [immunoblotting and immunohistochemistry for smooth muscle actin (SMA) and collagen]. Treatment of PCLS with 25 mM ethanol induced significant oxidative stress within 24 h, including depletion of cellular GSH and increased lipid peroxidation compared with controls ( P < 0.05). Ethanol treatment also elicited a significant and sustained increase in interleukin-6 (IL-6) production ( P < 0.05). Importantly, ethanol treatment accelerates a fibrogenic response after 48 h, represented by significant increases in SMA and collagen 1α(I) production ( P < 0.05). These ethanol-induced effects were prevented by the addition of 4-MP. Ethanol metabolism induces oxidative stress (GSH depletion and increased lipid peroxidation) and sustained IL-6 expression in rat PCLS. These phenomena precede and coincide with myofibroblast activation, which occurs within 48 h of treatment. These results indicate the PCLS can be used as in vitro model for studying multicellular interactions during the early stages of ethanol-induced liver injury and fibrogenesis.

Studies of Lipid Peroxidation Products in Cerebrospinal Fluid and Serum in Multiple Sclerosis and Other Conditions

1992 ◽  
Vol 38 (12) ◽  
pp. 2449-2454 ◽  
Author(s):  
R Naidoo ◽  
M L Knapp
Keyword(s):  
Multiple Sclerosis ◽  
Lipid Peroxidation ◽  
Cerebrospinal Fluid ◽  
Protein Concentration ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Significant Negative Correlation ◽  
Control Subjects ◽  
Csf Proteins ◽  
Relapse Time

Abstract Lipid peroxides were measured in cerebrospinal fluid (CSF) and sera from patients with multiple sclerosis (MS) or other conditions and from control subjects. In serum, visible fluorescence, A240nm, and free and protein-bound thiobarbituric acid (TBA)-reactive substances were significantly greater in MS patients than in control subjects. No such differences were observed in CSF. There was no correlation between lipid peroxides and disease severity or relapse time. We observed a significant positive correlation between CSF protein-bound TBA-reactive substances and CSF protein, suggesting that production of the former depends on protein concentration. A significant negative correlation between free TBA-reactive substances in serum and ultraviolet fluorescence indicated that production of free TBA-reactive substances may be associated with decreased production of fluorescent lipid peroxides. This study provides evidence for increased lipid peroxidation in serum but not CSF from MS patients, suggesting that either there is no increase in CSF lipid peroxidation in MS patients or that CSF lipid peroxides are rapidly removed, possibly by binding to CSF proteins that can be reabsorbed into the blood.

scholarly journals β-Carotene and α-tocopherol concentration and antioxidant status in buccal mucosal cells and plasma after oral supplementation

2002 ◽  
Vol 87 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Jürgen G. Erhardt ◽  
Heidrun Mack ◽  
Ulrike Sobeck ◽  
Hans K. Biesalski
Keyword(s):  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substance ◽  
Antioxidative Effect ◽  
Tocopherol Concentration ◽  
Antioxidative Status ◽  
Oral Supplementation ◽  
Oral Application ◽  
Mucosal Cells ◽  
And Oxidative Stress ◽  
Β Carotene

The uptake of α-tocopherol and β-carotene and their antioxidative effect in plasma and buccal mucosal cells after oral application in twelve subjects is demonstrated in our study. The effect on the antioxidative status was evaluated using a modified thiobarbituric acid-reactive substance (TBARS) method. As expected, the supplement of 134·2 mg α-tocopherol/d and 25 mg β-carotene/d for 7 d resulted in a significant increase of α-tocopherol and β-carotene concentration in plasma (P<0·05). In buccal mucosal cells, the concentration of β-carotene increased after supplementation (P<0·05), whereas the concentration of α-tocopherol remained constant. A decrease in TBARS (P<0·05) was found in buccal mucosal cells but not in plasma. In conclusion, an uptake of the supplemented antioxidants was detected in plasma and in buccal mucosal cells. There was significant change in β-carotene concentration and oxidative stress as measured using a modified TBARS test in buccal mucosal cells, but not in the plasma.

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