scholarly journals Alterations in the Plasma and Red Blood Cell Properties in Patients with Varicose Vein: A Pilot Study

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lukasz Gwozdzinski ◽  
Anna Pieniazek ◽  
Joanna Bernasinska-Slomczewska ◽  
Pawel Hikisz ◽  
Krzysztof Gwozdzinski
Keyword(s):  
Oxidative Stress ◽  
Varicose Vein ◽  
Ache Activity ◽  
Plasma Membranes ◽  
Varicose Veins ◽  
Blood Stasis ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Thiobarbituric Acid Reactive Substance

The varicose vein results from the inefficient functioning of the valves in the lower limb veins, making the blood flow slow down and leading to blood stasis and hypoxia. This type of vein dysfunction might be a result of the development of oxidative stress. We compared oxidative stress markers in the plasma and erythrocytes obtained from peripheral veins and varicose veins in the same patients (glutathione, nonenzymatic antioxidant capacity (NEAC), catalase (CAT) and acetylcholinesterase (AChE) activity, thiols, thiobarbituric acid-reactive substance (TBARS), and protein carbonyls). We found a decrease in NEAC in the plasma obtained from the varicose veins compared to the peripheral veins. We detected a decrease in thiols in the plasma, hemolysate, and plasma membranes and increase in protein carbonyl compounds and TBARS levels in the varicose veins. These changes were accompanied by a decrease in CAT and AChE activity. For the first time, our results show changes in the plasma, erythrocyte membrane, and hemolysate protein properties in varicose vein blood in contrast to the plasma and erythrocytes in peripheral vein blood from the same patients. The increased oxidative stress accompanying varicose vein disease might result from the local inefficiency of the antioxidant defense system.

scholarly journals The Role of Oxidative Stress in Decreased Acetylcholinesterase Activity at the Neuromuscular Junction of the Diaphragm during Sepsis

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Hua Liu ◽  
Jin Wu ◽  
Jun-yan Yao ◽  
Hong Wang ◽  
Shi-tong Li
Keyword(s):  
Oxidative Stress ◽  
Neuromuscular Junction ◽  
Ache Activity ◽  
Thiobarbituric Acid ◽  
Acetylcholinesterase Activity ◽  
Protein Carbonyls ◽  
Low Grade ◽  
Caecal Ligation And Puncture ◽  
Septic Group

Our recent study demonstrated that acetylcholinesterase (AChE) activity at the neuromuscular junction (NMJ) of the diaphragm decreased during sepsis. However, the mechanisms were not clearly identified. In this study, we aimed to investigate whether the decreased AChE activity was related to oxidative stress by observing AChE activity in different grades of sepsis induced by caecal ligation and puncture (CLP). At 24 h after surgery, an assay of thiobarbituric acid reactive species (TBARS) and protein carbonyls, as well as the myeloperoxidase (MPO), superoxide dismutase (SOD), and catalase (CAT) activity, was conducted. AChE activity was measured by biochemical and histological detection. AChE and CAT activity in the diaphragm decreased, while the contents of TBARS and protein carbonyls, the activity of MPO and SOD, and the SOD/CAT ratios increased. The above changes were much more significant in the mid-grade septic group than in the low-grade septic group. The colour of the AChE activity staining at the NMJ gradually lightened from the sham surgery group to the mid-grade septic group. AChE activity was significantly negatively correlated with the levels of TBARS and protein carbonyls. We consider that oxidative stress might be responsible for decreased AChE activity in the diaphragms of rats induced with sepsis.

Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Antioxidant Vitamin ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protein Carbonyl Content ◽  
Trained Subjects ◽  
Exercise Induced ◽  
Sedentary Subjects

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

scholarly journals Association of Hypoadiponectinemia with Hypoglutathionemia in NAFLD Subjects with and without Type 2 Diabetes

2010 ◽  
Vol 29 (5) ◽  
pp. 213-221 ◽  
Author(s):  
Narasimhan Sandhya ◽  
Kuppan Gokulakrishnan ◽  
Radhakrishnan Ravikumar ◽  
Viswanathan Mohan ◽  
Muthuswamy Balasubramanyam
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Thiobarbituric Acid ◽  
Normal Glucose Tolerance ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Diabetic Patients ◽  
Thiobarbituric Acid Reactive Substances ◽  
Type 2 Diabetic Patients

Objective: The aim of this study is to measure the extent of oxidative stress and to see whether it has any correlation to changes in adiponectin levels in NAFLD subjects with and without Type 2 diabetes.Methods: Subjects recruited from the Chennai Urban Rural Epidemiology Study comprise of 1: Normal Glucose Tolerance (NGT) subjects without NAFLD; 2: NGT with NAFLD; 3: Type 2 Diabetic patients [T2DM] without NAFLD and 4: T2DM with NAFLD. Thiobarbituric acid reactive substances (TBARS), protein carbonyl (PCO), glutathione and adiponectin levels were measured by standard methods. Ultrasound of the liver was used to diagnose NAFLD.Results: T2DM subjects with NAFLD had significantly (p< 0.001) higher levels of thiobarbituric acid reactive substances (TBARS) and protein carbonyls (PCO) but lower (p< 0.001) GSH/GSSG ratio and adiponectin levels compared to other three groups. The association of hypoadiponectinemia withNAFLD/Type 2 diabetes was significant even after adjusting for age, gender and BMI, but lost when adjusted for parameters of oxidative stress. While palmitate significantly reduced GSH/GSSG ratio in hepatocytes, addition of exogenous recombinant adiponectin restored the GSH/GSSG ratio comparable to those of untreated cells.Conclusion: There exists an association of hypoglutathionemia and hypoadiponectinemia in subjects with NAFLD and/or T2DM. In addition to the known beneficial effects, out study also exposes the antioxidant nature of adiponectin.

scholarly journals PSIV-5 Can dietary oxidized protein induce oxidative stress in pigs?

2019 ◽  
Vol 97 (Supplement_2) ◽  
pp. 181-181
Author(s):  
Carl A Frame ◽  
Logan R Kilburn ◽  
Erika M Johnson ◽  
Mariana C Rossoni Serao
Keyword(s):  
Oxidative Stress ◽  
Companion Animals ◽  
Thiobarbituric Acid ◽  
Oxidation Products ◽  
Protein Carbonyls ◽  
P Value ◽  
Thiobarbituric Acid Reactive Substance ◽  
Oxidation Treatment ◽  
Crypt Depth ◽  
Lipid Oxidation Products

Abstract Endogenous protein oxidation as a result of oxidative stress is known to reduce the efficiency of livestock species (Boler et al., 2012; DeRouchey et al., 2004; Dibner, Atwell, Kitchell, Shermer, & Ivey, 1996). Additionally, rendered by-products are common feedstuffs in livestock diets. During processing, these sources have the potential to become oxidized. While most research on oxidative stress has focused on consumption of dietary oxidized lipids, little research has been done in the area of dietary oxidized proteins and the potential to induce oxidative stress. The objective of this study was to determine the effects of dietary oxidized protein on oxidative stress in pigs. For this study, 30 pigs 6 weeks old were divided into three dietary treatments of control, medium, and high dietary oxidized protein. Each treatment was fed the same diet, with the exception of the degree of oxidation in bovine plasma which was included in the diet at 10 percent. Pigs were fed for 19 days and then euthanized for tissues collected. Jejunum, liver, and colon were collected along with urine and plasma samples on day 0 and 18. Jejunum samples were also collected for histology. Markers of oxidative stress included protein carbonyls, thiobarbituric acid reactive substance (TBARS), 8-hydroxyguanine, and glutathione peroxidase activity. Pigs in the high oxidation treatment had an increase in crypt depth of 16 percent (p-value less than 0.05) when compared to control further resulting in an 11 percent decrease in villi height to crypt depth ratio (p-value less than 0.05). Additionally, lipid oxidation products, measured by TBARS, was 28 percent greater in the liver of pigs in the medium oxidation treatment (p-value less than 0.05) when compared to control. Even with the short duration of this study, dietary oxidized protein did impact the oxidative status of the animal. Using pigs as a model for companion animals, it could be hypothesized then that long-term exposure could have implications on longevity.

Diallyl trisulfide ameliorates arsenic-induced hepatotoxicity by abrogation of oxidative stress, inflammation, and apoptosis in rats

2014 ◽  
Vol 34 (5) ◽  
pp. 506-525 ◽  
Author(s):  
NC Sumedha ◽  
S Miltonprabu
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Oxidation ◽  
Structural Changes ◽  
Histopathological Examination ◽  
Thiobarbituric Acid ◽  
Hepatic Function ◽  
Protein Carbonyl ◽  
Thiobarbituric Acid Reactive Substance ◽  
Diallyl Trisulfide

The present study investigates the possible ameliorative effects of diallyl trisulfide (DATS) against arsenic (As)-induced hepatotoxicity and oxidative stress in rats. The four experimental groups evaluated include: (1) vehicle control; (2) As (5 mg/kg/day); (3) DATS (80 mg/kg/day) + As; and (4) DATS. Induction of As in rats caused severe hepatotoxicity as evidenced by an elevation of serum aspartate aminotransferase and alanine aminotransferase activities and increased total bilirubin concentration, indicating hepatic function abnormalities. Histopathological examination revealed various structural changes in the liver, characterized by hepatocyte degeneration/necrosis, congestion, sinusoidal dilatation, vacuolation, and inflammatory cell infiltration. The significant decrease in reduced glutathione content, catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and the significant increase in lipid peroxidation (thiobarbituric acid reactive substance) and protein oxidation (protein carbonyl) contents indicated that As-induced hepatotoxicity was mediated through oxidative stress. As intoxication also elevated the levels of Cas-3 and nitric oxide and increased the expression of nuclear factor-κB p65 in the liver. In contrast, DATS pretreatment significantly improved As-induced serum biochemical, immunohistochemical, and histopathological alterations reflecting hepatic dysfunction. These results may contribute to a better understanding of the hepatoprotective role of DATS, emphasizing the influence of this garlic trisulfide in the diet for human health, possibly preventing the hepatic injury associated with As intoxication, presumably due to its ability to inhibit lipid peroxidation, protein oxidation, and restoration of antioxidant status.

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 Effect of Acacia Polyphenol Supplementation on Exercise-Induced Oxidative Stress in Mice Liver and Skeletal Muscle

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 29 ◽  
Author(s):  
Koichi Yada ◽  
Llion Arwyn Roberts ◽  
Natsumi Oginome ◽  
Katsuhiko Suzuki
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Muscle Protein ◽  
Thiobarbituric Acid ◽  
Exhaustive Exercise ◽  
Protein Carbonyls ◽  
High Dose ◽  
Thiobarbituric Acid Reactive Substance ◽  
Skeletal Muscle Protein ◽  
Exercise Induced

The purpose of this study was to investigate the effects of acacia polyphenol (AP) supplementation on exercise-induced oxidative stress in mouse liver and skeletal muscle. Plasma aspartate aminotransferase (AST), liver and skeletal muscle levels of thiobarbituric acid reactive substance (TBARS), and levels of skeletal muscle protein carbonyls increased immediately after exhaustive exercise. Exhaustive exercise also decreased liver glutathione (GSH). These results suggest that the exhaustive exercise used in this study induced tissue damage and oxidative stress. Contrary to our expectations, AP supplementation increased plasma AST and alanine aminotransferase activities, liver levels of TBARS, and protein carbonyls. Furthermore, AP supplementation decreased glutathione and glutathione peroxidase activity in the liver. On the other hand, AP supplementation decreased TBARS levels in skeletal muscle. These results suggest that oral high-dose AP administration decreased oxidative stress in skeletal muscle but induced oxidative stress in the liver and increased hepatotoxicity.

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.

scholarly journals TUALANG HONEY ATTENUATES KAINIC ACID-INDUCED OXIDATIVE STRESS IN RAT CEREBELLUM AND BRAINSTEM

2017 ◽  
Vol 9 (12) ◽  
pp. 155 ◽  
Author(s):  
Nur Shafika Mohd Sairazi ◽  
K. N. S. Sirajudeen ◽  
Mustapha Muzaimi ◽  
Mummedy Swamy ◽  
Mohd Asnizam Asari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Total Antioxidant Status ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Multiple Time ◽  
Rat Cerebellum ◽  
Total Antioxidant ◽  
Multiple Time Points ◽  
Tualang Honey

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property.

scholarly journals Protein carbonyls and protein thiols in rheumatoid arthritis

2018 ◽  
Vol 6 (5) ◽  
pp. 1738 ◽  
Author(s):  
Pullaiah P. ◽  
Suchitra M. M. ◽  
Siddhartha Kumar B.
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Protein Modification ◽  
Antioxidant Properties ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Carbonyl Content ◽  
Protein Thiol ◽  
Protein Carbonyl Content ◽  
Protein Thiols

Background: Oxidative stress (OS) has an important role in the pathogenesis and progression of rheumatoid arthritis (RA). OS causes protein modification, thereby impairing the biological functions of the protein. This study was conducted to assess the oxidatively modified protein as protein carbonyl content and the antioxidant status as protein thiols, and to study the association between protein carbonyls and protein thiols in RA.Methods: Newly diagnosed RA patients who were not taking any disease modifying anti-rheumatic drugs were included into the study group (n=45) along with age and sex matched healthy controls (n=45). Serum protein carbonyl content and protein thiols were estimated.Results: Elevated protein carbonyl content and decreased protein thiol levels (p<0.001) were observed in RA. A significant negative correlation was observed between protein carbonyl content and protein thiol levels (p<0.001).Conclusions: Oxidative stress in RA is evidenced by enhanced protein oxidation and decreased antioxidant protein thiol levels. Decreased protein thiols may also reflect protein modifications leading to compromise in the antioxidant properties. This oxidant and antioxidant imbalance needs to be addressed by therapeutic interventions to prevent disease progression.

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