scholarly journals Ascorbic acid and dehydroascorbic acid as biomarkers of oxidative stress caused by smoking

1997 ◽  
Vol 65 (4) ◽  
pp. 959-963 ◽  
Author(s):  
J Lykkesfeldt ◽  
S Loft ◽  
J B Nielsen ◽  
H E Poulsen
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Dehydroascorbic Acid ◽  
Biomarkers Of Oxidative Stress

scholarly journals Concentration-Dependent Antioxidant/Pro-Oxidant Activity of Ascorbic Acid in Chickens

2012 ◽  
Vol 66 (6) ◽  
pp. 256-260
Author(s):  
Nadežda Berzina ◽  
Jurijs Markovs ◽  
Mirdza Apsīte ◽  
Svetlana Vasiļjeva ◽  
Galina Smirnova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Cadmium Concentration ◽  
Dehydroascorbic Acid ◽  
Cadmium Accumulation ◽  
Suppressive Effect ◽  
High Dose ◽  
Dependent Manner ◽  
Treatment Groups ◽  
Liver And Kidney

The effects of ascorbic acid supplementation on biomarkers of oxidative stress, cadmium accumulation in organs, immune system activity and kidney function in chickens were investigated. The treatment groups of chickens were fed either plain diet or diet supplemented with ascorbic acid at 100, 500, 1000 and 2000 mg/kg for four weeks. Liver and kidney tissues were assayed for cadmium concentration, and the hepatic levels of ascorbic acid and dehydroascorbic acid (DHAA; the oxidised form), malondialdehyde, glutathione, activity of glutathione peroxidase, blood serum uric acid, creatinine, lysozyme and circulating immune complexes were measured. Supplementation with a high dose of ascorbic acid (1000 and 2000 mg/kg in the diet) caused an imbalance between pro-oxidative and antioxidative activities, and induced a suppressive effect on innate immunity. The results suggest that oxidative stress compromises renal function. We observed that ascorbic acid increased cadmium accumulation in a dose-dependent manner.

scholarly journals Content of vitamine C metabolites in rats organs at acute blood loss

2018 ◽  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Blood Loss ◽  
Dehydroascorbic Acid ◽  
Acute Blood Loss ◽  
Acid System ◽  
Control Value ◽  
Vitamine C ◽  
Acid Metabolites ◽  
Oxidative Processes

There has been studied the effect of acute blood loss, which was modeled by a single loss of 30% of the circulating blood, on the fluctuations in the content of ascorbic (AA), dehydroascorbic (DAA), diketogulonic (DKGA) acid and their sum in the organs of rats in dynamics for the fifth, twelfth, nineteenth and twenty-sixth days after the blood loss. Acute blood loss caused a significant decrease in the content of all parameters of the system of metabolites of ascorbic acid – their sum, AA, DAA and DKGA – by 10–73 % compared to the control. The most significant decrease was in the content of AA, which was not restored in all organs until the end of the study period. The DAA content in all organs increased from the 12th day, and then decreased during the experiment. The content of the DKGA increased from the 19th day of the experiment. At the same time, it was found that on 26th day in the kidneys, the DAA content exceeded the control value by 42%, and the content of DKGA in the liver and blood – by 25–60 %. The content of the amount of ascorbic acid metabolites at the end of the experiment was almost restored, but this recovery occurred in various ways: in the kidneys – due to an increase in the DAA content, in other organs – by increasing the concentration of DKGA. The parts of AA from the sum of acids (in %) after blood loss significantly decreased, starting from the 5th day, and the process of its recovery began to occur only after the 19th day. The ratio of the amount of the vitamin component of the acids of the ascorbic acid system to the content of the non-vitamin DKGA was increased in the kidneys on the 12th and 26th days of the experiment, in other organs this index decreased 2.3–3.1 times in comparison with the control. The obtained data can be explained by the increased consumption of ascorbic acid to neutralize the effects of the intensification of oxidative processes under oxidative stress, which were activated by the action of acute blood loss, due to its reversible conversion to dehydroascorbic acid, and the latter irreversibly to diketogulonic acid.

scholarly journals Physical Exercise and Redox Balance in Type 2 Diabetics: Effects of Moderate Training on Biomarkers of Oxidative Stress and DNA Damage Evaluated through Comet Assay

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Monica Pittaluga ◽  
Antonio Sgadari ◽  
Ivan Dimauro ◽  
Barbara Tavazzi ◽  
Paolo Parisi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Dna Damage ◽  
Ascorbic Acid ◽  
Exercise Training ◽  
Comet Assay ◽  
Redox Homeostasis ◽  
Diabetic Patients ◽  
Biomarkers Of Oxidative Stress

Objective.Hyperglycemia leads to increased production of reactive oxygen species (ROS) in type 2 diabetes, which reduces cellular antioxidant defenses and induces DNA lesions. The aim of this study was to investigate the effects on redox homeostasis and DNA oxidative damage of exercise training in patients with type 2 diabetes compared with nondiabetic individuals.Methods and Results.12 sedentary type 2 diabetic males (62.1 ± 4.3 yrs) and 12 sedentary healthy males (61.7 ± 3.9 yrs) were exposed to 4-month moderate training, 3 times per week, to evaluate the effect on plasma biomarkers of oxidative stress malondialdehyde and antioxidant status (GSSG, GSH/GSSG, and ascorbic acid) as well as basal and H2O2-induced DNA damage trough alkaline comet assay in peripheral blood lymphocytes. After training, glutathione and ascorbic acid levels increased in both groups, but only in diabetics the malondialdehyde as well as the DNA damage decreased.Conclusion.Our study demonstrates for the first time that moderate exercise training is not only effective in improving the redox homeostasis, through an increase of the endogenous antioxidant defences in healthy as well as in diabetic patients, but also, specifically in diabetic patients, effective in lowering the susceptibility to oxidative DNA damage and the lipid peroxidation levels.

scholarly journals Lutein Interacts with Ascorbic Acid More Frequently than with α-Tocopherol to Alter Biomarkers of Oxidative Stress in Female Zucker Obese Rats

2003 ◽  
Vol 133 (9) ◽  
pp. 2838-2844 ◽  
Author(s):  
Shirley Blakely ◽  
Arnetra Herbert ◽  
Michelle Collins ◽  
Mamie Jenkins ◽  
Geraldine Mitchell ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Obese Rats ◽  
Biomarkers Of Oxidative Stress

scholarly journals Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis

Gut ◽  
1998 ◽  
Vol 42 (6) ◽  
pp. 850-855 ◽  
Author(s):  
K Tsai ◽  
S-S Wang ◽  
T-S Chen ◽  
C-W Kong ◽  
F-Y Chang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Acute Pancreatitis ◽  
Ascorbic Acid ◽  
Disease Severity ◽  
Clinical Manifestations ◽  
Dehydroascorbic Acid ◽  
Superoxide Radicals ◽  
Severity Scores ◽  
Mild Acute Pancreatitis

Background—Reactive oxygen species and related oxidative damage have been implicated in the initiation of acute pancreatitis. Changes in these parameters during disease progression merit further investigation.Aims—To evaluate changes and the clinical relevance of superoxide radicals, endogenous antioxidants, and lipid peroxidation during the course of acute pancreatitis.Patients and methods—Superoxide radicals (measured as lucigenin amplified chemiluminescence), ascorbic acid, dehydroascorbic acid, α tocopherol, and lipid peroxidation (measured as thiobarbiturate reactive substances) were analysed in blood samples from 56 healthy subjects, 30 patients with mild acute pancreatitis, and 23 patients with severe acute pancreatitis. The association with grades of disease severity was analysed. Measurements were repeated one and two weeks after onset of pancreatitis.Results—In the blood from patients with acute pancreatitis, there were increased levels of the superoxide radical as well as lipid peroxides. There was notable depletion of ascorbic acid and an increased fraction of dehydroascorbic acid. Changes in α tocopherol were not great except in one case with poor prognosis. Differences between severe and mild acute pancreatitis were significant (p<0.01). Variable but significant correlations with disease severity scores were found for most of these markers. The normalisation of these indexes postdated clinical recovery one or two weeks after onset of disease.Conclusions—Heightened oxidative stress appears early in the course of acute pancreatitis and lasts longer than the clinical manifestations. The dependence of disease severity on the imbalance between oxidants and natural defences suggests that oxidative stress may have a pivotal role in the progression of pancreatitis and may provide a target for treatment.

Chronically and acutely exercised rats: biomarkers of oxidative stress and endogenous antioxidants

2000 ◽  
Vol 89 (1) ◽  
pp. 21-28 ◽  
Author(s):  
Jiankang Liu ◽  
Helen C. Yeo ◽  
Eva Övervik-Douki ◽  
Tory Hagen ◽  
Stephanie J. Doniger ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Treadmill Running ◽  
Tissue Type ◽  
Tissue Homogenate ◽  
Glutamine Synthetase Activity ◽  
Chronic Exercise ◽  
Endogenous Antioxidants ◽  
The Brain ◽  
Biomarkers Of Oxidative Stress

The responses to oxidative stress induced by chronic exercise (8-wk treadmill running) or acute exercise (treadmill running to exhaustion) were investigated in the brain, liver, heart, kidney, and muscles of rats. Various biomarkers of oxidative stress were measured, namely, lipid peroxidation [malondialdehyde (MDA)], protein oxidation (protein carbonyl levels and glutamine synthetase activity), oxidative DNA damage (8-hydroxy-2′-deoxyguanosine), and endogenous antioxidants (ascorbic acid, α-tocopherol, glutathione, ubiquinone, ubiquinol, and cysteine). The predominant changes are in MDA, ascorbic acid, glutathione, cysteine, and cystine. The mitochondrial fraction of brain and liver showed oxidative changes as assayed by MDA similar to those of the tissue homogenate. Our results show that the responses of the brain to oxidative stress by acute or chronic exercise are quite different from those in the liver, heart, fast muscle, and slow muscle; oxidative stress by acute or chronic exercise elicits different responses depending on the organ tissue type and its endogenous antioxidant levels.

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