scholarly journals EFFECTS OF VITAMIN C SUPPLEMENTATION ON THE CHRONIC PHASE OF CHAGAS DISEASE

2015 ◽  
Vol 57 (3) ◽  
pp. 245-250 ◽  
Author(s):  
Ricardo Guimarães MARIM ◽  
Alex Silva de GUSMÃO ◽  
Roberto Esteves Pires CASTANHO ◽  
Rafael DEMINICE ◽  
Altino Luiz Silva THEREZO ◽  
...  
Keyword(s):  
Vitamin C ◽  
Chagas Disease ◽  
Chronic Phase ◽  
Thiobarbituric Acid ◽  
Dose Equivalent ◽  
Thiobarbituric Acid Reactive Substances ◽  
Vitamin C Supplementation ◽  
Histopathologic Analysis ◽  
Different Doses ◽  
Oxidative Insult

Introduction: In order to examine the effectiveness of vitamin C (ascorbic acid) in combating the oxidative insult caused by Trypanosoma cruzi during the development of the chronic phase of Chagas disease, Swiss mice were infected intraperitoneally with 5.0 × 104 trypomastigotes of T. cruzi QM1strain. Methods: Mice were given supplements of two different doses of vitamin C for 180 days. Levels of lipid oxidation (as indicated by thiobarbituric acid reactive substances-TBARS), total peroxide, vitamin C, and reduced glutathione were measured in the plasma, TBARS, total peroxide and vitamin C were measured in the myocardium and histopathologic analysis was undertaken in heart, colon and skeletal muscle. Results: Animals that received a dose equivalent to 500 mg of vitamin C daily showed increased production of ROS in plasma and myocardium and a greater degree of inflammation and necrosis in skeletal muscles than those that received a lower dose or no vitamin C whatsoever. Conclusion: Although some research has shown the antioxidant effect of vitamin C, the results showed that animals subject to a 500 mg dose of vitamin C showed greater tissue damage in the chronic phase of Chagas disease, probably due to the paradoxical actions of the substance, which in this pathology, will have acted as a pro-oxidant or pro-inflammatory.

scholarly journals Effects of vitamin C supplementation on acute phase Chagas disease in experimentally infected mice with Trypanosoma cruzi QM1 strain

2012 ◽  
Vol 54 (6) ◽  
pp. 319-323 ◽  
Author(s):  
Ricardo Guimarães Marim ◽  
Alex Silva de Gusmão ◽  
Roberto Esteves Pires Castanho ◽  
Rafael Deminice ◽  
Altino Luiz Silva Therezo ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin C ◽  
Chagas Disease ◽  
Acute Phase ◽  
Immune Reaction ◽  
Parasite Clearance ◽  
Vitamin C Supplementation ◽  
Affected Tissue ◽  
Tissue Changes ◽  
High Doses

The tissue changes that occur in Chagas disease are related to the degree of oxidative stress and antioxidant capacity of affected tissue. Studies with vitamin C supplementation did not develop oxidative damage caused by Chagas disease in the host, but other studies cite the use of peroxiredoxins ascorbate - dependent on T. cruzi to offer protection against immune reaction. Based on these propositions, thirty "Swiss" mice were infected with T. cruzi QM1 strain and treated with two different vitamin C doses in order to study the parasitemia evolution, histopathological changes and lipid peroxidation biomarkers during the acute phase of Chagas disease. The results showed that the parasite clearance was greater in animals fed with vitamin C overdose. There were no significant differences regarding the biomarkers of lipid peroxidation and inflammatory process or the increase of myocardium in animals treated with the recommended dosage. The largest amount of parasite growth towards the end of the acute phase suggests the benefit of high doses of vitamin C for trypomastigotes. The supplementation doesn't influence the production of free radicals or the number of amastigote nests in the acute phase of Chagas disease.

scholarly journals Patients Undergoing Myeloablative Chemotherapy and Hematopoietic Stem Cell Transplantation Exhibit Depleted Vitamin C Status in Association with Febrile Neutropenia

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1879 ◽  
Author(s):  
Anitra C. Carr ◽  
Emma Spencer ◽  
Andrew Das ◽  
Natalie Meijer ◽  
Carolyn Lauren ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Febrile Neutropenia ◽  
Vitamin C ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
C Reactive Protein ◽  
Hematopoietic Stem ◽  
Reactive Protein ◽  
Myeloablative Chemotherapy ◽  
And Oxidative Stress

Patients undergoing myeloablative chemotherapy and hematopoietic stem cell transplantation (HSCT) experience profound neutropenia and vulnerability to infection. Previous research has indicated that patients with infections have depleted vitamin C status. In this study, we recruited 38 patients with hematopoietic cancer who were undergoing conditioning chemotherapy and HSCT. Blood samples were collected prior to transplantation, at one week, two weeks and four weeks following transplantation. Vitamin C status and biomarkers of inflammation (C-reactive protein) and oxidative stress (protein carbonyls and thiobarbituric acid reactive substances) were assessed in association with febrile neutropenia. The vitamin C status of the study participants decreased from 44 ± 7 µmol/L to 29 ± 5 µmol/L by week one (p = 0.001) and 19 ± 6 µmol/L by week two (p < 0.001), by which time all of the participants had undergone a febrile episode. By week four, vitamin C status had increased to 37 ± 10 µmol/L (p = 0.1). Pre-transplantation, the cohort comprised 19% with hypovitaminosis C (i.e., <23 µmol/L) and 8% with deficiency (i.e., <11 µmol/L). At week one, those with hypovitaminosis C had increased to 38%, and at week two, 72% had hypovitaminosis C, and 34% had outright deficiency. C-reactive protein concentrations increased from 3.5 ± 1.8 mg/L to 20 ± 11 mg/L at week one (p = 0.002), and 119 ± 25 mg/L at week two (p < 0.001), corresponding to the development of febrile neutropenia in the patients. By week four, these values had dropped to 17 ± 8 mg/L (p < 0.001). There was a significant inverse correlation between C-reactive protein concentrations and vitamin C status (r = −0.424, p < 0.001). Lipid oxidation (thiobarbituric acid reactive substances (TBARS)) increased significantly from 2.0 ± 0.3 µmol/L at baseline to 3.3 ± 0.6 µmol/L by week one (p < 0.001), and remained elevated at week two (p = 0.003), returning to baseline concentrations by week four (p = 0.3). Overall, the lowest mean vitamin C values (recorded at week two) corresponded with the highest mean C-reactive protein values and lowest mean neutrophil counts. Thus, depleted vitamin C status in the HSCT patients coincides with febrile neutropenia and elevated inflammation and oxidative stress.

Dehydroepiandrosterone administration prevents the oxidative damage induced by acute hyperglycemia in rats

1997 ◽  
Vol 155 (2) ◽  
pp. 233-240 ◽  
Author(s):  
M Aragno ◽  
E Brignardello ◽  
E Tamagno ◽  
V Gatto ◽  
O Danni ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Properties ◽  
Thiobarbituric Acid ◽  
Alpha Tocopherol ◽  
Thiobarbituric Acid Reactive Substances ◽  
Acute Hyperglycemia ◽  
Tissue Resistance ◽  
In Vivo Administration ◽  
Different Doses

Free radical overproduction contributes to tissue damage induced by acute hyperglycemia. Dehydroepiandrosterone, which has recently been found to have antioxidant properties, was administered i.p. to rats at different doses (10, 50 or 100 mg/kg body weight) 3 h before treatment with dextrose (5 g/kg). Lipid peroxidation was evaluated on liver, brain and kidney homogenates, measuring both steady-state concentrations of thiobarbituric acid reactive substances, and fluorescent chromolipids, evaluated as hydroxynonenal adducts. Formation of thiobarbituric acid reactive substances was significantly higher in hyperglycemic than in normoglycemic animals. Three hours (but not 1 h) dehydroepiandrosterone-pretreatment protected tissues against lipid peroxidation induced by dextrose; both thiobarbituric acid reactive substances and hydroxynonenal adducts in liver, kidney and brain homogenates were significantly lower in dehydroepiandrosterone-pretreated animals. Dehydroepiandrosterone did not modify the cytosolic level of antioxidants, such as alpha-tocopherol or glutathione, nor the activities of glutathione peroxidase, reductase or transferase. The results of this study indicate that the 'in vivo' administration of dehydroepiandrosterone increases tissue resistance to lipid peroxidation triggered by acute hyperglycemia.

Vitamin C and Thiobarbituric Acid Reactive Substances (TBARS) in Psoriasis Vulgaris Related to Psoriasis Area Severity Index (PASI)

2017 ◽  
Vol 68 (1) ◽  
pp. 43-47 ◽  
Author(s):  
Mircea Tampa ◽  
Ilinca Nicolae ◽  
Corina Daniela Ene ◽  
Isabela Sarbu ◽  
Clara Matei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Vitamin C ◽  
Psoriasis Vulgaris ◽  
Thiobarbituric Acid ◽  
Severity Index ◽  
Thiobarbituric Acid Reactive Substances ◽  
Psoriasis Area Severity Index ◽  
Pathogenic Potential ◽  
Antioxidant Mechanisms

Oxidative stress is caused by an imbalance between the production of pro-oxidants and the capacity of a biological system of rapid detoxification of free radicals. In this paper the level of pro-oxidants and antioxidants was quantified in patients with psoriasis vulgaris. The results of this study show that the level of oxygen reactive species dramatically increases and the physiologic antioxidant mechanisms are inefficient in patients with psoriasis vulgaris. These findings re-confirm that oxidative stress has a destructive and pathogenic potential in psoriasis.

scholarly journals Interaction between vitamins C and E affects their tissue concentrations, growth, lipid oxidation, and deficiency symptoms in yellow perch (Perca flavescens)

2003 ◽  
Vol 89 (5) ◽  
pp. 589-596 ◽  
Author(s):  
Kyeong-Jun Lee ◽  
Konrad Dabrowski
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Yellow Perch ◽  
Perca Flavescens ◽  
Thiobarbituric Acid ◽  
Deficient Diet ◽  
Deficiency Symptoms ◽  
Supplemental Vitamin ◽  
Vitamin C Supplementation

We have conducted studies with juvenile yellow perch (Perca flavescens) over a period of 20 weeks to address the question of the interaction between water- and lipid-soluble antioxidant vitamins. Fish (2·25±0·14 g) were divided into twelve groups, and triplicate groups were fed one of four casein-based, semi-purified diets formulated to contain low or high vitamin E levels of either 5 or 160 mg/kg without or with vitamin C supplementation (250 mg/kg). Diets were designated as −C−E, −C+E, +C−E, or +C+E, respectively. The fish fed the +C+E diet showed significantly higher weight gain, feed intake, and feed efficiency than the groups fed vitamin C-deficient diets. Total ascorbate concentrations of liver were significantly higher in fish fed vitamin C-supplemented diets than in fish fed the vitamin C-deficient diet after 16 and 20 weeks. The liver α-tocopherol concentrations were increased by supplemental vitamin C in vitamin E-deficient dietary groups which indicates a sparing or regenerating effect of vitamin C on vitamin E. Fish fed vitamin C-deficient diets (−C−E and −C+E) exhibited severe deficiency symptoms, such as scoliosis, lens cataracts, anorexia, and haemorrhages. The cumulative mortality was significantly higher in the −C−E groups. The thiobarbituric acid-reactive substances value was significantly higher in blood plasma of fish fed a diet unsupplemented with both vitamins. The findings in the present study with yellow perch support the hypothesis that vitamin C regenerates and/or spares vitamin E in vivo.

Vitamin C Supplementation Affects Oxidative-Stress Blood Markers in Response to a 30-Minute Run at 75% VO2max

2005 ◽  
Vol 15 (3) ◽  
pp. 279-290 ◽  
Author(s):  
Allan H. Goldfarb ◽  
Stephen W. Patrick ◽  
Scott Bryer ◽  
Tongjian You
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Repeated Measures ◽  
Thiobarbituric Acid ◽  
Protein Carbonyls ◽  
Dependent Manner ◽  
Total Blood ◽  
Intensity Measures ◽  
Vitamin C Supplementation ◽  
Dose Dependent

Vitamin C supplementation (VC) (either 500 or 1000 mg/d for 2 wk) was compared to a placebo treatment (P) to ascertain if VC could influence oxidative stress. Twelve healthy males (25 ± 1.4 y) were randomly assigned in a counter-balanced design with a 2-wk period between treatments. Data were analyzed using repeated measures ANOVA. Exercise intensity measures (VO2, RER, RPE, HR, lactate) were similar across treatments. Resting blood oxidative-stress markers were unaffected by treatment. Exercise decreased total blood glutathione (TGSH) and reduced glutathione (GSH) and increased oxidized glutathione (GSSG) (P < 0.01) independent of treatment. Protein carbonyls (PC) increased 3.8 fold in the P (P < 0.01). VC attenuated the PC exercise response in a dose-dependent manner (P < 0.01). Thiobarbituric acid reactive substances (TBARS) was not influenced by exercise (P = 0.68) or VC. These data suggest that VC supplementation can attenuate exercise-induced protein oxidation in a dose-dependent manner with no effect on lipid peroxidation and glutathione status.

Endothelium-dependent vasodilation in the brachial artery is impaired in smokers: effect of vitamin C

1997 ◽  
Vol 273 (4) ◽  
pp. H1644-H1650 ◽  
Author(s):  
Takeshi Motoyama ◽  
Hiroaki Kawano ◽  
Kiyotaka Kugiyama ◽  
Osamu Hirashima ◽  
Masamichi Ohgushi ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cigarette Smoking ◽  
Vitamin C ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Sublingual Nitroglycerin ◽  
Thiobarbituric Acid Reactive Substances ◽  
Lower Vitamin

Cigarette smoking has been shown to cause endothelial dysfunction. To examine the effects of vitamin C and cigarette smoking on endothelium-dependent vasodilation, we measured the lumen diameter and flow velocity of the brachial arteries at rest, during reactive hyperemia following transient arterial occlusion, and after sublingual nitroglycerin (0.3 mg) in smokers ( n = 20) and nonsmokers ( n = 20) with high-resolution ultrasound after infusion of saline or saline plus vitamin C (10 mg/min for 20 min). We also performed the same study in smokers ( n = 15) before and 10 min after cigarette smoking. In addition, we measured the serum levels of vitamin C and the plasma levels of thiobarbituric acid-reactive substances (TBARS) as an index of lipid peroxidation. The smokers had lower vitamin C levels, higher TBARS levels, and showed impairment of flow-dependent vasodilation (5.3 ± 1.9 vs. 9.2 ± 1.5%, P < 0.0001) compared with nonsmokers. Vitamin C administration improved the impairment of flow-dependent vasodilation (5.3 ± 1.9 to 9.0 ± 3.2%, P < 0.001) and decreased TBARS in smokers but not in nonsmokers. Furthermore, cigarette smoking acutely worsened the impairment of flow-dependent vasodilation (5.4 ± 1.8 to 1.5 ± 1.3%, P < 0.01) and increased TBARS. We conclude that 1) endothelium-dependent vasodilation in the brachial arteries is impaired in smokers and this impairment is improved by vitamin C administration in association with a decrease in TBARS and 2) cigarette smoking produces acute impairment of endothelium-dependent vasodilation in smokers in association with an increase in TBARS.

Complete lack of vitamin C intake generates pulmonary emphysema in senescence marker protein-30 knockout mice

2010 ◽  
Vol 298 (6) ◽  
pp. L784-L792 ◽  
Author(s):  
Kengo Koike ◽  
Yoshitaka Kondo ◽  
Mitsuaki Sekiya ◽  
Yasunori Sato ◽  
Kazunori Tobino ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Lung Development ◽  
Pulmonary Emphysema ◽  
Collagen Synthesis ◽  
Thiobarbituric Acid ◽  
Sirtuin 1 ◽  
Plain Water ◽  
Marker Protein ◽  
Thiobarbituric Acid Reactive Substances

Vitamin C (VC) is a potent antioxidant and plays an essential role in collagen synthesis. As we previously reported, senescence marker protein-30 (SMP30) knockout (KO) mice cannot synthesize VC due to the genetic disruption of gluconolactonase (i.e., SMP30). Here, we utilized SMP30 KO mice deprived of VC and found that VC depletion caused pulmonary emphysema due to oxidative stress and a decrease of collagen synthesis by the third month of age. We grew SMP30 KO mice and wild-type (WT) mice on VC-free chow and either VC water [VC(+)] or plain water [VC(−)] after weaning at 4 wk of age. Morphometric findings and reactive oxygen species (ROS) in the lungs were evaluated at 3 mo of age. No VC was detected in the lungs of SMP30 KO VC(−) mice, but their ROS increased 50.9% over that of the VC(+) group. Moreover, their collagen content in the lungs markedly decreased, and their collagen I mRNA decreased 82.2% compared with that of the WT VC(−) group. In the SMP30 KO VC(−) mice, emphysema developed [21.6% increase of mean linear intercepts (MLI) and 42.7% increase of destructive index compared with VC(+) groups], and the levels of sirtuin 1 (Sirt1) decreased 16.8%. However, VC intake increased the MLI 16.2% and thiobarbituric acid reactive substances 22.2% in WT mice, suggesting that an excess of VC can generate oxidative stress and may be harmful during this period of lung development. These results suggest that VC plays an important role in lung development through affecting oxidant-antioxidant balance and collagen synthesis.

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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