scholarly journals Synergistic Action of Vitamin E and Vitamin C in Vivo Using a New Mutant of Wistar-Strain Rats, ODS, Unable to Synthesize Vitamin C.

1991 ◽  
Vol 37 (4) ◽  
pp. 359-369 ◽  
Author(s):  
Osamu IGARASHI ◽  
Yukako YONEKAWA ◽  
Yoko FUJIYAMA-FUJIHARA
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Synergistic Action ◽  
Wistar Strain

scholarly journals Effectiveness of Vitamin C and Vitamin E Antioxidant Combination on Caspase-3 Expression in Wistar White Rat Pulmonum Contusion

2020 ◽  
Vol 3 (1) ◽  
pp. 31-44
Author(s):  
Bermansyah ◽  
Gama Satria ◽  
Ahmad Umar
Keyword(s):  
Cell Death ◽  
Vitamin E ◽  
Vitamin C ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Cell Function ◽  
Pulmonary Contusion ◽  
Tnf Α ◽  
Male Wistar Rats

Introduction.Pulmonary contusions can cause a progressive inflammatory response. Activation of TNF-α cytokines and reactive oxygen species (ROS) can cause pulmonary cell death. Antioxidants can have the potential to neutralize ROS. The purpose of this study is to determine the effectiveness of antioxidant administration in maintaining pulmonary cell function in wistar rats that have been induced to experience pulmonary contusions through caspase-3 levels. Methods.This study was an in vivo experimental study conducted on thirty male wistar rats and divided into five groups (n = 6): control, pulmonary contusion + asthaxanthine 5 mg/kgBW, pulmonary contusion + vitamin C and E 50 mg/kgBW, pulmonary contusion + vitamin C and E 100 mg/kgBW, pulmonary contusion + vitamin C and E 200 mg/kgBW. The value of Caspase-3 is evaluated by the IHC. All data analyzes used SPSS 18. Results. Low doses of antioxidants have the potential to reduce pulmonary cell death in wistar rats induced by pulmonary contusions.Conclussion. Vitamin C and E effective to reduce polmonary cell death in pulmonary contusion.Keywords: antioxidants, vitamin C, vitamin E, pulmonary contusions animal model, apoptosis, caspase-3

scholarly journals Determination of tissue-specific interaction between vitamin C and vitamin E in vivo using senescence marker protein-30 knockout mice as a vitamin C synthesis deficiency model

2021 ◽  
pp. 1-33
Author(s):  
Ayami Sato ◽  
Yuka Takino ◽  
Tomohiro Yano ◽  
Koji Fukui ◽  
Akihito Ishigami
Keyword(s):  
Gene Expression ◽  
Vitamin E ◽  
Vitamin C ◽  
Specific Interaction ◽  
Marker Protein ◽  
Tissue Specific ◽  
Transfer Protein

Abstract Vitamin E (α-tocopherol; VE) is known to be regenerated from VE radicals by vitamin C (L-ascorbic acid; VC) in vitro. However, their in vivo interaction in various tissues is still unclear. Therefore, we alternatively examined the in vivo interaction of VC and VE by measurement of their concentrations in various tissues of senescence marker protein-30 (SMP30) knockout (KO) mice as a VC synthesis deficiency model. Male SMP30-KO mice were divided into four groups (VC+/VE+, VC+/VE-, VC-/VE+, and VC-/VE-), fed diets with or without 500 mg/kg VE and given water with or without 1.5 g/L VC ad libitum. Then, VC and VE concentrations in the plasma and various tissues were determined. Further, gene expression levels of transporters associated with VC and VE, such as α-tocopherol transfer protein (α-TTP) and sodium-dependent vitamin C transporters (SVCTs), were examined. These results showed that the VE levels in the VC-depleted (VC-/VE+) group were significantly lower than those in the VC+/VE+ group in the liver and heart; the VC levels in the VE-depleted (VC+/VE-) group were significantly lower than those in the VC+/VE+ group in the kidneys. The α-TTP gene expression in the liver and kidneys were decreased by VC and/or VE depletion. Moreover, SVCT1 gene expression in the liver was decreased by both VC and VE depletion. In conclusion, these results indicate that VC spares VE mainly in the liver and heart, and that VE spares VC in the kidneys of SMP30-KO mice. Thus, interaction between VC and VE is likely to be tissue specific.

scholarly journals Effects of vitamin C and vitamin E on in vivo lipid peroxidation: results of a randomized controlled trial

2002 ◽  
Vol 76 (3) ◽  
pp. 549-555 ◽  
Author(s):  
Han-Yao Huang ◽  
Lawrence J Appel ◽  
Kevin D Croft ◽  
Edgar R Miller ◽  
Trevor A Mori ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Randomized Controlled Trial ◽  
Vitamin E ◽  
Vitamin C ◽  
Controlled Trial ◽  
Randomized Controlled

Protection From Oxidized LDL–Induced Leukocyte Adhesion to Microvascular and Macrovascular Endothelium In Vivo by Vitamin C but Not by Vitamin E

Circulation ◽  
1995 ◽  
Vol 91 (5) ◽  
pp. 1525-1532 ◽  
Author(s):  
Hans-Anton Lehr ◽  
Balz Frei ◽  
A. Maria Olofsson ◽  
Thomas E. Carew ◽  
Karl-E. Arfors
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Leukocyte Adhesion ◽  
Oxidized Ldl

Estrogen and Gender Effects on Muscle Damage, Inflammation, and Oxidative Stress

2000 ◽  
Vol 25 (4) ◽  
pp. 274-287 ◽  
Author(s):  
Peter M. Tiidus
Keyword(s):  
Oxidative Stress ◽  
Gender Differences ◽  
Creatine Kinase ◽  
Vitamin E ◽  
Vitamin C ◽  
Muscle Damage ◽  
Antioxidant Properties ◽  
Gender Effects ◽  
Gender Based

Information suggests that there may be gender-based differences in skeletal muscle responses to damaging exercise. Evidence demonstrates that estrogen has strong antioxidant properties and may be an important factor in maintaining postexercise membrane stability and limiting creatine kinase (CK) leakage from damaged muscle in female animals. Research demonstrates effects of estrogen and possible gender differences in other morphological and biochemical indices of postexercise muscle damage and leukocyte invasion. Nevertheless, there are conflicting findings suggesting that in some in vivo exercise models, estrogen administration has limited ability to affect exercise-induced oxidative stress and muscle damage and max cause loss of tissue vitamin C. Gender differences appear to exist in tissue levels of other important antioxidants such as vitamin E and glutathione. More research is needed to fully define the potential for estrogen to influence postexercise muscle damage and the inflammatory response and to determine the mechanisms by which it may operate. Key words: exercise, neutrophils, creatine kinase, vitamin E, vitamin C

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.

scholarly journals The effect of vitamin C or vitamin E supplementation on basal and H2O2-induced DNA damage in human lymphocytes

2000 ◽  
Vol 84 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Lisa A. Brennan ◽  
Gerard M. Morris ◽  
Gillian R. Wasson ◽  
Bernadette M. Hannigan ◽  
Yvonne A. Barnett
Keyword(s):  
Dna Damage ◽  
Superoxide Dismutase ◽  
Vitamin E ◽  
Vitamin C ◽  
Glutathione Peroxidase ◽  
Human Lymphocytes ◽  
Peripheral Blood Lymphocytes ◽  
Supplementation Period ◽  
Before And After

There is a wealth of epidemiological information on antioxidants and their possible prevention of disease progression but very little of the research on antioxidants has involved intervention studies. In this study, the potential protective effect of vitamin C or E supplementation in vivo against endogenous and H2O2-induced DNA damage levels in lymphocytes was assessed. The supplementation involved fourteen healthy male and female non-smokers mean age 25·53 (SD 1·82) years, who were asked to supplement an otherwise unchanged diet with 1000 mg vitamin C daily for 42 d or 800 mg vitamin E daily for 42 d. DNA damage in H2O2-treated peripheral blood lymphocytes (PBL) and untreated PBL before and after supplementation, and during a 6-week washout period was assessed using an ELISA. At each sampling time-point, the red cell concentrate activities of superoxide dismutase, catalase and glutathione peroxidase were also determined. Supplementation with vitamin C or vitamin E decreased significantly H2O2-induced DNA damage in PBL, but had no effect on endogenous levels of DNA damage. The activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were suppressed during the supplementation period. These supplementation regimens may be used to limit the possible adverse effects of reactive oxygen species (including those produced during the course of an immune response) on lymphocytes in vivo, and so help to maintain their functional capacity.

Sign in / Sign up

Export Citation Format

Share Document