Vitamin E Treatment (vitamin + e_treatment)

Distribution by Scientific Domains


Selected Abstracts


Determination of Reactive Oxygen Species in Myringotomized Tympanic Membranes: Effect of Vitamin E Treatment

THE LARYNGOSCOPE, Issue 4 2004
Senol Polat MD
Abstract Objectives/Hypothesis Recent studies have established a strong relationship between the development of myringosclerosis and reactive oxygen species (ROS). The aims of the present study were to directly detect ROS in the tympanic membrane and middle ear mucosa of rats by measuring luminol amplified chemiluminescence, to evaluate the changes in the levels of ROS after treatment with vitamin E, and to examine the possible changes in the tympanic membranes otomicroscopically and histologically. Study Design Prospective controlled animal study. Methods Forty healthy Sprague-Dawley rats were divided into five groups of eight animals each. Animals in all groups except group 1 were bilaterally myringotomized. Group 2 received no treatment, group 3 was treated with topical olive oil, group 4 received topical vitamin E, and group 5 received intramuscular vitamin E. After 24 hours of myringotomy, tympanic membranes were examined otomicroscopically; thereafter, tympanic membranes and middle ear mucosa were peeled off. The right ears of the animals were used for biochemical assay, and the left ears were used for histological study. Results Reactive oxygen species levels were significantly decreased in group 4 with topical application of vitamin E compared with untreated and myringotomized animals in group 2. Reactive oxygen species levels were also decreased in group 5, although the decrease was not statistically significant when compared with groups 2 and 3. Histological studies confirmed sclerotic changes in the untreated myringotomized animals. The tympanic membranes of animals in groups 2 and 3 showed a white, chalk-like pattern of sclerotic changes, whereas animals in groups 4 and 5, with the exception of two animals in group 5, lacked these changes. Conclusion Although the relationship between the development of myringosclerosis and ROS had been well documented previously, the present study is the first that has directly measured the levels of ROS in the tympanic membrane and middle ear mucosa. These results are relevant because they correlate with histological findings. It has also been demonstrated that topically applied vitamin E is effective in decreasing the ROS levels. [source]


,-tocopherol improves impaired physiology of rat type II pneumocytes isolated from experimentally injured lungs

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 11 2000
B. Müller
Background Oxidant stress delivered by nitrogen dioxide (NO2) inhalation impairs the function of extracellular surfactant as well as surfactant phospholipid metabolism in type II pneumocytes. Because protection against oxidant stress is important to normal lung function, the lung contains a variety of antioxidants, including vitamin E. Whether administration of this antioxidant during NO2 inhalation attenuates NO2 -induced alterations in phospholipid metabolism in type II pneumocytes has not been studied. Methods We exposed rats to identical NO2 body doses (720 p.p.m. x h) using continuous, intermittent, or repetitive protocols. During exposure periods, the animals received daily intramuscular injections of vitamin E (25 mg kg,1). We isolated type II pneumocytes from NO2 -exposed rats and evaluated them for cell yield and viability, as well as for synthesis and secretion of phosphatidylcholine (PC) as measures of surfactant metabolism. Results The yield of type II pneumocytes was significantly elevated from animals that had been exposed continuously to NO2 whereas in intermittently and repeatedly exposed rats, cell yield was similar to yield from control animals. Viability of the isolated cells was similar in controls and all NO2 exposure protocols. Vitamin E treatment of the NO2 -exposed rats neither changed cell yield nor cell viability. Phospholipid de novo synthesis, as estimated by choline incorporation into PC, was increased most after continuous NO2 inhalation whereas in the other conditions there was only a slight increase. Vitamin E administration further increased phospholipid synthesis; this difference reached statistical significance only in the case of intermittent NO2 exposure. Secretion of phosphatidylcholine from type II cells was only reduced after continuous NO2 inhalation and administration of the antioxidant reduced the impairment. Conclusion Because vitamin E appears to preserve the ability of type II pneumocytes isolated from NO2 -exposed rats to synthesize and secrete surfactant lipid, we conclude that administration of vitamin E may mitigate NO2 -induced lung injury. [source]


Vitamin E uncouples joint destruction and clinical inflammation in a transgenic mouse model of rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 2 2002
Michel De Bandt
Objective Reactive oxygen species are thought to play a role in rheumatoid arthritis (RA) in humans. We postulated that antioxidant treatment could have a beneficial effect in this disease. We therefore investigated the effects of vitamin E in the transgenic KRN/NOD mouse model of RA. Methods Mice were treated by gavage with oral vitamin E (,-tocopherol). Clinical, histologic, and biochemical parameters were assessed for 6 weeks. Results Vitamin E treatment did not modify the clinical features of the disease (date of onset or disease intensity, as measured by the articular index), but it did prevent joint destruction, as measured by qualitative and semiquantitative analyses. Redox status did not differ between treated and control mice. White blood cell chemiluminescence was higher in transgenic KRN/NOD mice than in controls, but vitamin E treatment attenuated this difference. Vitamin E treatment of the transgenic animals led to a significant decrease in the levels of interleukin-1, (IL-1,) but not tumor necrosis factor ,. Conclusion Vitamin E seems to uncouple joint inflammation and joint destruction in this model of RA, with a beneficial effect on joint destruction. Since many investigations are currently in progress to evaluate the benefit of interventions targeted toward anti-IL-1,, our findings suggest opportunities of therapeutic interest in human RA. [source]


Oxidative-inflammatory damage in cirrhosis: Effect of vitamin E and a fermented papaya preparation

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2007
Francesco Marotta
Abstract Background and Aim:, Oxidative DNA damage occurs as an early event in hepatitis C virus (HCV) infection and is an indication of the potential for carcinogenesis. The aim of this study was to test a novel antioxidant/immunomodulator in patients with HCV-related cirrhosis. Methods:, The study group consisted of 50 patients with HCV-related cirrhosis with transaminase values less than twofold increased (alanine aminotransferase [ALT] < 80 IU/L). Patients underwent a standardized food-vitamin composition assessment and were assessed for dietary intake, nutritional status and iron level. Patients were randomly allocated into two groups and then given either ,-tocopherol 900 IU/day or 9 g/day of a fermented papaya preparation (FPP, Immun-Age, Osato Research Institute, Gifu, Japan) at bedtime for 6 months. Ten healthy subjects served as controls. Patients were checked monthly for: routine tests, redox status (reduced glutathione, glutathione peroxidase, oxidized glutathione, malondialdehyde), plasma ,-tocopherol, 8-hydroxy-deoxy-guanidine (8-OHdG) level in circulating leukocyte DNA and serum levels of cytokines. Results:, Patients with cirrhosis showed a significant imbalance of redox status (low antioxidants/high oxidative stress markers) (P < 0.005 vs controls). Neither treatment regimen affected transaminases as a whole. However, vitamin E supplementation almost normalized ALT only in the limited vitamin-E-deficient subgroup. A significant improvement of redox status was obtained by both regimens. However, only FPP significantly decreased 8-OHdG and the improvement of cytokine balance with FPP was significantly better than with vitamin E treatment (P < 0.05). Conclusions:, Although the present data seem to suggest a potential supportive role of antioxidants/immunomodulators as FPP in HCV patients, more studies are needed to substantiate their effect on the natural history of the disease. [source]


Effects of testosterone and vitamin E on the antioxidant system in rabbit testis

ANDROLOGIA, Issue 5 2004
N. Aydilek
Summary. The aim of the study was to investigate the effects of testosterone propionate and vitamin E on the antioxidant system in the testis. Thirty-two male New Zealand White rabbits were randomly divided into four groups. The first group was used as control. The second group was injected with testosterone propionate, the third group vitamin E and the fourth group vitamin E and testosterone propionate combination. All treatments were carried out during 6 weeks and oxidative parameters were evaluated in homogenized testicular tissue. The levels of vitamin E and the activity of glutathione peroxidase were lower (P < 0.05) in the testosterone group than in controls. However, vitamin C and malondialdehyde levels were higher (P < 0.05) in this group than in controls. The levels of reduced glutathione, , -carotene, vitamin C and E increased, but malondialdehyde levels decreased in the vitamin E group, when compared with controls (P < 0.05). Vitamin E and , -carotene levels were significantly higher (P < 0.05) in the combination group than in testosterone group. However, MDA levels were lower (P < 0.05) in combination group than in the testosterone group. In conclusion, administration of testosterone propionate led to a significant elevation of oxidative stress. Vitamin E is quite an effective antioxidant which protects rabbit testis against lipid peroxidation, and, testosterone-induced lipid peroxidation could be improved by additional vitamin E treatment. [source]


Influence of glutamine and vitamin E on growth and antioxidant capacity of fish enterocytes

AQUACULTURE NUTRITION, Issue 4 2009
J. JIANG
Abstract The present study explored the effect of glutamine and vitamin E on growth and anti-oxidation capacity of isolated fish enterocytes. Fish enterocytes were cultured with six medium, respectively, containing 0, 2.0, 4.7, 6.8, 8.1, 9.2 mmol L,1 glutamine for 64 h. The results showed that glutamine could promote fish enterocytes proliferation and differentiation. Fish enterocytes were cultured with different medium containing 0, 2.5, 3.5, 4.5, 6.0, 7.0 ,g mL,1 vitamin E for 96 h. The results showed that cells proliferation and differentiation were not significantly enhanced, but anti-superoxide anion activity, anti-hydroxy radical activity, reduced glutathione concentration, the ratio between reduced and total glutathione in the cells were significantly enhanced, and the malondialdehyde concentration in the culture medium was significantly depressed with the vitamin E treatment. In the whole, the present results firstly indicated that glutamine could promote fish enterocytes growth, but vitamin E could not. Vitamin E could promote fish enterocytes antioxidant capacity and cellular structural integrity. These data would be instructive for glutamine and vitamin E supplement in aquaculture diets. [source]


Vitamin E uncouples joint destruction and clinical inflammation in a transgenic mouse model of rheumatoid arthritis

ARTHRITIS & RHEUMATISM, Issue 2 2002
Michel De Bandt
Objective Reactive oxygen species are thought to play a role in rheumatoid arthritis (RA) in humans. We postulated that antioxidant treatment could have a beneficial effect in this disease. We therefore investigated the effects of vitamin E in the transgenic KRN/NOD mouse model of RA. Methods Mice were treated by gavage with oral vitamin E (,-tocopherol). Clinical, histologic, and biochemical parameters were assessed for 6 weeks. Results Vitamin E treatment did not modify the clinical features of the disease (date of onset or disease intensity, as measured by the articular index), but it did prevent joint destruction, as measured by qualitative and semiquantitative analyses. Redox status did not differ between treated and control mice. White blood cell chemiluminescence was higher in transgenic KRN/NOD mice than in controls, but vitamin E treatment attenuated this difference. Vitamin E treatment of the transgenic animals led to a significant decrease in the levels of interleukin-1, (IL-1,) but not tumor necrosis factor ,. Conclusion Vitamin E seems to uncouple joint inflammation and joint destruction in this model of RA, with a beneficial effect on joint destruction. Since many investigations are currently in progress to evaluate the benefit of interventions targeted toward anti-IL-1,, our findings suggest opportunities of therapeutic interest in human RA. [source]