			Home About us Contact

Vit E (vit + e)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency

EUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001
S. Gabsi
Ataxia with vitamin E (Vit E) defciency (AVED) is an autosomal recessive disorder caused by mutations of the , tocopherol transfer protein gene. The Friedreich ataxia phenotype is the most frequent clinical presentation. In AVED patients, serum Vit E levels are very low in the absence of intestinal malabsorption. As Vit E is a major antioxidant agent, Vit E deficiency is supposed to be responsible for the pathological process. Twenty-four AVED patients were fully investigated (electromyography, nerve conduction velocity (NVC) studies, somatosensory evoked potentials, cerebral computed tomography scan, sural nerve biopsy, genetic studies) and supplemented with Vit E (800 mg daily) during a 1-year period. Clinical evaluation was mainly based on the Ataxia Rating Scale (ARS) for cerebellar ataxia assessment and serum Vit E levels were monitored. Serum Vit E levels normalized and ARS scores decreased moderately but significantly suggesting clinical improvement. Better results were noted with mean disease duration , 15 years. Reflexes remained abolished and posterior column disturbances unchanged. Vitamin E supplementation in AVED patients stabilizes the neurological signs and can lead to mild improvement of cerebellar ataxia, especially in early stages of the disease. [source]

Varicocelectomy reduces reactive oxygen species levels and increases antioxidant activity of seminal plasma from infertile men with varicocele

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 5 2001
T. Mostafa
Several theories have been advanced to explain the mechanisms by which varicocele impairs male fertility. These theories include scrotal hyperthermia, retrograde flow of adrenal or renal metabolites, Leydig cell dysfunction and hypoxia. Varicocele is reported to be associated with elevated reactive oxygen species (ROS) production in spermatozoa and diminished seminal plasma antioxidant activity. The aim of this study was to investigate whether surgical correction of varicocele might reduce ROS or increase the antioxidant capacity of seminal plasma from infertile patients with varicocele. The study group consisted of 68 infertile males, selected from patients scheduled for varicocelectomy at Cairo University Hospital during the year 1999. Seminal plasma levels of two ROS [malondialdehyde (MDA), hydrogen peroxide (H2O2)] and one ROS radical [nitric oxide (NO)] were estimated as well as six antioxidants [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), vitamin C (Vit C), vitamin E (Vit E), albumin) on the day prior to varicocelectomy. For comparison, the same parameters were measured again 3 and 6 months post-operatively. A statistically significant reduction in the 3 month post-operative levels of MDA, H2O2 and NO was observed when compared with the pre-operative values. A further significant reduction took place during the following 3 months. Four of the six antioxidants tested (SOD, CAT, GPx, and Vit C) showed a significant increase in seminal levels when comparing 3-month post-operative with pre-operative values. A further significant increase of the four antioxidant levels took place during the following 3 months. No significant change in the level of seminal plasma albumen took place during the first 3 months after varicocelectomy, however, a significant increase was noted during the next 3 months. In contrast to other antioxidants, seminal plasma levels of Vit E showed a significant decrease when comparing 3-month post-operative with pre-operative values. A further significant decrease took place during the following 3 months. It is concluded that varicocelectomy reduces ROS levels and increases antioxidant activity of seminal plasma from infertile men with varicocele. [source]

Therapeutic Effects of Vitamin E on Cyclic Mastalgia

THE BREAST JOURNAL, Issue 5 2009
Sousan Parsay PhD
Abstract:, Cyclic mastalgia is one of the most prevalent disorders among fertile women. To date, hormonal agents, despite their side effects, have been widely used for treatment of this ailment. This study was performed to clarify the therapeutic effects of Vitamin E (Vit E) as a safe treatment for cyclic mastalgia among fertile women. This study was conducted as a double blind clinical trial; 150 women with cyclic mastalgia, referred by three public health centers in Qazvin City in Iran, were enrolled in the trial and randomly divided into two distinct case and control groups; each containing 75 patients. The severity and duration of breast pain were measured according to both the Cardiff Breast Pain Chart and the Visual Analog Scale. Simple, chewable tablets of either Vit E or a placebo were prescribed twice a day for 4 months for case and control participants, respectively. Follow-up was performed at the end of both the second and the fourth months and, at that time, the severity, duration and side effects of intervention were evaluated. The administration of Vit E had significant curative results as tested at both the 2- and 4-month benchmarks. Chi-square testing indicated that after both 2 and 4 months of therapy, the efficacy demonstrated by the Vit E recipient case group was superior to that of the group that received a placebo. Applying the Mc Nemar Test, it also was shown that there was no significant difference in the benefits received between treatment courses of 2 versus 4 months. A 2-month prescription of Vit E has positive therapeutic effects on cyclic mastalgia. Given its lack of significant side effects, Vit E, therefore, can be considered a safe alternative to hormonal therapies currently being used in the treatment of cyclic mastalgia. [source]

Differential retention of ,-vitamin E is correlated with its transporter gene expression and growth inhibition efficacy in prostate cancer cells

THE PROSTATE, Issue 5 2007
Jing Ni
Abstract BACKGROUND Epidemiological studies showed Vit E has protective effects against prostate cancer (PCa). Interestingly, different prostate cancer cells have different sensitivity to ,-Vit E or VES treatment. The goal of this study is to determine whether cellular Vit E bioavailability and its transport proteins are important contributing factors. METHODS ,-Vit E and its ester form, VES, were used to treat prostate cancer LNCaP, PC3, and DU145 cells, and their growth rates were determined by MTT assay. Cellular levels of Vit E were quantified using HPLC as the index of bioavailability. The expression levels of Vit E transport proteins were determined by real-time PCR. RESULTS Among these PCa cells, only LNCaP cells were sensitive to 20 µM ,-Vit E treatment, while both LNCaP and PC3 cells were sensitive to 20 µM VES treatment. Coordinately, cellular levels of ,-Vit E and VES positively correlated to their inhibitory effects. Further study found expression levels of Vit E transport proteins, including tocopherol associated protein (TAP), scavenger receptor class B type I (SR-BI), ,-tocopherol transfer protein (TTP), and ATP binding cassette transporter A1 (ABCA1), were different in various PCa cells, which may contribute to cellular Vit E bioavailability. This notion is further supported by the findings that overexpression or knockdown of TTP could coordinately alter cellular ,-Vit E levels in PCa cells. CONCLUSION Antiproliferative efficacy of ,-Vit E is correlated with its cellular bioavailability in PCa cells. Modulating the expression of the efflux or influx transporters could sensitize the growth inhibition efficacy of Vit E in prostate cancer cells. Prostate 67: 463,471, 2007. © 2007 Wiley-Liss, Inc. [source]

Vitamins E and C prevent the impairment of retention of an inhibitory avoidance task caused by arginine administration

JOURNAL OF NEUROCHEMISTRY, Issue 2002
E. A. Reis
Hyperargininemia is an inherited metabolic disease of urea cycle caused by the deficiency of arginase I activity, resulting in tissue accumulation of arginine (Arg). Patients affected by this disease usually develop spasticity, epilepsy and mental retardation as principal symptoms. Previous studies from our laboratory have showed that acute administration of Arg impairs retention of the inhibitory avoidance task and that l -NAME (NOS inhibitor) prevents this effect. In the present study, we investigated the effect of chronic treatment with antioxidants (vitamins E and C) on the retrieval of the inhibitory avoidance task in adults rats subjected to experimental model of acute hyperargininemia in order to investigate the participation of oxidative stress on this phenomenon. Sixty-day-old-rats were treated for one week with i.p. injection of saline (0.9%) or vitamins E and C (vit E 40 mg/kg and vit C 100 mg/kg). Twelve hours after the last injection Arg (0.8 g/kg) or an equivalent volume of saline were administered 1 h before training, 1 h before testing or immediately after training sessions. Memory was significantly impaired in Arg-treated group, whereas the rats chronically treated with vitamins E and C had this effect prevented. Present data strongly indicate that Arg administration impairs memory, an effect probably mediated by oxidative stress since treatment with vitamins E and C prevented amnesia. Assuming the possibility that this might occur in the human condition, reported results may be relevant to explain, at least in part, neurologic dysfunction associated with hyperargininemia. [source]