Protective Effect Of Vitamin Research Articles

The possible protective effects of vitamin E and selenium administration in oxidative stress caused by high doses of glucocorticoid administration in the brain of rats

Acute exposure to high doses of glucocorticoids (GCs) may potentially increase the basal levels of reactive oxygen species (ROS) by altering the defence capacity against oxidative damage. Also, antioxidants may affect the oxidative breakdown of tissues. Therefore, the aim of this work was to determine the effects of dietary intake vitamin E and selenium (Se) on lipid peroxidation (LPO) as thiobarbituric acid reactive substances (TBARS) and on the antioxidative defence mechanisms in the brain of rats treated with high doses of prednisolone. Two hundred and fifty adult male Wistar rats were randomly divided into five groups. The rats were fed a normal diet, but groups 3, 4, and 5 received a daily supplement in their drinking water of 20mg vitamin E, 0.3mg Se, and a combination of vitamin E and Se, respectively, for 30days. For 3days subsequently, the control (group 1) was treated with a placebo, and the remaining 4 groups were injected intramuscularly with 100mg/kg body weight (bw) prednisolone. After the last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48h and the activities of enzymes selenium-glutathione peroxidase (Se-GSH-Px) and catalase (CAT), and the levels of reduced glutathione (reduced GSH) and TBARS in their brains were measured. Se-GSH-Px and CAT enzyme activities, and reduced GSH levels in the prednisolone treatment group (group 2) began to decrease gradually at 4h (p<0.01, p<0.05, respectively), falling respectively to 60, 50, and 40% of the control levels by 24h (p<0.001, p<0.01), and recovering to the control levels at 48h. In contrast, prednisolone administration caused an increase in the brain TBARS, reaching up to six times the level of the control at 24h (p<0.001). However, supplementation with vitamin E and Se had a preventive effect on the elevation of the brain TBARS and improved the diminished activities of antioxidative enzymes and the levels of reduced GSH. Therefore, the present study attempts to determine the sequence of cellular membrane damage in the brain of the rats after high doses GC administration and the possible roles in vivo of vitamin E and Se, and their combination.

The protective role of vitamin E on Oreochromis niloticus exposed to ZnONP

The present study evaluated if ZnONPs induce oxidative stress, immunological impairment and cellular damage in tilapia (Oreochromis niloticus), as well as the possible protective effect of vitamin E. Fish were fed for ten days and five study groups were investigated: controls, two ZnONPs concentrations (1.5 and 2.5mgL−1) and 1.5 and 2.5mgL−1 of ZnONPs + vitamin E (500mgkg−1 of food). O. niloticus treated with ZnONPs, showed decreased health in comparison with the control group and the groups that combined nanoparticles and vitamin E-supplemented diet. ZnONPs caused cell impairment by increasing ALT, AST and ALP activity and generated oxidative stress by inhibiting SOD and CAT activity. Biochemical changes of these biomarkers were prevented by vitamin E, although this compound did not confer complete protection. In conclusion, ZnONPs are toxic to O. niloticus, affecting antioxidant defenses, with vitamin E acting protectively against this toxic effect.

Rectal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

Rectal cancer: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up.

Protective effects of vitamins C and E on dichlorodiphenyltrichloroethane-induced genotoxicity and hepatotoxicity in human liver cells

Dichlorodiphenoxytrichloroethane (DDT), a persistent organic pollutant and hepatotoxicant, is used to control the malaria. However, scarce information exists on relevant effective inhibitors of DDT’ toxicity. The aim of this study was to investigate protective effects of natural antioxidants vitamin C (VC) or/and vitamin E (VE) on p,p′-DDT-induced genotoxicity and hepatotoxicity in human liver cells. p,p′-DDT exposure increased levels of chromatin condensation, comet parameter, micronucleus induction and DPC co-efficient of HL-7702 cells in a dose-dependent manner. Also, an increase in mRNA levels of CYP1A1 as well as CYP3A4, and a decrease in UGT along with GST were observed. Interestingly, supplementation with VC or/and VE prevented p,p′-DDT-caused alterations in DNA damage and phase metabolism gene expressions, and the combination of VC and VE had a more protective effect than VC or VE alone. These findings illustrated that VC or/and VE could be beneficial for the alleviation of p,p′-DDT-incurred toxicity in human liver cells.

Analysis of serum vitamin D levels and prognosis in stage III colon carcinoma patients treated with adjuvant FOLFOX+/- cetuximab chemotherapy: NCCTG N0147 (Alliance).

3516 Background: Epidemiological data suggest a protective effect of vitamin D on CC risk. However, association of serum vitamin D level with clinical outcome in pts with surgically resected CC remains unknown. We analyzed total circulating 25-hydroxyvitamin D [25(OH)D)] with clinical outcome in pts with resected stage III CC treated with FOLFOX +/- cetuximab in a phase III trial. Methods: Association of pre-treatment level of plasma 25(OH)D with disease-free survival (DFS) and time-to-recurrence (TTR) was analyzed with 25(OH)D as a continuous variable by a relative risk model with splines and as a binary variable (vitamin D deficient [&lt;30 ng/mL]) using multivariable Cox regression. Results: Overall, 49% (291/600) of pts were vitamin D deficient. Prevalence of vitamin D deficiency was significantly higher in women vs men (52% vs. 48%, p=0.030) and in blacks vs whites (74% vs. 45%, p=0.0003). The continuous 25(OH)D level and pt sex were associated by the interaction test (pinteraction=0.044). There were no statistically significant associations with DFS/TTR for either continuous 25(OH)D level (DFS, p=0.22; TTR, p=0.26) nor for vitamin D deficiency (DFS, adjusted hazard ratio [HRadj]=1.01, 95% CI, 0.74-1.38; padj=0.94; TTR, HRadj=1.00; CI, 0.72-1.38; padj=0.99. A comparison of the highest vs lowest tertile showed a significant association between the highest 25(OH)D level and better outcomes in men (DFS, HRadj.=0.18, CI, 0.04-0.76, padj=0.020; TTR, HRadj.=0.12, CI, 0.02-0.64, padj=0.014), but not in women (DFS, pinteraction=0.039; TTR, pinteraction=0.033). Conclusions: Nearly one-half of pts in the clinical trial cohort were vitamin D deficient with lowest 25(OH)D levels found in women and blacks. While vitamin D deficiency was not associated with adverse outcome, high levels of vitamin D in men, but not women, were associated with longer survival. Support: U10CA180821, U10CA180882, U10CA180820, U10CA180863, U10CA180888, U10CA077202, CCSRI 021039. ClinicalTrials.gov Identifier: NCT00079274.

Histological and Ultrastructure Study of the Testes of Acrylamide Exposed Adult Male Albino Rat and Evaluation of the Possible Protective Effect of Vitamin E Intake.

Acrylamide (AA) is a hazardous unavoidable gonadal toxin. Hence, the aim of this study is to clarify its harmful effects on the testis of adult albino rat by light and electron microscope and to evaluate the possible role of Vitamin E (Vit E) in the prevention of such effects. Thirty-five adult male albino rats were enrolled in this study. They were divided into three groups: Group I (control); Group II (AA exposed), and Group III (AA and concomitant Vit E treated group). Animals of Groups II and III were further subdivided into two equal subgroups (each subgroup included five rats): (a) rats were sacrificed after 4 weeks and (b) rats were sacrificed after 6 weeks. The testes of each rat were dissected out, processed, and examined by Hematoxylin and Eosin, Periodic acid–Schiff and Mallory's trichrome stains as well as electron microscopic study. The study revealed that AA induces testicular damage at the histological and ultrastructural level in the form of degeneration and arrested spermatogenesis. Moreover, decreased seminiferous tubules diameters and epithelial height were detected. These changes are maximally improved in Vit E treated group. Hence, we could conclude that AA causes degenerative changes of the testes of albino rats and arrest of spermatogenesis. The AA-induced histological and ultrastructural changes of the testes could be explained by oxidative stress. These effects changes are proportional to the duration of exposure. Moreover, it could be concluded that Vitamin E has a protective role against AA-induced testicular damage by its antioxidant and anti-apoptotic effects.

Histological Study of the Effects of Olanzapine on the Liver of Adult Male Albino Rat with and without Vitamin C

Introduction: Olanzapine is an atypical antipsychotic drug widely used in treatment of schizophrenia for prolonged time.Aim of the work: The present study was carried out to evaluate the effect of olanzapine on the liver and the possible protective effect of vitamin C.Material and Methods: Forty adult male albino rats were used in this work. They were divided into: Group I as a control, group II was given Olanzapine (2mg/kg B. wt. orally once daily) for one month, group III was given Olanzapine (at the same previous dose) plus vitamin C (15 mg /Kg. B. wt of orally once daily) for one month and group IV was given only vitamin C (for the same dose and period of the previous group). At the end of the experiment, liver specimens were processed for histological study by light and electron microscopes. Also blood samples were collected for estimation of liver enzymes.Result: Significant increase in the level of liver enzymes was observed in Olanzapine treated group. While the microscopic examination of the liver sections of this group revealed several histological changes including, dilatation and congestion of central veins and blood sinusoids, inflammatory cellular infiltration in the portal areas and cytoplasmic vacuolation of hepatocytes that present mainly around the central veins. Mitochondrial degeneration, bile ducts dilatation and excessive deposition of lipid droplets were also observed. These changes were ameliorated by vitamin C administration.Conclusion: Results of this experimental work revealed that administration of vitamin C greatly reduced the histological alterations induced by Olanzapine, suggesting that vitamin C has a protective effect on the liver.

WITHDRAWN: Histological and ultrastructure study of the testes of acrylamide exposed adult male albino rat and evaluation of the possible protective effect of vitamin E intake

WITHDRAWN: Histological and ultrastructure study of the testes of acrylamide exposed adult male albino rat and evaluation of the possible protective effect of vitamin E intake

Protective Effect of Vitamin E in Combination with Vitamin D and Calcium Against Osteoporosis in Ovariectomized Rats

Protective Effect of Vitamin E in Combination with Vitamin D and Calcium Against Osteoporosis in Ovariectomized Rats

Biochemical and histopathological changes in the brain of albino rats treated with profenofos and the possible protective effect of vitamins C and E

Objective The aim of this study was to evaluate the changes in the brain of albino rats treated with profenofos and the possible protective effect of vitamins C and E against the acute effect of profenofos. Background During the last decades the use of pesticides has increased steadily in developing countries in an effort to increase food production and control vector-borne diseases in plants. Organophosphorus (OP) compounds are widely used in agriculture as insecticides. OP poisoning is common due to its wide availability. Profenofos is a widely used insecticide and has been classified as moderately hazardous. OP pesticides are known to inhibit cholinesterase activity in target tissues. Oxidative stress is one of the possible mechanisms that could be involved in OP toxicity. Patients and methods Eighty adult male albino rats were divided randomly into four main groups: the control group (I), the profenofos toxicity group (group II), the profenofos + antidote-treated group (group III), and the profenofos + antidote + antioxidant-treated group (group IV). Each treated group was divided equally into two subgroups. Ten rats from each subgroup were killed after 24 h to demonstrate the toxicity. The other 10 rats were killed after 7 days to demonstrate the recovery. Brain samples were obtained for biochemical, histopathological, and immunohistochemical studies. Results Acute exposure to profenofos causes biochemical and histopathological changes in brain tissue. These changes were minimized with atropine and oxime treatment. However, this recovery was more prominent in the group administered vitamins C and E. Conclusion Treatment with vitamins C and E exerts an antioxidative effect and this may be responsible for the amelioration of profenofos-provoked toxicity.

The effect of tramadol on seminiferous epithelium of albino rats and the protective effect of vitamin C

Objective The aim of the study was to assess the effect of tramadol on the testes of adult male albino rats and to elucidate the possible protective effect of vitamin C. Background Tramadol is an opioid pain medication used to treat mild to severe pain, both acute and chronic, and premature ejaculation and as an antidepressant. Materials and methods Sixty adult male albino rats were used in the present study. Animals were divided into four groups: group I, the control group; group II, which received 500 mg/kg/day vitamin C orally for 4 weeks; group III, which was divided into two subgroups, subgroup IIIa and subgroup IIIb (receiving 50 mg/kg/day tramadol orally for 4 weeks) and subgroup IIIb, which was left without treatment for another 4 weeks; and group IV, which received tramadol and vitamin C in the doses same as the previous ones. At the end of the experiment, the testes were excised and specimens were processed for light, electron microscopic, morphometric studies and statistical analyses. Results Tramadol-treated rats showed degeneration, irregularity of seminiferous tubules with disorganization and exfoliation of spermatogenic cells in the lumen, which showed absence of sperms. Vascular dilatation and congestion was present. In addition, there was collagen fiber deposition in the interstitium and around the blood vessels with thickening of tunica albuginea. Cessation of tramadol administration showed reversibility of the previous changes but not complete recovery. However, coadministration of vitamin C with tramadol showed improvement. Conclusion Tramadol has harmful effect on the testes of rats. This effect is reversible when tramadol administration is stopped but complete recovery is not achieved. Vitamin C and tramadol in combination revealed improvement.

Protective effects of vitamin E isoforms in models of non-alcoholic fatty liver disease

Protective effects of vitamin E isoforms in models of non-alcoholic fatty liver disease

The protective impact of vitamin E against atenolol effect on Ca+2, Testosteron and FSH in male rats

Background and objective: Atenolol is β1-selective antagonist nonetheless this selectivity is not absolute and at higher dosages atenolol represses β-2 Adrenoceptors mainly located in bronchial and vascular musculature, alsoβ-blocker atenolol effects on testosterone and FSH production. Therefore ,this study was designed to investigate the possible protective effect of vitamin E on reproductive efficiency in male rats exposed to atenolol. Materials and methods:Thirty-two healthy adult males Wistar rats at random divided into four equal groups and treatment for 56 days as follows:-First group (control):Animals in this group received tap water and served as control.Second group (group T1):Animal in this group will be receive atenolol orally at dose (100mg/kg/day).Third group (group T2):Animal in this group will be receive Vit.E (800IU /B.W.) orally and Fourth group (group T3):Animal in this group will be receive Vit.E (800IU/B.W.) and atenolol at dose (100mg/kg/B.W.) orally. Results: serum level of serum testosterone in control group was 1.51±0.21 ng/ml, and it significantly decreased in atenolol treated group (0.74±0.008 ng/ml),.Serum level of FSH in the control group was (4.87±0.03 mIU /ml) while it significantly reduced in atenolol treated group (2.69±0.15mIU/ml), also the results showed that atenolol was a significantly decrease the Ca+2 concentration to (1.20 ± 0.15 mg/dl) in contrast to control group.Conclusion: Vitamin E improve significantly the levels of serum FSH and testosterone in in atenolol treated rats.

Protective effects of vitamin C and vitamin E against hysterosalpingography-induced epithelial degeneration and proliferation in rat endometrium.

AimThe aim of this study was to examine the protective effects of vitamin C (VC) and vitamin E (VE) against hysterosalpingography (HSG)-induced epithelial degeneration and proliferation in rat endometrium.Materials and methodsA total of 28 female Wistar albino rats were randomized into four groups: G1 (n=7; abdomen was opened and closed), G2 (n=7; 0.1 mL Lipiodol [ethiodized oil] was administered to each uterine horn in conjunction with X-ray irradiation), G3 (n=7; 50 mg/kg of intraperitoneal (ip) VC was administered, followed by the administration of 0.1 mL of ethiodized oil into the uterine horns after 15 minutes), and G4 (n=7; 50 mg/kg of ip VE was administered, followed by the administration of 0.1 mL of ethiodized oil into the uterine horns after 15 minutes). After abdominal closure, rats in G2, G3 and G4 groups were exposed to whole-body X-irradiation three times with 2-minute intervals at a total dose of 15–20 mrad. Three hours after exposure, abdominal cavities of all the rats were reopened and uterine horns were removed. The right uterine horns were embedded into paraffin blocks after fixing in 10% formaldehyde for histopathological and immunohistochemical examination. Uterine horns on the other side were rapidly excised and stored at −80°C for the examination of expression of microRNAs (miRNAs) and oxidant, antioxidant, apoptotic and antiapoptotic gene expression using real-time polymerase chain reaction (RT-PCR) method.ResultsNo differences were observed in terms of expression of miRNAs and oxidant, antioxidant, apoptotic and anti-apoptotic gene expression between the study groups. Congestion, epithelial degeneration and malondialdehyde immunoreactivity were significantly lower in G3 and G4 groups than in G2 group; no differences were observed between G1, G3 and G4 groups. Ki-67 immunoreactivity score was significantly higher in G2 group when compared with G1, G3 and G4 groups. Caspase-3 immunoreactivity was not statistically different between the groups.ConclusionVC and VE may confer cellular protection against radiation injury induced by HSG in endometrial epithelium.

Protective effects of vitamin E on sodium arsenite-induced toxicity, testicular measurements and histopathological studies of testes in Teddy goat bucks.

The objective of this study was to investigate the toxic effects of arsenic on testicular measurements and histology of adult Teddy goats bucks and to examine whether these toxic effects are scavenged by vitamin E. Twelve adult Teddy goat bucks were divided randomly into three groups, A, B and C. Group A was kept as control, the B was given sodium arsenite 5 mg/kg BW per day, and group C was fed with vitamin E 200mg/kg BW per day+arsenic 5mg/kg BW per day. This treatment was continued for 84days. Analysis of data revealed that the testicular measurements (scrotal circumference, width, length and weight) were significantly reduced in arsenic-treated animals, whereas there were ameliorating effects of vitamin E on these parameters. The major histopathological changes were present in the form of loss of germinal epithelium, atrophy of Leydig cells and vacuolations. Vitamin E in combination with sodium arsenite increased the active spermatogenesis as well as restoration of germinal epithelium. It can be concluded from the present findings that sodium arsenite causes toxicity in the male reproductive system of Teddy goat bucks with major changes in parenchyma of testes. Supplementation of vitamin E has protective effects on the toxicity of sodium arsenite on the reproductive system of male Teddy goat bucks.

Protective effect of vitamin E on zearelanone induced cytotoxicity and oxidative damage in leydig cells

Protective effect of vitamin E on zearelanone induced cytotoxicity and oxidative damage in leydig cells

Protective effect of vitamin E on lipid peroxidation, antioxidant status in hexachlorobenzene-induced toxicity in rats

Protective effect of vitamin E on lipid peroxidation, antioxidant status in hexachlorobenzene-induced toxicity in rats

Protective effect of vitamin E on sperm motility and oxidative stress in valproic acid treated rats

Long-term administration of valproic acid (VPA) is known to promote reproductive impairment mediated by increase in testicular oxidative stress. Vitamin E (VitE) is a lipophilic antioxidant known to be essential for mammalian spermatogenesis. However, the capacity of this vitamin to abrogate the VPA-mediated oxidative stress has not yet been assessed. In the current study, we evaluated the protective effect of VitE on functional abnormalities related to VPA-induced oxidative stress in the male reproductive system. VPA (400 mg kg−1) was administered by gavage and VitE (50 mg kg−1) intraperitoneally to male Wistar rats for 28 days. Analysis of spermatozoa from the cauda epididymides was performed. The testes and epididymides were collected for measurement of oxidative stress biomarkers. Treatment with VPA induced a decrease in sperm motility accompanied by an increase in oxidative damage to lipids and proteins, depletion of reduced glutathione and a decrease in total reactive antioxidant potential on testes and epididymides. Co-administration of VitE restored the antioxidant potential and prevented oxidative damage on testes and epididymides, restoring sperm motility. Thus, VitE protects the reproductive system from the VPA-induced damage, suggesting that it may be a useful compound to minimize the reproductive impairment in patients requiring long-term treatment with VPA.

The effect of vitamin E on lung pathology in sulfur mustard-exposed guinea pigs.

Pulmonary complications of exposure to sulfur mustard (SM) gas range from no effect or mild symptoms to severe bronchial stenosis. In the present study, the protective effect of vitamin E on the lung inflammation of SM-exposed guinea pigs was examined. Guinea pigs (n = 5 for each group) were exposed to ethanol (control group), 40 mg/m3 inhaled SM (SME group), SME treated with vitamin E (SME + E), SME treated with dexamethasone (SME + D), and SME treated with both treatments (SME + E + D). Pathological evaluation of the lung was done 14 days postexposure. The epithelial desquamation of trachea and other pathologic changes in the lung of the SME group were significantly higher than those in the control group. Furthermore, the pathological changes of trachea and lung in the SME + E and SME + E + D groups were significantly improved compared with those of SME group. In addition, the pathological changes of trachea and lung of SME + E and SME + E + D animals were significantly less than those of SME + D group.

Fipronil-induced genotoxicity and DNA damage in vivo: Protective effect of vitamin E.

Fipronil, an insecticide of the phenylpyrazole class has been classified as a carcinogen by United States Environmental Protection Agency, yet very limited information is available about its genotoxic effects. Adult male and female animals were gavaged with various doses of fipronil (2.5, 12.5, and 25 mg/kg body weight (bw)) to evaluate micronucleus test (mice), chromosome aberration (CA), and comet assay (rats), respectively. Cyclophosphamide (40 mg/kg bw; intraperitoneal) was used as positive control. Another group of animals were pretreated with vitamin E orally (400 mg/kg bw) for 5 days prior to administration of fipronil (12.5 mg/kg). Fipronil exposure in both male and female mice caused significant increase in the frequency of micronuclei (MN) in polychromatic erythrocytes. Similarly, structural CAs in bone marrow cells and DNA damage in the lymphocytes was found to be significantly higher in the male and female rats exposed to fipronil as compared to their respective controls. The average degree of protection (male and female animals combined together) shown by pretreatment of vitamin E against fipronil-induced genotoxicity was 63.28%: CAs; 47.91%: MN formation; and 74.70%: DNA damage. Findings of this study demonstrate genotoxic nature of fipronil regardless of gender effect and documents protective role of vitamin E.