Protective Effect Of Vit Research Articles

Vitamin E protects dopaminergic neurons against manganese-induced neurotoxicity through stimulation of CHRM1 and KCNJ4

BackgroundManganese (Mn) overexposure can induce neurotoxicity and lead to manganism. Vitamin E (Vit E) has neuroprotective effects by acting as an ROS scavenger, preventing mitochondrial dysfunction and neuronal apoptosis. However, the effects of Vit E on Mn-induced nigrostriatal system lesions remains unknown. ObjectivesWe aim to investigate whether Vit E has protective effects on Mn-induced nigrostriatal system lesions and mRNA expression profiles in the SN of mice. MethodsSixty 8-week-old C57BL/6 male mice were randomly divided into the Control, MnCl2, MnCl2 +Vit E, and Vit E group. Twenty-four hours after the last injection, the behaviour test was performed. The numbers of dopaminergic neurons in Substantia nigra (SN), the contents of dopamine and its metabolite levels in striatium, and the morphology of mitochondria and nuclei in the dopaminergic neurons in SN were detected by immunofluorescence staining, high-performance liquid chromatography, and transmission electron microscopy. Transcriptome analysis was used to analyze the signaling pathways and RT-PCR was used to verify the mRNA levels. ResultsVit E ameliorates behavioral disorders and attenuates the loss of nigral dopaminergic neurons in the Mn-induced mouse model. In addition, Vit E antagonized Mn-induced toxicity by restoring mitochondrial function. The results of transcriptome sequencing and RTPCR show that the protective effect of Vit E was related to the upregulation of CHRM1 and KCNJ4 mRNA in the SN. ConclusionsVit E has neuroprotective effects on Mn-induced neurodegeneration in the nigrostriatal system. This effect may be related to the upregulation of CHRM1 and KCNJ4 mRNA stimulated by Vit E in the SN.

Investigation of the toxicity of a glyphosate-based herbicide in a human liver cell line: Assessing the involvement of Nrf2 pathway and protective effects of vitamin E and α-lipoic acid

Glyphosate-based herbicides (GBHs) are the most widely used herbicides all over the world and has gained more attention in recent years because of health safety concerns. In this study, Roundup, one of the most popular glyphosate formulations, was used to evaluate cytotoxic, oxidative stress and apoptosis inducing effects of GBHs in a human hepatocellular cell line (HepG2). Roundup was shown to significantly increase cellular reactive oxygen species (ROS) levels, which lead to activation of the nuclear factor-erythroid-2-related factor 2 (Nrf2) antioxidant defense pathway including reduced levels of heme oxygenase 1 (HO-1). Furthermore, Roundup was found to induce apoptosis and further analysis confirmed involvement of a mitochondrial-dependent pathway verified by increased Bax/Bcl-2 ratios. Investigation of the protective effects of antioxidants vitamin E (Vit E) and α-lipoic acid (LA) against Roundup toxicity showed that both antioxidants significantly reduced the cytotoxicity, ROS formation, HO-1 downregulation, and apoptosis and that Vit E did so more efficiently than LA. In conclusion, our findings highlight the ROS producing and apoptosis inducing effects associated with GBHs, the activation of Nrf2 pathway as a defense mechanism and the protective effects of Vit E and LA against GBH toxicity.

Protective effects of vitamin D on learning and memory deficit induced by scopolamine in male rats: the roles of brain-derived neurotrophic factor and oxidative stress.

The beneficial effects of vitamin D (vit D) on central nervous system disorders have been suggested. In the current research, the protective effects of vit D on learning and memory deficit induced by scopolamine, oxidative stress criteria, brain-derived neurotrophic factor (BDNF), and nitric oxide (NO) in the brain were investigated. Rats were divided into five groups, including (1) Control, (2) Scopolamine (2 mg/kg), (3-5) Scopolamine + Vit D (100, 1000, and 10,000 IU/kg) groups. Vit D administrated for 2 weeks and in the third week scopolamine co-administrated with vit D and behavioral tests, including Morris water maze (MWM) and passive avoidance (PA) tests, were carried out. The cortical and hippocampal tissues were analyzed for BDNF, catalase (CAT), and superoxide dismutase (SOD) activities, thiol content, NO metabolites, and malondialdehyde (MDA) concentration. Scopolamine injection significantly impaired rats' performance on the MWM and PA test. It further enhanced the MDA and nitrite level while decreased thiol content and BDNF levels and SOD and CAT activities in the brain. Administration of both 1000 and 10,000 IU/kg vit D improved cognitive outcome in MWM and PA tests. In addition, vit D elevated thiol content, SOD and CAT activities, and BDNF levels, while reduced nitrite and MDA concentration. Vit D also increased the levels of vit D and calcium in the serum. The results demonstrated that vit D has protective effects on scopolamine-associated learning and memory impairment by improving BDNF levels and attenuating NO and brain tissue oxidative damage.

Efecto citomolecular de la vitamina E combinada con sulfato ferroso: un modelo in vitro sobre el tratamiento preventivo de la anemia durante la primera infancia

Dado que la anemia afecta el normal crecimiento y desarrollo de los niños, la Sociedad Argentina de Pediatría recomienda la suplementación preventiva diaria con sulfato ferroso. Sin embargo, el tratamiento diario puede llevar a la sobrecarga tisular de hierro provocando daño sobre proteínas, lípidos y ADN. Con el propósito de eludir estos efectos no deseados, ha surgido como alternativa la posibilidad de implementar un tratamiento alternativo que consiste en la suplementación semanal. Por otra parte, la vitamina E, es el antioxidante no enzimático liposoluble más importante y esencial en la defensa celular. A raíz de esto, el presente trabajo tiene como objetivo evaluar el efecto de la vitamina E sobre el sulfato ferroso en sus dos formas de administración (semanal y diaria) en linfocitos de sangre periférica humana cultivados in vitro. Se llevó a cabo el ensayo de micronúcleos con bloqueo de la citocinesis, y se realizaron 8 tratamientos que incluyen los respectivos controles y tratamientos combinados de sulfato ferroso diario y semanal con dos dosis de vitamina E. Se evidenciaron diferencias estadísticamente significativas para la frecuencia de micronúcleos (F= 840,04; p= 0,0). Los resultados obtenidos en este trabajo demostraron un efecto protector de la vitamina E, disminuyendo el daño que el sulfato ferroso ocasiona. Sumado a esto, se corroboró que la administración del mismo en dosis únicas semanales provoca menor daño cromosómico que en dosis diarias.

The protective effect of vitamin U on valproic acid-induced lung toxicity in rats via amelioration of oxidative stress.

Vitamin U (Vit U) is a novel free-radical scavenger. The protective effect of Vit U on valproic acid (VPA)-induced lung damage was examined. Rats were divided into four groups: control rats; rats given Vit U (50 mg/kg/d, by gavage) for 15 days; rats treated with VPA (500 mg/kg/d, intraperitoneally) for 15 days; and rats were given VPA + Vit U (in same dose and time). On the 16th day of the experiment, the lungs were collected from rats. Lung structure, pulmonary oxidant/antioxidant parameters and Nrf2, α-SMA, and collagen-1 were evaluated by microscopic and biochemical analysis. Additionally, it was determined the interactions of Vit U with Nrf2 and Keap1 by in silico analysis. VPA administration increased lipid peroxidation and the activity of lactate dehydrogenase and myeloperoxidase. However, it decreased the glutathione level, and the activities of glutathione peroxidase, glutathione-S-transferase, catalase, and superoxide dismutase. VPA-mediated oxidative stress prompted structural distortion and fibrotic alterations in the lung. Vit U supplementation reversed structural and biochemical alterations, induced antioxidant system through Nrf2 activation, and attenuated fibrosis by reducing collagen expression in VPA-administered rats. However, Vit U pretreatment was unable to reduce α-SMA levels in the lung of VPA-treated rats. Molecular docking analysis showed the binding of Vit U to ETGE motif leads to dissociation of Nrf2 from the Nrf2/Keap1 complex and its transfer to nuclei. In conclusion, Vit U attenuated VPA-induced tissue damage by restoring antioxidative systems through amelioration of Nrf2 activity in the lung under oxidative stress.

α-Tocopherol succinate enhances pterostilbene anti-tumor activity in human breast cancer cells in vivo and in vitro.

Vitamin E (Vit. E) is considered an essential dietary nutrient for humans and animals. An enormous body of evidence indicates the biological and protective effects of Vit. E consumption. Tocopherol-associated protein (TAP) is a major tocopherol-binding protein affecting Vit. E stimulation and downstream signaling transduction. However, how Vit. E utilizes TAP as an anti-cancer mechanism remains unclear. Microarray analysis of signature gene profiles in breast cancer cells treated with α-tocopheryl succinate (α-TOS, a Vit. E isoform) resulted in cell cycle arrest and anti-cancer activity in breast cancer cells. Pterostilbene (PS), a natural dietary antioxidant found in blueberries, in combination with α-TOS synergistically maximized breast cancer cell growth inhibition by disrupting signal transduction, transcription factors and cell cycle proteins. In a xenograft mouse model, PS treatment with Vit. E inhibited breast tumor growth and cell invasion, which were evaluated using our recently developed circulating tumor cell (CTC) detection assay. Because dietary Vit. E and PS supplementation contributed to preventative and therapeutic effects in vitro and in vivo, this combination may benefit breast cancer therapy in the clinic.

Time course of changes in oxidative stress and stress-induced proteins in cardiomyocytes exposed to doxorubicin and prevention by vitamin C.

We previously reported that Vitamin C (Vit C) protects against doxorubicin (Dox)-induced cardiotoxicity by reducing oxidative stress, p38 mitogen-activated kinase (MAPK) and p53 activation and rescuing cell death in isolated adult cardiomyocytes. The pattern of activation and the role of oxidative stress as well as down-stream mechanisms for such protection remain elusive. Therefore the present study aims to analyze time-dependant generation of reactive oxygen species (ROS) and the activation of stress induced signalling pathways in cardiomyocytes treated with Dox and Vit C. The data provides further understanding of heart pathophysiology in response to Dox at the cellular level, and may help to optimize the timing of various therapeutic approaches. Cardiomyocytes isolated from adult Sprague-Dawley rats were exposed to Dox (10 μM), Vit C (25 μM), and Dox + Vit C for different time intervals up to 24 h. p38-JNK (SB203580) and p53 (pifithrin-α) inhibitors were used to determine the role of each respective signalling protein. Dox administration to cardiomyocytes increased the levels of ROS in a time-dependent manner that followed the activation of stress-induced proteins p53, p38 and JNK MAPKs, culminating in an increase in autophagy and apoptosis markers. Dox-induced increase in ROS was alleviated by Vit C adjuvant treatment at all time-points and this was also correlated with blunting of the activation of the studied signaling pathways leading to the prevention of apoptosis and preservation of cell viability. Protective effect of Vit C against the activation of stress induced proteins, autophagy and apoptosis was mainly attributed to its antioxidant properties even though blockage of p38, JNK and p53 by pharmacological inhibitors also suppressed Dox-induced apoptosis. ROS is defined as a key inducer of cardiomyocyte damage under Dox exposure; Vit C could effectively counteract all Dox-induced changes in cardiomyocytes and may potentially be used as an antioxidant adjuvant therapy to protect against Dox-induced cardiomyopathy.

Study the Effects of Methotrexate with and without Vitamin A on Some Biochemical and Histological Parameters in Male Rabbits

The present study aims to evaluate the effects of methotrexate (MTX) with and without vitamin A (Vit. A) on some biochemical parameters and histological structure in male rabbits liver. Twenty male rabbits weighing 1250-1480 gm were divided into four equal number groups. The first group was given 2 ml distilled water as control group. The second group was given MTX (20 mg/kg), the third group was given Vit. A (5000 IU), while the fourth group was given MTX (20 mg/kg) +Vit. A (5000 IU) in alternative days. Following four weeks of treatment, lipid profile total cholesterol (TC), triglycerides (TG), high-density lipoprotein (HDL), [low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL)]; in addition to thyroid hormones triiodothyronine (T3) and thyroxin (T4)] and liver enzymes [glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT)] were determined in the serum. Also, the histological examination of liver of all the experimental groups were carried out. The results were revealed that the treatment with MTX caused a significant P≤0.05 increases in TC, HDL, LDL, T4, and GPT when compared with the control group. The treatment with Vit. A did not cause any significant P≥0.05 differences in all the studied parameters. The MTX+Vit. A treated group showed a significant P≤0.05 increases only in GPT compared with the control group; while a significant P≤0.05 decreases was found in TC, HDL, T3, T4, and GOT when compared with the MTX treated group. The histological examination of the liver sections showed that MTX administration caused major histological changes in comparison with the control such as inflammatory cell infiltrations, vascular congestion, sinusoidal dilatation and granular degeneration of hepatocytes. Treatment with Vit. A showed a typical structure in liver tissue. While in MTX+Vit. A group, the histological changes were less severe than those in the MTX treated group; these changes were granular degeneration of hepatocytes and sinusoidal dilatation at low levels. The overall results of this study confirmed that administration of Vit. A decreased the side effects of MTX; this protective effect of Vit. A may have clinical applications in chemotherapy.

L-Ascorbate Protects Against Methamphetamine-Induced Neurotoxicity of Cortical Cells via Inhibiting Oxidative Stress, Autophagy, and Apoptosis.

Methamphetamine (METH)-induced cell death contributes to the pathogenesis of neurotoxicity; however, the relative roles of oxidative stress, apoptosis, and autophagy remain unclear. L-Ascorbate, also called vitamin (Vit.) C, confers partial protection against METH neurotoxicity via induction of heme oxygenase-1. We further investigated the role of Vit. C in METH-induced oxidative stress, apoptosis, and autophagy in cortical cells. Exposure to lower concentrations (0.1, 0.5, 1mM) of METH had insignificant effects on ROS production, whereas cells exposed to 5mM METH exhibited ROS production in a time-dependent manner. We confirmed METH-induced apoptosis (by nuclear morphology revealed by Hoechst 33258 staining and Western blot showing the protein levels of pro-caspase 3 and cleaved caspase 3) and autophagy (by Western blot showing the protein levels of Belin-1 and conversion of microtubule-associated light chain (LC)3-I to LC3-II and autophagosome staining by monodansylcadaverine). The apoptosis as revealed by cleaved caspase-3 expression marked an increase at 18h after METH exposure while both autophagic markers, Beclin 1 and LC3-II, marked an increase in cells exposed to METH for 6 and 24h, respectively. Treating cells with Vit. C 30min before METH exposure time-dependently attenuated the production of ROS. Vitamin C also attenuated METH-induced Beclin 1 and LC3-II expression and METH toxicity. Treatment of cells with Vit. C before METH exposure attenuated the expression of cleaved caspase-3 and reduced the number of METH-induced apoptotic cells. We suggest that the protective effect of Vit. C against METH toxicity might be through attenuation of ROS production, autophagy, and apoptosis.

Dietary vitamin E in White Leghorn layer breeder hens: a strategy to combat aflatoxin B1-induced damage

Mycotoxins are unavoidable contaminants of animal and human feed and food respectively. This study was designed to investigate the protective activity of vitamin E (Vit E) in White Leghorn breeder hens and their progeny against aflatoxin B1 (AFB1)-induced damage. The results indicated a significant decrease in egg production and quality in the groups exposed to dietary AFB1. A detectable amount of AFB1 residue appeared in the eggs during the first week of mycotoxin exposure at levels ≥ 2.5 mg kg−1, which reached its peak (0.403 ± 0.04 ng/g [mean ± standard deviation]) during the second week of the experiment (in the group fed 10 mg kg−1). Feeding Vit E + AFB1 resulted in higher AFB1 residues (0.467 ± 0.03) when compared with the hens fed AFB1 alone. The resistance of red blood cells to oxidative damage was decreased, while embryonic mortalities and deformities were increased in the AFB1-fed groups. The protective effect of Vit E on these parameters was noted in the groups fed lower doses of AFB1. After the withdrawal of mycotoxin-contaminated feed, most of the parameters returned towards normal within 2 weeks, except AFB1 residues that were still detectable. From the findings of this study one can conclude that the addition of Vit E in the diet of hens provided only partial protection against AFB1-induced damage.

Vitamin C protected human retinal pigmented epithelium from oxidant injury depending on regulating SIRT1.

The purpose was to investigate the protective effects of Vitamin C (Vit C) and the regulatory mechanism between Vit C and sirtuin 1 (SIRT1) in PREs during oxidative stress as Vit C and SIRT1 exerted famous effects as antioxidants. We found that moderate Vit C (100 µM) prevented ARPE-19 cells from damages induced by H2O2, including increasing viability, reducing apoptosis, and attenuating intracellular ROS levels. But lower and higher concentration of Vit C had no effects. Further results indicated that Vit C caused the dysregulation of some stress responses factors (SIRT1, p53 and FOXO3) in ARPE-19 cells response to H2O2. Moreover we found that SIRT1 activator resveratrol (SRV) stimulated significantly the protective effects of moderate Vit C, provided the property of antioxidative stress for the lower and higher concentration of Vit C in ARPE-19 cells as well. Consistently, nicotinamide (NA) relieved the protective functions of moderate Vit C. Interestingly, data also revealed the dysregulation of p53 and FOXO3 was dependent on the regulation of SIRT1 rather than Vit C. Summarily, the protective effect of Vit C against oxidative stress was involved in regulation of SIRT1. It suggested that combined application of Vit C and RSV might be a promising therapeutic method for AMD.

Abstract 669: Disparities in head and neck cancer: A case for chemoprevention with vitamin D

Abstract Worldwide head and neck cancer (HNC) is the sixth most frequently diagnosed cancer in men and is associated with significant morbidity, mortality and economic loss. African Americans (AA) experience significantly more HNC compared to Caucasian Americans (CA) and they have markedly reduced 5-year survival rates, 40% compared to 61% among CA. AA bear a disproportionate burden of HNC for reasons that are incompletely understood, but likely due to the complex interplay of environmental, genetic and health care access issues. An inverse association for vitamin (vit) D status and HNC cancer has been reported and hypovitaminosis D in AA is well documented; yet, vit D status has not been assessed in HNC patients stratified by race. Thus, objective of this prospective pilot study is to access vit D status in newly diagnosed AA and CA HNC patients by measuring the circulating metabolite of vit D, vit-D 25-OH and by assessing dietary levels utilizing the Block vit D/Calcium screener. Circulating calcium, parathyroid, and 1,25-Dihydroxy vit D are also being measured. In addition, to improve our understanding of mechanisms associated with the potential cancer protective effects of vit D in the context of HNC two HNC cell lines were treated with 2 µM cholecalciferol for 6 hours and protein harvested for proteome profiling. To date, 18 HNC patients have been evaluated, 8 AA and 10 CA. Mean circulating vit D 25-OH levels were 27.3 (+ 9.9) and 20.0 (+ 5.9) ng/mL in CA and AA, respectively supporting that vit D levels are suppressed to a greater extent in AA compared to CA HNC patients, even in sunny Florida. Dietary vit D estimates were non-significantly higher in AA HNC patients compared to CA who had higher total vit D levels, supporting differences in metabolism or potentially supplement use. None of the AA patients had vit D 25-OH levels > 30 ng/mL, a level suggested for optimum regulation of PTH, calcium absorption and bone density; 30% of CA patients expressed levels above 30 ng/mL. Proteome profiling of CAL27 and SSC25 HNC cell lines following vit D treatment revealed inverse modulation of proteins linked to HNC. Proteins down-regulated by vit D treatment included nucleophosmin (NPM), lactoylglutathione, heat shock protein beta-1 (HSPB1) Peroxiredoxin-1 (PRDX1) and Ras-related protein Rap-2b. Recent reports have linked NPM with the regulation of the oncogene FOXM1, also a potential biomarker for early detection. Disease-free survival rate is improved in HNC patients with low NPM expression. Similarly, HSPB1 has been shown to be over expressed in HNC and silencing of HSPB1 has been shown to decrease metastatic behavior in HSNCC. PRDX1 displays upregulation in oral premalignancy and is an indicator for local recurrence. Histone H2A type was up-regulated by Vitamin D. Study results support that newly diagnosed AA HNC patients have depressed vit D levels compared to CA cases and that vit D treatment inversely targets select proteins dysregulated in HNC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 669. doi:1538-7445.AM2012-669

Endosulfan-induced neurotoxicity and serum acetylcholinesterase inhibition in rabbits: The protective effect of Vit C

The neurotoxic effects and acetylcholinesterase inhibition induced by endosulfan, and the amelioration of these effects by Vitamin C (Vit C), were studied in the brains of New Zealand white rabbits. The cerebrum and cerebellum of each rabbit was examined grossly and histopathologically, and caspase-3 activity was determined by immunohistochemical methods. Twenty-four rabbits were divided into four groups ( n = 6). Rabbits in Group I (END) were given a sublethal dose of endosulfan (1 mg/kg bw) in corn oil daily by oral gavage for 6 weeks. Group II (END + C) received the same dose of endosulfan and also Vit C (20 mg/kg bw) every second day during the 6 week period. Group III (OIL + C) received oral corn oil daily and Vit C every second day for 6 weeks. Group IV (OIL) received corn oil daily by oral gavage throughout the experiment. A significant reduction in acetylcholinesterase activity was observed in the END group, which was ameliorated in the END + C group. Hyperemia and slight hemorrhages in brains and cerebellums were seen in some rabbits in the END group. There were no gross cerebral or cerebellar lesions in the other groups. Hemorrhages, degenerations and slight gliosis were the marked histopathological findings of some rabbits belonging to the END group. A positive caspase-3 reaction was more severe in the END group than in the others. An ameliorating effect of Vit C on gross, histopathological, and immunohistochemical findings was observed in the END + C group. Thus, although endosulfan could cause neurotoxic effects in rabbits, this toxicity was decreased by Vit C treatment, which increased serum acetylcholinesterase activity.

Metallothionein, an Endogenous Antioxidant, Protects against Retinal Neuron Damage in Mice

To clarify the functional role of metallothionein (MT) in retinal damage in mice deficient in both MT-I and -II (MT-I/-II-deficient mice [C57BL/6J background]) and wild-type (C57BL/6J) mice and MT induction (zinc sulfate [ZnSO4] and 1alpha, 25-dihydroxyvitamin D3 [Vit. D3]). Retinal, cell damage was induced by intravitreous injection of N-methyl-D-aspartate (NMDA; 40 nmol/eye). Retinal MT-I, -II, and -III mRNA expression was monitored by real-time reverse-transcription-PCR of total retinal RNA from eyes injected or not injected with NMDA. In wild-type mice, MT-I and -II immunohistochemistry was performed (with antibody that recognizes both proteins) 12 and 24 hours after intravitreous NMDA injection. To examine the involvement of induced retinal MT, ZnSO4 (10 nmol/eye) or Vit. D3 (0.2 or 2 ng/eye) was intravitreously injected 24 hours before NMDA injection in wild-type or MT-I/-II-deficient mice, and ganglion cell layer (GCL) cell loss and inner plexiform layer (IPL) thinning were evaluated 7 days after the NMDA injection. The protective effect of Vit. D3 was assessed against the RGC-5 cell death induced by oxidative stress (using buthionine sulfoximine [BSO] to deplete glutathione in combination with glutamate to inhibit cystine uptake). In wild-type mice, MT-II mRNA expression was time-dependently elevated by NMDA (5.9 and 7.4 times versus the nontreated control at 4 and 12 hours, respectively, after injection), with the normal level being regained within 24 hours. In contrast, MT-I and -III showed persistent decreases (to <50% control) from 4 to 24 hours. In wild-type mice, MT-like immunoreactivity was increased in the inner retina (GCL and IPL) 12 and 24 hours after NMDA injection. At 7 days after NMDA injection in MT-I/-II-deficient mice (versus wild-type mice), GCL cell loss was increased, but IPL thickness was not different. Pretreatment with ZnSO4 or Vit. D3 increased inner retinal MT-like immunoreactivity 24 hours after NMDA injection and significantly attenuated NMDA-induced GCL cell loss in wild-type mice, but ZnSO4 pretreatment did not protect against such cell loss in MT-I/-II-deficient mice. In vitro, Vit. D3 pretreatment (100 nM) reduced BSO+glutamate-induced RGC-5 cell death. These findings suggest that MT, especially MT-II, protects against retinal neuron damage, by acting as an endogenous antioxidant.

Vitamin E protects against acetone-induced oxidative stress in rat red blood cells

Acetone may induce oxidative stress leading to disturbance of the biochemical and physiological functions of red blood cells (RBCs) thereby affecting membrane integrity. Vitamin E (vit E) is believed to function as an antioxidant in vivo protecting membranes from lipid peroxidation. The aim of the present study was the evaluation of possible protective effects of vit E treatment against acetone-induced oxidative stress in rat RBCs. Thirty healthy male Wistar albino rats, weighing 200-230 g and averaging 12 weeks old were randomly allotted into one of three experimental groups: Control (A), acetone-treated (B) and acetone + vit E-treated groups (C), each containing ten animals. Group A received only drinking water. Acetone, 5% (v/v), was given with drinking water to B and C groups. In addition, C group received vit E dose of 200 mg/kg/day i.m. The experiment continued for 10 days. At the end of the 10th day, the blood samples were obtained for biochemical and morphological investigation. Acetone treatment resulted in RBC membrane destruction and hemolysis, increased thiobarbituric acid reactive substance (TBARS) levels in plasma and RBC, and decreased RBC vit E levels. Vit E treatment decreased elevated TBARS levels in plasma and RBC and also increased reduced RBC vit E levels, and prevented RBC membrane destruction and hemolysis. In conclusion, vit E treatment appears to be beneficial in preventing acetone-induced oxidative RBC damage, and therefore, it can improve RBC rheology.

Carbamate Toxicity and Protective effect ofvit. A and vit. E on some biochemicalaspects of male albino rats

The effect of daily oral administration of carbamate (1/10 L.D50) on rats for 30 successive days were studied. The male rats were divided into five groups (control, control + oil, carbamate, carbamate + vit. A and carbamate + vit. E). Each group (except control and control + oil) was daily administrated carbamate (0.012 mg/kg B.wt.). Two groups of carbamate – intoxicated animals provided with vit. A (700 mg/kg.B.wt) or vit. E (10 mg/kg.B.wt). Poisoning symptoms were recorded, e.g. unbalanse, diarrhea, have poor health and posterior limbs rigidity. Haematological parameters showed a significant decrease in red blood corpuscles (R.B.Cs), white blood corpuscles (W.B.Cs) count, Haemoglobin concentration and haematocrit value in groups treated with carbamate, and an improvement in these values was observed in groups treated with the anti-oxidants (vit. A and vit. E). Total lipids cholesterol, total proteins, albumin, glucose, LDH, AST, ALT, adrenaline and noradrenaline were measured in serum. Total proteins, total lipids, of tissues (liver, heart, muscle and kidney) were investigated. The present study declare that, carbamate induced a significant elevetion in serum LDH, glucose. total lipids,cholesterol, AST, ALT, adrenaline and noradrenaline. On the other hand, causes a significant reduction in total proteins and albumin. The total lipids and total proteins of the tissue were recorded highly significant decrease in the group treated with carbamate only. From another point of view, antioxidant ameliorated the effect of carbamate on tissues. So, it is clear that administration of vit. E or vit. A. reduced the effect of carbamate on biochemical alteration to various extent. The antioxidant property of vitamin A and vitamin E seem to be responsible for the observed protection against carbamate intoxication

Carbamate Toxicity and Protective effect ofvit. A and vit. E on some biochemicalaspects of male albino rats

The effect of daily oral administration of carbamate (1/10 L.D50) on rats for 30 successive days were studied. The male rats were divided into five groups (control, control + oil, carbamate, carbamate + vit. A and carbamate + vit. E). Each group (except control and control + oil) was daily administrated carbamate (0.012 mg/kg B.wt.). Two groups of carbamate – intoxicated animals provided with vit. A (700 mg/kg.B.wt) or vit. E (10 mg/kg.B.wt). Poisoning symptoms were recorded, e.g. unbalanse, diarrhea, have poor health and posterior limbs rigidity. Haematological parameters showed a significant decrease in red blood corpuscles (R.B.Cs), white blood corpuscles (W.B.Cs) count, Haemoglobin concentration and haematocrit value in groups treated with carbamate, and an improvement in these values was observed in groups treated with the anti-oxidants (vit. A and vit. E). Total lipids cholesterol, total proteins, albumin, glucose, LDH, AST, ALT, adrenaline and noradrenaline were measured in serum. Total proteins, total lipids, of tissues (liver, heart, muscle and kidney) were investigated. The present study declare that, carbamate induced a significant elevetion in serum LDH, glucose. total lipids,cholesterol, AST, ALT, adrenaline and noradrenaline. On the other hand, causes a significant reduction in total proteins and albumin. The total lipids and total proteins of the tissue were recorded highly significant decrease in the group treated with carbamate only. From another point of view, antioxidant ameliorated the effect of carbamate on tissues. So, it is clear that administration of vit. E or vit. A. reduced the effect of carbamate on biochemical alteration to various extent. The antioxidant property of vitamin A and vitamin E seem to be responsible for the observed protection against carbamate intoxication

Lipid peroxidation in liver of mice administrated with nickel chloride: with special reference to trace elements and antioxidants.

The relationship between Ni-induced hepatic lipid peroxidation (LPO) and the concentrations of Ni and trace elements was investigated in male ICR mice. The protective effects of antioxidants were also examined. Hepatic LPO and the concentrations of Ni, Fe, Cu, and Zn in the liver were enhanced after an ip injection of nickel chloride (NiCl2). Dose-response studies were conducted on male mice with different groups being injected with 50, 85, and 170 micromol Ni/kg. LPO increased significantly in a dose-dependent manner. In time-course studies, mice were administrated NiCl2 (170 micromol Ni/kg) and killed at intervals of 6, 12, 24, and 48 h after injection. Both LPO and the accumulation of Ni, Fe, Cu, and Zn in the liver showed a significantly positive time-course relationship after NiCl2 injection. At 1 h and 24 h after a single ip injection of 170 micromol Ni/kg, the mice were given an ip injection of ascorbic acid (vit C), glutathione (GSH), and selenium (Se). Vit C and GSH significantly decreased both the level of hepatic LPO and the concentration of Ni in the liver, but did not decrease the accumulation of Fe, Cu, and Zn. However, LPO in the experimental group of mice was different significantly from that in the control group. In conclusion, the results suggest that Ni-induced hepatic LPO may result from increasing the amounts of Ni, Fe, and Cu, since these elements are involved in the generation of hydroxyl radical by inducing the Fenton reaction, thus instigating the Ni-mediated hepatic LPO. The protective effects of vit C and GSH in hepatic LPO result not only from removing the oxygen reactive species, but also from decreasing the Ni concentration.