Chronic Administration Of Vitamin Research Articles

Dietary Vitamin E as a Protective Factor for Parkinson's Disease: Clinical and Experimental Evidence.

Effective disease-modifying treatments are an urgent need for Parkinson's disease (PD). A putative successful strategy is to counteract oxidative stress, not only with synthetic compounds, but also with natural agents or dietary choices. Vitamin E, in particular, is a powerful antioxidant, commonly found in vegetables and other components of the diet. In this work, we performed a questionnaire based case-control study on 100 PD patients and 100 healthy controls. The analysis showed that a higher dietary intake of Vitamin E was inversely associated with PD occurrence independently from age and gender (OR = 1.022; 95% CI = 0.999–1.045; p < 0.05), though unrelated to clinical severity. Then, in order to provide a mechanistic explanation for such observation, we tested the effects of Vitamin E and other alimentary antioxidants in vitro, by utilizing the homozygous PTEN-induced kinase 1 knockout (PINK1−/−) mouse model of PD. PINK1−/− mice exhibit peculiar alterations of synaptic plasticity at corticostriatal synapses, consisting in the loss of both long-term potentiation (LTP) and long-term depression (LTD), in the absence of overt neurodegeneration. Chronic administration of Vitamin E (alpha-tocopherol and the water-soluble analog trolox) fully restored corticostriatal synaptic plasticity in PINK1−/− mice, suggestive of a specific protective action. Vitamin E might indeed compensate PINK1 haploinsufficiency and mitochondrial impairment, reverting some central steps of the pathogenic process. Altogether, both clinical and experimental findings suggest that Vitamin E could be a potential, useful agent for PD patients. These data, although preliminary, may encourage future confirmatory trials.

Vitamin E improved redox homeostasis in heart and aorta of hypothyroid rats.

The objective of this study was to evaluate the effect of vitamin E on the oxidative stress parameters and antioxidant defense enzymes in the heart and aorta of 6-n-propylthiouracil (PTU)-induced hypothyroid rats. The animals were divided into 4 experimental groups: Group 1 (Euthyroid) received tap water, Group 2 (Hypothyroid) received 0.05 % of PTU in dissolved in their drinking water, Group 3 (PTU+Vit E) hypothyroid rats treated with vitamin E, and Group 4 (Euthyroid+Vit E). Vitamin E was injected daily (20 mg/kg) to groups 3 and 4 via daily gavage for 6 weeks. Malondialdehyde (MDA) levels, total thiol levels, and the activities of Cu, Zn-superoxide dismutase (SOD) and catalase (CAT) were evaluated in the aortic and cardiac tissues. A significant decrease of thyroxine (T4) serum levels confirmed hypothyroidism in rats, which received PTU. The MDA level increased and total thiol level decreased in the hypothyroid group compared to control group (p<0.001). Th e activities of SOD and CAT significantly decreased in the hypothyroid rats in comparison to the control. Vitamin E treatment resulted in increased levels of total thiol, SOD, and CAT within aortic and cardiac tissues and decreased levels of MDA in comparison with the hypothyroid group (p<0.01-p<0.001). PTU-induced hypothyroidism resulted in oxidative stress. Chronic administration of vitamin E to hypothyroid rats decreased the oxidative stress markers in the aortic and cardiac tissues.

Chronic administration of vitamin E elevates brain derived neurotrophic factor and nerve growth factor in chronic stress induced wistar rats.

Chronic administration of vitamin E elevates brain derived neurotrophic factor and nerve growth factor in chronic stress induced wistar rats.

Chronic administration of Vitamin C increases cognitive function in chronic stress induced rats

Background: Stress and increase in free radicals levels are known to alter cognition, learning, memory, and emotional responses. There is a marked impairment of hippocampus-dependent memory and suppression of long-term potentiation in the CA1 region of the hippocampus during stress. Aim and Objective: The aim of this study is to evaluate the hypothesized neuroprotective effect of oral antioxidants and piracetam in chronic restraint stress-induced rats. Materials and Methods: Healthy Wistar rats were divided into 5 groups (n = 6) each. Control group received neither stress nor oral antioxidant. Stress group received chronic restraint stress for 6 h per day for 21 days. Three experimental groups were administered vitamin C (100 mg/kg), beta-carotene (7 mg/kg), and caffeine (8 mg/kg), respectively. Evaluation parameters were measurement of serum nerve growth factor (NGF) using ELISA method. The oxidative stress markers, glutathione peroxidase (GPx), glutathione reductase, and malondialdehyde were measured. Histological analysis of CA1 region of the hippocampus was done to evaluate the structural changes of pyramidal neurons. Results: Vitamin C caused statistically significant (P < 0.001) increase in serum NGF. The results revealed that vitamin C caused statistically significant (P < 0.05) increase in antioxidant enzymes GPx, glutathione reductase. Vitamin C caused increase in neuronal cell size and volume in CA1 pyramidal layer of hippocampus. Conclusion: The findings of study are suggestive of neuroprotection, offered by administration of vitamin C compared to other antioxidants against chronic restraint stress-induced rats. These naturally available dietary vitamins might serve as an adjuvant therapy to avoid progression of brain damage during stress.

Vitamin E prevents high-fat high-carbohydrates diet-induced memory impairment: The role of oxidative stress

Memory and learning are impaired by imbalanced diet consumption. High-fat high-carbohydrate diet (HFCD) induces oxidative stress, which results in neuronal damage and interference with synaptic transmission; hence, a decline in cognitive function. Vitamin E is a fat soluble antioxidant that is believed to have positive effects on learning and memory. In this study, we tested the hypothesis that chronic administration of vitamin E prevents learning and memory impairment induced by HFCD. In addition, possible molecular targets for HFCD, and vitamin E that lead to cognitive effects were examined. Vitamin E and/or HFCD were concurrently administered to animals for 6weeks. Thereafter, behavioral studies were conducted to test the spatial learning and memory using radial arm water maze (RAWM). Additionally, brain derived neurotrophic factor (BDNF) level and antioxidant markers were assessed in the hippocampus. The results of this project revealed that HFCD impairs both short-term and long-term memories (p<0.05). The administration of vitamin E prevented the memory impairment induced by HFCD consumption (p<0.05). The consumption of HFCD reduced activities of hippocampal superoxide dismutase (SOD) and catalase (p<0.05); whereas the levels of thiobarbituric acid reactive substances (TBARS) and oxidized glutathione (GSSG) were elevated (p<0.05). The administration of vitamin E normalized the effect of HFCD on the oxidative stress markers. None of the treatments induced changes in the levels of BDNF or glutathione peroxidase (GPx). In conclusion, HFCD induces memory impairment, and the administration of vitamin E prevented this impairment probably through normalizing antioxidant mechanisms in the hippocampus.

Effect of chronic administration of vitamin E on the hemopoietic system in hypercholesterolemia

Hypercholesterolemia induces oxidative stress, which is known to have adverse effects on the integrity of cells. Hence, hypercholesterolemia may have adverse effects on the hemopoietic system. Vitamin E, an antioxidant, is being used by normo- and hypercholesterolemic subjects. It is, however, not known if vitamin E has any beneficial or adverse effects on the hemopoietic system. The objectives of this study are to determine if (i) hypercholesterolemia has any adverse effects on the hemopoietic system [red blood cell (RBC) count, mean corpuscular volume (MCV), red blood cell distribution width (RDW), hematocrit (Hct), hemoglobin (Hb), mean corpuscular hemoglobin (MCH), MCH concentration (MCHC), white blood cell (WBC), and platelet counts, and mean platelet volume (MPV)], and (ii) vitamin E has any effect on the hemopoietic system in hypercholesterolemia. Blood samples were collected before and at various intervals during a high cholesterol diet (0.25% cholesterol) for 2 and 4 months, and while on high cholesterol diet with vitamin E (2 months) following a high cholesterol diet (2 months). Serum cholesterol was measured on an automated Clinical System Analyzer and hemopoietic parameters were measured on an automated Cell-dyn-4000. The results show that hypercholesterolemia decreased RBC count, Hct and Hb, increased MCV, RDW, MCH, and MCHC, and had no effect on WBC and platelet counts, and MPV. Vitamin E did not affect any of the parameters of the hemopoietic system. In conclusion, hypercholesterolemia of short duration has adverse effects on certain elements of the hemopoietic system. Vitamin E does not affect the hemopoietic system during hypercholesterolemia.

Chronic administration of vitamin E in type 2 diabetic Nigerians

Chronic administration of vitamin E in type 2 diabetic Nigerians

Protective Effects of Vitamin C on Cisplatin-Induced Renal Damage: A Light and Electron Microscopic Study

The present study was performed to investigate whether the chronic administration of antioxidant vitamin C provided morphological protection on cisplatin-induced renal damage. Wistar albino male rats were divided into control and two experiment groups, each consisting of six rats. Cisplatin (5 mg/kg/month) was administered intravenously to the second and third group for three months. After the first application of cisplatin, vitamin C (8 mg/kg/day) to the third group was administered intramuscular for 3 months. At the end of the third month, the kidney specimens of the all groups were obtained. All of these kidney specimens were processed for light and electron microscopical examination. In the second group, most of the renal corpuscle lost their normal appearance and size, especially in the corticomedullary region. The most obvious changes were encountered in the proximal tubules. These changes were tubular dilation, thickening of basement membrane, loss of brush border, vacuolization, and swollenness of mitochondria in the proximal tubule epithelial cells. In addition, infiltration foci were observed mainly in the cortical region. In the third group, which was administered cisplatin plus vitamin C, although the structural damages and morphometric changes were lessened, mononuclear cell infiltration was still observed. This study suggests that the chronic administration of vitamin C may be of therapeutic benefit on cisplatin nephrotoxicity.

Effects of chronic administration of Vitamin C on haemodynamic responses to postural stress or cutaneous cold stimulation in healthy young men

Effects of chronic administration of Vitamin C on haemodynamic responses to postural stress or cutaneous cold stimulation in healthy young men

Chronic vitamin C administration induces thermal hyperalgesia in male rats

Against a backdrop of neurological effects, the effects of acute and chronic administration of vitamin C (600mg/kg) on pain processing were investigated in male rats. Chronic administration of vitamin C induced significant thermal hyperalgesia while acute administration had no effect. In addition, the intraperitoneal administration of vitamin C produced observable abdominal writtings similar to what has been observed with acetic acid. We conclude that chronic vitamin C exerts facilitatory central nervous system effects and a possibility of using intraperitoneal injection of vitamin C as an animal model of pain is suggested. Keywords: vitamin C, pain, hyperalgesia, nociception, ascorbic acidNigerian Journal of Health and Biomedical Sciences Vol. 4(2) 2005: 153-155

Effect of Vitamin C on the Availability of Tetrahydrobiopterin in Human Endothelial Cells

Vitamin C has long been known for its beneficial vascular effects, but its mechanism of action remains unclear. Recent reports suggest that vitamin C may prevent endothelial dysfunction by scavenging free radicals and increasing the bioavailability of nitric oxide. To investigate this area further, we studied the effect of vitamin C (10(-4) M) and Mn(III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP; 10(-5) M), a scavenger of superoxide, hydrogen peroxide, and peroxynitrite, on endothelial nitric oxide synthase (eNOS) enzymatic activity in cultured human umbilical vein endothelial cells. L-Citrulline formation (a measure of eNOS enzymatic activity) was significantly increased in cells treated for 24 h with vitamin C. No effect was observed after MnTBAP treatment. Chronic administration of vitamin C also had no effect on eNOS protein expression. Treatment with vitamin C for 24 h significantly increased levels of the eNOS co-factor tetrahydrobiopterin (BH4), whereas MnTBAP did not affect its levels. Sepiapterin (10(-4) M), a precursor of BH4, significantly increased eNOS activity, whereas addition of vitamin C to cells treated with sepiapterin did not cause any further increase in eNOS activity. Our results suggest that the beneficial effect of vitamin C on endothelial function is best explained by increased intracellular BH4 content and subsequent enhancement of eNOS activity. This effect appears to be independent of the ability of vitamin C to scavenge superoxide anions.

Enhancement of nitroxide-reducing activity in rats after chronic administration of vitamin E, vitamin C, and idebenone examined by an in vivo electron spin resonance technique.

Rats were given vitamin E (Vit-E), idebenone (ID), or vitamin C (Vit-C) in their food for 2 or 4 weeks. After feeding, the ability of rats to reduce 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) in terms of the half-life of Tempol was examined as a specific marker. Tempol was repeatedly injected intravenously, and its half-life was serially evaluated by an in vivo electron spin resonance (ESR) technique. The radical-reducing ability in rats was enhanced differently by Vit-E, ID, and Vit-C, i.e., slow onset of the ability after Vit-E and ID (lipid-soluble antioxidants) and fast onset after Vit-C (a water-soluble antioxidant).

Vitamin E ameliorates enhanced renal lipid peroxidation and accumulation of F2-isoprostanes in aging kidneys.

Aging results in progressive glomerular sclerosis and reductions in glomerular filtration rate (GFR). Oxidative stress may be an important mechanism for the aging process, but to date the role of oxidative stress on renal aging has not been determined. The present study was performed to determine whether age-related alterations in renal hemodynamics and morphology were associated with oxidative stress and whether this could be attenuated by chronic administration of vitamin E. Rats, aged 13 mo, were given either control diet containing vitamin E 50 IU/kg (n = 6) or a high-vitamin E diet (5,000 IU/kg; n = 6) for 9 mo. Another group of rats (3-4 mo old; n = 7) served as young controls. Aging was accompanied by a 60% reduction in GFR, a threefold increase in renal F2 isoprostanes, newly discovered vasoconstrictive F2-like prostaglandins generated by free radical-mediated lipid peroxidation. Renal aging was also associated with an increase in oxidant-sensitive heme oxygenase, advanced glycosylation end products (AGEs), and the AGE receptor, RAGE. AGE-RAGE interaction has been shown to induce oxidative stress. With high-vitamin E diet, GFR was increased by 50%, F2 isoprostanes were suppressed, and expression of heme oxygenase and RAGE was attenuated. There was also a tendency for glomerular sclerosis to be attenuated. These data demonstrate that age-related decline in renal function is accompanied by oxidative stress and that administration of antioxidants, such as vitamin E, could attenuate the decline in renal function.