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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although no absolute certainty exists about the role of nutrition in the etiology of cancer, many facts in favor of the relationship became available during the last decades. Correlation studies, experimental work and to a lesser extent case-control studies made it possible to clarify the role of certain nutrients and foods in carcinogenesis. The most important cancer sites where nutrition could play a role are esophagus, stomach, colon, rectum, prostate and breast. Esophageal cancer is of a very complex etiology, in which alcohol intake plays an important role, at least in western countries. The cancer-promoting properties of alcohol intake are enhanced by smoking. Three factors from nutrition are probably related to stomach cancer, namely salt, nitrate/nitrite and vitamin C. Salt is caustic to the stomach mucosa, resulting in atrophic gastritis. Salt is also co-carcinogenic and stomach cancer-promoting in experimental animals. Nitrate is probably important at the stage of atrophic gastritis, where bacterial overgrowth, due to the high pH, converts nitrates in nitrites, making the loco synthesis possible of potent nitrosocarcinogens. Vitamin C inhibits the latter step. The epidemiological evidence for the role of those factors is provided. The most important among them is the strong and consistent association of stomach cancer mortality with stroke. Rectum, colon, prostate and breast cancer are related in some way to fat intake. They all seem positively related to saturated fat intake, whereas breast cancer is probably also promoted by polyunsaturated fat intake. However, polyunsaturated fat seems to be without effect on rectum cancer. Colon and prostate cancer are probably also influenced by polyunsaturated fat but to a lesser degree than breast cancer. An important argument for this are the positive ecological correlations between changes in rectum, colon and breast cancer mortality from 1968 on, and changes occurring in coronary heart diseases, stroke and diabetes mortality. Those six types of mortality are decreasing, or only slightly increasing in the USA, Belgium, France, the Netherlands, etc. They are strongly increasing in East European countries. The intake of saturated fat has generally decreased in the first group of countries, and has markedly increased in the second group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and cancer. 353 16

The accuracy of the Ischemic Score (IS) of Hachinski in the differential diagnosis between senile dementia (SDAT) and multi-infarct dementia (MID) is evaluated in this study. Ninety-four demented patients were subdivided on the basis of CT scan in three subgroups: 1) CT-SDAT (ventricular enlargement and widening of cortical sulci), 2) CT-MID (multiple low density areas attributable to ischemic lesions), 3) CT-VASC (single low density area attributable to ischemic lesion). Sixty-nine percent of patients with SDAT and 94% of patients with MID had an Ischemic Score in agreement with the diagnosis established by CT scan. With the purpose of improving the accuracy of the I.S., a modified ischemic score consisting of five items (abrupt onset; history of strokes; focal symptoms; focal signs; focal (single or multiple) CT-low density areas) is proposed as a useful tool in the differential diagnosis between SDAT and MID.
Stroke
PMID:Diagnostic evaluation of degenerative and vascular dementia. 665 9

Of particular physiological interest, ascorbate, the ionized form of ascorbic acid, possesses strong reducing properties. However, it has been shown to induce oxidative stress and lead to apoptosis under certain experimental conditions. Ascorbate in the brain is released during hypoxia, including stroke, and is subsequently oxidized in plasma. The oxidized product (dehydroascorbate) is transported into neurons via a glucose transporter (GLUT) during a reperfusion period. The dehydroascorbate taken up by cells is reduced to ascorbate by both enzymatic and non-enzymatic processes, and the ascorbate is stored in cells. This reduction process causes an oxidative stress, due to coupling of redox reactions, which can induce cellular damage and trigger apoptosis. Ascorbate treatment decreased cellular glutathione (GSH) content, and increased the rates of lipid peroxide production in rat cortical slices. Wortmannin, a specific inhibitor of phosphatidylinositol (PI)-3-kinase (a key enzyme in GLUT translocation), prevented the ascorbate induced-decrease of GSH content, and suppressed ascorbate-induced lipid peroxide production. However, wortmannin was ineffective in reducing hydrogen peroxide (H(2)O(2))-induced oxidative stress. The oxidative stress caused ceramide accumulation, which was proportionally changed with lipid peroxides when the cortical slices were treated with ascorbate. These differential effects support the hypothesis that GLUT efficiently transports the dehydroascorbate into neurons, causing oxidative stress.
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PMID:Oxidative stress induced by ascorbate causes neuronal damage in an in vitro system. 1125 61

The human organism is incapable of producing vitamin C by biosynthesis. We are therefore totally dependent on the presence of this vitamin in our diet. Vitamin C is capable of essentially influencing the course of many metabolic processes, and it is therefore used in the treatment and prophylaxis of many diseases, including those that are a consequence of the activity of the so-called reactive forms of oxygen. The presence of vitamin C in the anti-oxidant protective system is believed to be very important, since it can react with the free radicals of oxygen and other oxidants, and "sweep" them away. Therefore, attention is more and more frequently focused on the possibility of using vitamin C in the treatment of those circulatory diseases that are believed to be associated with the action of free radicals. Routine administration of vitamin C should be therefore recommended in the treatment of patients with coronary arterial disease, treatment of patients after cardiac infarction or cerebral stroke, or in the treatment of arterial hypertension.
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PMID:[Vitamin C in treatment of certain cardiovascular diseases]. 1132 May 79

Ascorbate is a reducing agent, but it is also known to oxidize cellular components under specific conditions. The mechanism of this oxidative action, however, is not well established. Ascorbate treatment increased lipid peroxide content in PC12 cells, but did not increase quantities of lipid peroxide when homogenates of PC12 cells were treated with ascorbate, suggesting that cellular integrity is required for ascorbate to generate lipid peroxidation. However, dehydroascorbate increased lipid peroxide production in both intact PC12 cells and the cell homogenates. These differential effects of ascorbate and dehydroascorbate on intact cells versus homogenates suggest that the dehydroascorbate in cytosol induces an oxidative stress. Ascorbate in culture medium is rapidly oxidized to dehydroascorbate, which is transported into cells by a glucose transporter (GLUT). The GLUT antagonists wortmannin and cytochalasin B, or a high concentration of glucose, blocked (14)C uptake (from ascorbate) in a time-dependent manner and suppressed lipid peroxide production in PC12 cells. These observations support the concept that ascorbate is oxidized to dehydroascorbate, which is transported into cells via GLUT. The dehydroascorbate induces oxidative stress. The oxidative stress triggered apoptosis according to ceramide production, caspase-3 activation, and TUNEL. We have concluded that ascorbate is taken up after oxidation to dehydroascorbate via a "dehydroascorbate transporter" (GLUT), and the dehydroascorbate generates an oxidative stress which triggers apoptosis. These studies have significant implications for conditions under which a high concentration of ascorbate in a tissue is released during a period of hypoxia (e.g., stroke) and taken up during a reperfusion period as dehydroascorbate. Inhibiting uptake of dehydroascorbate may offer novel therapeutic strategies to alleviate brain damage during a reperfusion period.
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PMID:Involvement of oxidative stress in ascorbate-induced proapoptotic death of PC12 cells. 1135 56

Ascorbic acid (vitamin C) and alpha-tocopherol (vitamin E) have antioxidant properties that could improve redox-sensitive vascular changes associated with hypertension. We determined whether vitamins C and E influence vascular function and structure in hypertension by modulating activity of NADPH oxidase and superoxide dismutase (SOD). Adult stroke-prone spontaneously hypertensive rats (SHRSP) were divided into 3 groups: control (C; n=6), vitamin C-treated (vit C, 1000 mg/day; n=7), and vitamin E-treated (vit E, 1000 IU/day; n=8). All rats were fed 4% NaCl. Blood pressure was measured weekly. After 6 weeks of treatment, the rats were killed, and mesenteric arteries were mounted as pressurized preparations. Vascular O(2)(-) generation and NADPH oxidase activity were measured by chemiluminescence. Vascular SOD activity and plasma total antioxidant status (TAS) were determined spectrophotometrically. Blood pressure increased from 212+/-7 to 265+/-6 mm Hg in controls. Treatment prevented progression of hypertension (vit C, 222+/-6 to 234+/-14 mm Hg; vit E, 220+/-9 to 227+/-10 mm Hg). Acetylcholine-induced vasodilation was improved (P<0.05), and media-to-lumen ratio was reduced (P<0.05) in the treated rats. O(2)(-) was lower in vitamin-treated groups compared with controls (vit C, 10+/-4 nmol. min(-1). g(-1) dry tissue weight; vit E, 9.6+/-3.5 nmol. min(-1). g(-1) dry tissue weight; C, 21+/-9 nmol. min(-1). g(-1) dry tissue weight; P<0.05). Both vitamin-treated groups showed significant improvement (P<0.01) in TAS. These effects were associated with decreased activation of vascular NADPH oxidase (vit C, 46+/-10; vit E, 50+/-9; C, 70+/-16 nmol. min(-1). g(-1) dry tissue weight, P<0.05) and increased activation of SOD (vit C, 12+/-2; vit E, 8+/-1; C, 4.6+/-1 U/mg; P<0.05). Our results demonstrate that vitamins C and E reduce oxidative stress, improve vascular function and structure, and prevent progression of hypertension in SHRSP. These effects may be mediated via modulation of enzyme systems that generate free radicals.
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PMID:Antioxidant effects of vitamins C and E are associated with altered activation of vascular NADPH oxidase and superoxide dismutase in stroke-prone SHR. 1156 40

Vitamin C in humans must be ingested for survival. Vitamin C is an electron donor, and this property accounts for all its known functions. As an electron donor, vitamin C is a potent water-soluble antioxidant in humans. Antioxidant effects of vitamin C have been demonstrated in many experiments in vitro. Human diseases such as atherosclerosis and cancer might occur in part from oxidant damage to tissues. Oxidation of lipids, proteins and DNA results in specific oxidation products that can be measured in the laboratory. While these biomarkers of oxidation have been measured in humans, such assays have not yet been validated or standardized, and the relationship of oxidant markers to human disease conditions is not clear. Epidemiological studies show that diets high in fruits and vegetables are associated with lower risk of cardiovascular disease, stroke and cancer, and with increased longevity. Whether these protective effects are directly attributable to vitamin C is not known. Intervention studies with vitamin C have shown no change in markers of oxidation or clinical benefit. Dose concentration studies of vitamin C in healthy people showed a sigmoidal relationship between oral dose and plasma and tissue vitamin C concentrations. Hence, optimal dosing is critical to intervention studies using vitamin C. Ideally, future studies of antioxidant actions of vitamin C should target selected patient groups. These groups should be known to have increased oxidative damage as assessed by a reliable biomarker or should have high morbidity and mortality due to diseases thought to be caused or exacerbated by oxidant damage.
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PMID:Vitamin C as an antioxidant: evaluation of its role in disease prevention. 1256 11

Ascorbic acid (AA) is a well-known antioxidant. It also has pro-oxidant effects, however, in the presence of free transition metals. Because of the pro-oxidant effects of AA, dehydroascorbic acid (DHA), an oxidized form of AA, has been used as a substitute for AA. DHA has been shown recently to have a protective effect in an experimental stroke model. This study was carried out to determine if DHA has different effects from AA on hydrogen peroxide (H2O2)-induced oxidative cell death in primary astrocytes. DHA was found to prevent cell death and reverse mitochondrial dysfunction after exposure to H2O2. DHA significantly increased the glutathione peroxidase (GPx) and glutathione reductase (GR) activities 1 hr after H2O2 exposure. Moreover, DHA not only reversed the decrease in the glutathione (GSH) levels, but also significantly enhanced it by stimulating the pentose phosphate pathway (PPP) 15 hr after H2O2 exposure. DHA also reduced production of reactive oxygen species (ROS) after H2O2 exposure. In contrast, AA accelerated H2O2-induced cell death. To determine if the pro-oxidant effect of AA is related to iron, the effect of AA on cell death was examined using an iron chelator, desferrioxamine. Even though co-pretreatment with AA and desferrioxamine could abrogate the aggravating effects of AA on H2O2-induced cell death at early stages, it could not prevent H2O2-induced cell death over a 24-hr period. These results suggest that DHA has distinct effects from AA and prevent H2O2-induced cell death by increasing the GSH levels mediated by the GPx and GR activities and PPP.
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PMID:Dehydroascorbic acid prevents oxidative cell death through a glutathione pathway in primary astrocytes. 1566 57

L-Ascorbic acid (AsA, vitamin C) is an essential human nutrient that must be obtained in the diet, with the vast majority being obtained from plant foods. A vitamin C-deficient diet results in the onset of scurvy, which can have lethal consequences. However, vitamin C has also been implicated in the prevention of chronic diseases such as heart disease, stroke, cancer, and several neurodegenerative diseases. Although the supporting evidence for these claims is disputed, the dietary allowances for vitamin C have been recently increased in several countries, including the United States. This scenario, together with the general perception by consumers of vitamin C as being of benefit in the prevention of several lifestyle diseases and associated with general "well-being", contributes to a market rationale for enhancing the vitamin C content of crops. In recent years, there has been substantial progress in the understanding of vitamin C biochemistry in plants with a number of structural genes cloned. Here these findings are reviewed, and a description of how such knowledge could be applied to the nutritional enhancement of crops is given.
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PMID:Improving the nutritional value of crops through enhancement of L-ascorbic acid (vitamin C) content: rationale and biotechnological opportunities. 1596 4

Consumption of fruits and vegetables is associated with a reduced risk of death from all causes including heart disease and stroke. In this work, the bioavailability of vitamin C from a Mediterranean vegetable soup (gazpacho) constituted mainly of tomato, pepper and cucumber, and its influence on plasma vitamin C, 8-epi-prostaglandin F(2alpha) (8-epi-PGF2alpha), prostaglandin E2 (PGE2), monocyte chemotactic protein-1 (MCP-1), and the cytokines/tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 concentrations in a healthy human population were assessed. Six men and six women consumed 500 ml of commercial gazpacho per day for 14 days, corresponding to an intake of 78 mg of ascorbic acid per day. There were no differences (P = .22) in baseline plasma vitamin C concentrations between the men and women. The maximum increase (P < .05) in plasma vitamin C occurred 4 h postdose in both men and women. Vitamin C concentrations were significantly higher (P < .03) on Days 7 and 14 of the intervention. Baseline concentrations of uric acid and 8-epi-PGF2alpha were significantly higher (P < or = .032) in men than in women. Baseline concentrations of 8-epi-PGF2alpha decreased significantly (P < or = .05) by Day 14 of the intervention. A significant inverse correlation was observed between vitamin C and 8-epi-PGF2alpha (r = -.415, P = .049). Baseline concentrations of PGF2 and MCP-1 were significantly higher (P< or = .025) in men than in women but decreased significantly (P< or = .05) by Day 14 of the intervention. No effect on TNF-alpha, IL-1beta and IL-6 was observed at Day 14 of the intervention. Drinking gazpacho (500 ml/day) significantly increases plasma concentrations of vitamin C and significantly decreases 8-epi-PGF2alpha, PGE2 and MCP-1 concentrations in healthy humans.
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PMID:Mediterranean vegetable soup consumption increases plasma vitamin C and decreases F2-isoprostanes, prostaglandin E2 and monocyte chemotactic protein-1 in healthy humans. 1616 5


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