Vitamin E. An inhibitor of the platelet release reaction.

Steiner, Manfred; Anastasi, John

doi:10.1172/jci108331

Cited by 207 publications

(77 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The serum level in smokers increased from 8.8±0.7 ,ug/ml at baseline to 20.6±2.9 ,g/ml after vitamin E. A similar increase (10.5±1.6-22.7±1.9 ,Ag/ml) was seen in nonsmokers. Serum vitamin E levels (baseline and supplemented) did not differ significantly between smokers and nonsmokers (P > 0.1, both comparisons), and are consistent with previously reported values (42)(43)(44).…”

Section: Resultssupporting

confidence: 91%

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Pacht¹,

Kaseki²,

Mohammed³

et al. 1986

J. Clin. Invest.

174

View full text Add to dashboard Cite

Cigarette smoking produces oxidant-mediated changes in the lung important to the pathogenesis of emphysema. Since vitamin E can neutralize reactive oxygen species and prevent peroxidation of unsaturated lipids, it may constitute an important component ofthe lung's defense against oxidant injury. To better characterize the antioxidant protective role of vitamin E, young asymptomatic smokers and nonsmokers were evaluated by bronchoalveolar lavage before and immediately after a 3-wk course of oral vitamin E (2,400 IU/d). Smoker alveolar fluid at baseline was relatively deficient in vitamin E compared with nonsmoker fluid (3.1±0.7 ng/ml vs. 20.7±2A ng/ml, P < 0.005). Although smoker alveolar fluid vitamin E levels increased to 9.3±2.3 ng/ml after supplementation, the levels remained significantly lower than nonsmoker baseline levels (P < 0.01). This deficiency was explained, in part, by the increased oxidative metabolism of vitamin E to the quinone form in the lungs of smokers compared with nonsmokers. Although the significance of a lower concentration of alveolar fluid vitamin E is unclear, it may compromise the antioxidant protection afforded by the alveolar fluid as it coats the lung's epithelial surface. The protective role of vitamin E was assessed by cytotoxicity experiments, which demonstrated that the killing of normal rat lung parenchymal cells by smoker alveolar macrophages was inversely related to the vitamin E content of the parenchymal cells. These findings suggest that vitamin E may be an important lower respiratory tract antioxidant, and that the deficiency seen in young smokers may predispose them to an enhanced oxidant attack on their lung parenchymal cells.

show abstract

Section: Resultssupporting

confidence: 91%

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Pacht¹,

Kaseki²,

Mohammed³

et al. 1986

J. Clin. Invest.

174

View full text Add to dashboard Cite

show abstract

“…48 Several studies have shown that the antioxidant ␣-tocopherol inhibits platelet aggregation. 31,49,50 Nitrosothiols have also been shown to inhibit platelet aggregation. 24,51 Antioxidant flavonoids in tea may also inhibit platelet aggregation by a number of mechanisms.…”

Section: Duffy Et Al Tea Effects On Platelet Aggregationmentioning

confidence: 99%

Effect of Acute and Chronic Tea Consumption on Platelet Aggregation in Patients With Coronary Artery Disease

Duffy

Vita

Holbrook

et al. 2001

ATVB

View full text Add to dashboard Cite

Abstract-Epidemiological studies suggest that tea consumption is associated with a decreased risk of cardiovascular events, but the mechanisms of benefit remain undefined. Platelet aggregation is a precipitating event in cardiovascular disease, and tea contains antioxidant flavonoids that are known to decrease platelet aggregation in vitro. To test the effect of tea consumption on platelet aggregation, we randomized 49 patients with coronary artery disease to either 450 mL of black tea or water consumed initially, followed by 900 mL of tea or water daily for 4 weeks in a crossover design. Ex vivo platelet aggregation in platelet-rich plasma was assessed in response to ADP and thrombin receptor-activating peptide at baseline and 2 hours and 4 weeks after beverage consumption. We observed dose-dependent platelet aggregation in response to each agonist, and neither relation was altered by acute or chronic tea consumption. Plasma flavonoids increased with acute and chronic tea consumption, indicating adequate absorption of tea flavonoids. In conclusion, these results demonstrate that acute and chronic black tea consumption does not affect ex vivo platelet aggregation in patients with coronary artery disease. These findings suggest that an effect of tea flavonoids on platelet aggregation is unlikely to be the explanation for the reduction in risk of cardiovascular events noted in epidemiological studies. Key Words: platelet aggregation Ⅲ tea Ⅲ flavonoids Ⅲ coronary artery disease R ecent epidemiological studies strongly suggest an inverse relationship between tea consumption and cardiovascular disease risk, 1-5 with 1 notable exception. 6 There is also convincing evidence that dietary intake of antioxidant flavonoids from tea and other sources (eg, red wine, onions, apples, and broccoli) is associated with reduced cardiovascular risk. [1][2][3][4][5][7][8][9] The benefit of high flavonoid intake may be greater for individuals with established coronary artery disease (CAD), 1,10 although favorable effects have also been demonstrated in people without evidence of atherosclerosis. 5,8,9 One proposed mechanism for the apparent benefit of tea and other sources of flavonoids is their favorable effect on platelet aggregation. [11][12][13][14][15][16] These polyphenols may inhibit platelet aggregation by a number of different mechanisms, including inhibition of lipoxygenase, cyclooxygenase, 13,17 cAMP phosphodiesterase, 12,18 and cGMP phosphodiesterase. 19 Other platelet-inhibitory effects of flavonoids include thromboxane receptor antagonism, 15 scavenging of reactive oxygen species such as superoxide anion, 20 decreasing phospholipase C activation by blunting hydrogen peroxide production, 21 and inhibition of lipid peroxidation. 14 Flavonoids also enhance nitric oxide (NO) production from the endothelium. 22 NO is a potent inhibitor of platelet adhesion, aggregation, [23][24][25] and thrombosis, 26 and impaired platelet production of NO has been associated with acute coronary syndromes. 27 A recent study demonstrated dose-...

show abstract

“…It has an antioxidation function, and activates actions of tissue cells of living animals, such as hormone secretory cells and embryo cells4,5,11), and so it has been used for prophylaxis and therapy of reproductive disturbance in domestic animals and poultry2, 3,7,8).…”

mentioning

confidence: 99%

Effects of DL-α-Tocopherol on Body Weight Gains and Meat Qualities of Holstein Steers

茂樹¹,

興平²

1985

Nihon Chikusan Gakkaiho

View full text Add to dashboard Cite

living animals, was used to fatten steers at the finishing period for examining the effects on the body weight gain and the meat quality. Ten Holstein steers in NODAI's Fuji Experiment Farm were divided into two groups, and each group was further divided into two lots, the experimental and the control. In both groups, body weight and traits of carcass were measured.Blood properties after the fattening were also measured in one group. In Group I, the average daily gains were 1.17kg and 0.95kg in the lot of V. E and control, respectively.In Group II, they were 1.08kg and 1.06kg. The differences were not significant.Carcass weight, marbling, quality of meat, rib eye area and grading of the carcass were a little better in the lot of V. E than in control.Dressing percentage, price at the market and appearance of them were similar in both lots. The changes of erythrocyte, leucocyte, Hematocrit, total protein, cholesterol, calcium, inorganic phosphorus and uric acid during the experimental period of one month were not distinguished between both lots. Jpn. J. Zootech. Sci., 56 (10) In connection with fat, V. E prevents the disturbance of lipid peroxide, which arises from a peroxidation of fatty acid, while V. E itself is easily oxidized4). As the result, in a normal route, fatty acids in the body produceIn this papers, the accelerating effect of V. E on metabolism in tissues was focussed, and the effect on body weight gain and meat quality of Holstein steers was examined when it was given per os in the latter period of fattening. Materials and MethodsTen Holstein steers in NODAI's Fuji Experiment Farm that were fed for beef from 12 months of age were divided into two groups (Table I). Four steers of 20 months and 614-692kg in body weight were included in Group I, and two of them were given V. E mixed with grain ration for the last one month before slaughtering at the dose of 1g per head (1.54-1.64mg per kg of body weight). Other six steers of 18.5 months and 580-631kg were included in Group II, and three of them were Jpn. J. Zootech.Sci., 56 (10): 802-806 802 1985

show abstract

Vitamin E. An inhibitor of the platelet release reaction.

Cited by 207 publications

References 25 publications

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Deficiency of vitamin E in the alveolar fluid of cigarette smokers. Influence on alveolar macrophage cytotoxicity.

Effect of Acute and Chronic Tea Consumption on Platelet Aggregation in Patients With Coronary Artery Disease

Effects of DL-α-Tocopherol on Body Weight Gains and Meat Qualities of Holstein Steers

Contact Info

Product

Resources

About