Protective effects of vitamins C and E in hypoxia

The choanal atresia is a rare congenital malformation. Its clinical diagnosis is easy and must be done at the birth by the midwife or the obstetrician. We recommend the aspiration in all hospital maternity wards. This attitude avoids the unrecognized of an unilateral choanal atresia. The authors report three cases with a successfully treatment.     

Concentrations of vitamins A, C and E in elderly patients with Parkinson''s disease

Concentrations of the naturally occurring antioxidant vitamins A, C and E were measured in 27 patients with Parkinson's disease and 16 age-matched control subjects, from a similarly disabled patient group. There was no significant difference in the serum concentrations of vitamins A and E in the two groups. Vitamin C was significantly higher (P < 0.05) in the Parkinson's disease group, however, the mean leucocyte vitamin C concentration in the control group was low (101 nmol/10(8) WBCS) compared to established data in healthy young individuals (119-301 nmol/10(8) WBCS). There was no correlation between the severity or duration of Parkinson's disease and concentrations of vitamins A, C and E. There is therefore no evidence from this study that a deficiency of these antioxidants contributes to the onset or progress of Parkinson's disease.     

Low-density lipoprotein oxidation and vitamins E and C in sustained and white-coat hypertension

Low-density lipoprotein oxidation and antioxidant vitamins E and C were investigated in white-coat hypertension in comparison with sustained hypertension and normotension. We selected 21 sustained hypertensive subjects, 21 white-coat hypertensive subjects, and 21 normotensive subjects matched for gender, age, and body mass index. White-coat hypertension was defined as clinical hypertension and daytime ambulatory blood pressure <139/90 (subjects were also reclassified using 134/90 and 135/85 mm Hg as cutoff points for daytime blood pressure). Blood samples were drawn for lipid profile determination, assessment of fluorescent products of lipid peroxidation in native LDL, evaluation of susceptibility to LDL oxidation in vitro (lag phase and propagation rate), and determination of LDL vitamin E and plasma vitamins E and C contents. Compared with sustained hypertensive subjects, white-coat hypertensives had significantly lower fluorescent products of lipid peroxidation (15.4+/-3.4 versus 10.2+/-3 units of relative fluorescence/mg LDL protein, P<.05), longer lag phase (54+/-10 versus 88+/-10 minutes, P<.05), lower propagation rate (8.2+/-2.5 versus 5.95+/-2.1 nmol diene/min per mg LDL cholesterol, P<.05), higher LDL vitamin E content (8.3+/-1.1 versus 10.1+/-1.8 nmol/mg LDL cholesterol, P<.05), and plasma vitamin C content (40+/-13 versus 57+9 micromol/L, P<. 05). No significant difference was observed between white-coat hypertensive and normotensive subjects. The results did not change after reclassification of subjects. Our data show that white-coat hypertensive subjects do not show an enhanced propensity to LDL oxidation or reduction in antioxidant vitamins. Given the role of LDL oxidation in the development of atherosclerosis and that of vitamin E and C in protecting against it, these findings suggest that white-coat hypertension per se carries a low atherogenic risk.     

Plasma vitamins E and C concentrations of adult patients during cardiopulmonary bypass

The trajectories of change in CD4+ and CD8+ lymphocytes and serum neopterin and beta2-microglobulin (beta2M) levels were determined in 158 HIV-seropositive individuals during 5.5 years before a clinical AIDS diagnosis. Each patient was evaluated separately using a two-piece regression model with seven possible change points to identify any adverse change (inflection point) in the slopes of each immunologic marker of HIV infection. Two categories of subjects were distinguished for each marker--those with statistically significant inflection points and those who demonstrated a steady progression of changes to AIDS. Fifty-nine percent had an inflection point for CD4+ T cells. The frequency of inflection points for CD8+ was 49%, for serum neopterin -48% and for beta2M -38%. Inflection points were found over a 4-year span. Three distinctive categories of inflection points were observed on the basis of their independent occurrence: one was in CD4+ T cells, another in CD8+ T cells, and a third in the serum markers of immune activation. The inflection point for CD4+ usually occurred prior to those for CD8+ T cells (p=.0002). The HIV-positive persons with inflection points were diagnosed with AIDS when immunologic parameters were significantly more abnormal than in those with steady progression (p < .0003). Thus, these two groups differed in the course of immune changes and in the levels of immune abnormalities associated with the occurrence of clinical AIDS.     

Increased oxidation of LDL in patients with coronary artery disease is independent from dietary vitamins E and C

There is increasing experimental evidence that oxidation of LDL plays a major role in the pathogenesis of coronary artery disease (CAD). However, results from clinical studies on LDL oxidation and CAD are not consistent. In most studies only single plasma factors of LDL oxidation have been determined. We studied 207 patients who underwent coronary angiography. They were divided into subjects with CAD (n = 137) and those without CAD (n = 70). We determined the susceptibility of LDL to in vitro oxidation (lag phase), potential prooxidative and antioxidative plasma factors (plasma vitamin E, LDL vitamin E, ascorbate, iron, copper, ferritin, and ceruloplasmin), and markers of in vivo LDL oxidation (autoantibodies to malondialdehyde-modified LDL, oxidized LDL, and thiobarbituric acid-reactive substances), plasma lipids and lipoproteins, smoking habits, and other coronary risk factors in both groups. The lag phase was significantly shorter in patients with CAD than in patients without CAD (101 +/- 38.6 versus 119 +/- 40.6 minutes, P < .01). There was no correlation between the lag phase and the other oxidation parameters or the coronary risk factors. In multivariate regression analyses the lag phase remained significant in all tested models. Our data suggest that a short lag phase of LDL oxidation might be an independent risk factor of CAD.     

Vitamin E protection against tumor formation by transplanted murine sarcoma cells

Mice fed vitamin E at a level of 0.5 g DL-alpha-tocopheryl acetate/kg diet demonstrated decreased incidence and rate of appearance of tumors produced by transplanted sarcoma cells (K3T3), compared to control groups fed diets without the vitamin supplement. Protection was dependent on the degree of unsaturation of dietary fat and on the size of the tumor cell challenge. When vitamin E was increased 10-fold (to 5 g/kg diet), the protective effect was no longer observed. Protection may be mediated through the host immune system, because sublethal, whole-body X-irradiation abrogated differences in tumor development between the +E and the -E mice. Studies with in vitro immunization showed that treatment of the K3T3 cell with vitamin E enhanced its ability to induce a cytotoxic response. It appears that the direct effect of vitamin E is on the tumor cell rather than on the immune system, since spleen cells from mice fed diets with and without vitamin E supplementation were indistinguishable in their response to untreated K3T3 cells. K3T3 cells treated with excessive levels of vitamin E were unable to induce a cytotoxic response, a result that correlates with the loss of protection against tumor development when massive doses of vitamin E were fed.     

Inhibitory effect of vitamins C and E on the oxygen free radical production in human polymorphonuclear leucocytes

Beneficial effects of dietary supplementation with antioxidant vitamins are attributed mainly to the influence upon lipid metabolism, endothelial and vascular functions. Their effect upon leucocyte oxygen free radical producing capacity has not been investigated. In 13 healthy volunteers we examined the influence of oral supplementation with vitamins C and E (aa 600 mg per day for 14 days) upon leucocyte oxygen free radical production estimated by lucigenin-amplified chemiluminescence in isolated leucocytes stimulated with arachidonic acid. After supplementation with vitamins, significant increase in serum content of ascorbic acid and tocopherol was concomitant with significant (P < 0.001) decrease of leucocyte chemiluminescent response (mean 63.2 + 23.0 SD, % of initial values) and lowering of serum lipid peroxides (P < 0.05). These findings suggest that suppression of leucocyte capacity to produce oxygen free radicals as shown in this study, may contribute to vasoprotective action of vitamins C and E.     

Myocardial protection against cold stress with pravastatin

The CARE study showed that the myocardial infarction recurrence rate in patients with moderate cholesterol blood level decreases early during pravastatin treatment. Our goal is to evaluate the possible role of pravastatin in preventing the myocardial lesions induced by cold stress. Twenty Wistar-EPM rats were divided into four groups: Control (CON); PR (Pravastatin) treated with 10 mg/kg/d for 15 days; S (Stress group) in which the rats were submitted to cold stress (-8 degrees C for four hours); and PR + S group treated with pravastatin like PR group and also submitted to the cold stress. The animals were sacrificed and heart fragments were removed for optic and electronic microscopic analysis. The variable considered was mitochondria abnormality (edema, lyses and vacuolization) that was interpreted as crystolyses indices (CI) (n degree of abnormal mitochondria/n degree total of mitochondria). The following crystolyses indices, were found for each group respectively: CON, 2.0%; S, 95.5%; PR, 19.9% and PR + S group, 27.7%*(*p < 0.01). In conclusion, pravastatin prevented myocardial lesions induced by cold stress significantly.     

Relationships between cigarette smoking, oral contraceptives, and plasma vitamins A, E, C, and plasma triglycerides and cholesterol

Plasma vitamins A, E, and C, plasma triglycerides and cholesterol, and leukocyte vitamin C were examined in young healthy adult females who were cigarette and/or oral contraceptive users. It was found that cigarette smoking slightly increased the levels of vitamin A, triglycerides, and cholesterol while oral contraceptives significantly increased these plasma lipids. The effects of cigarette smoking and oral contraceptives on these substances were additive. Neither cigarette smoking nor oral contraceptives had any significant effect on plasma vitamins E and C. Oral contraceptives slightly decreased the level of leukocyte vitamin C in the cigarette smokers. Cigarette smoking did not impart and acute effect on these parameters.     

Murine antibodies against E2 and hypervariable region 1 cross-reactively capture hepatitis C virus

The purpose of this study was to determine whether supplemental estrogen influences cardiovascular hemodynamics at peak exercise in endurance trained and sedentary postmenopausal women. Subjects were 22 women between 3 and 10 yr past menopause who had engaged in endurance exercise at least three times per week for one or more years. Twelve of the women had taken estrogen replacement for at least 1 yr (ER) while the other 10 had never taken supplemental estrogen (NOER). Peak cardiac output (Qpeak) and, subsequently, peak cardiac index (QIpeak) were calculated by regressing submaximal cardiac output values on corresponding oxygen consumptions and extrapolating to peak exercise. Peak oxygen consumption in the two groups were almost identical; however, the ER group demonstrated a higher QIpeak in conjunction with a lower arteriovenous oxygen difference and a lower peripheral resistance. It was concluded that estrogen supplementation may be associated with higher peak cardiac outputs in exercise trained postmenopausal women via alterations in the peripheral vascular and oxygen kinetic responses to maximal exercise.     

Methods for determination of vitamins A and E our simple HPLC assay

Biological effects of reactive oxygen species and other radicals which are controlled by antioxidant mechanism are exerted on the basis of enzymes and substrates. Antioxidant substrates are divided into lipophilic and hydrophilic groups. Main representants of lipophilic antioxidants are retinol and tocopherol which are closely related to ascorbate in the hydrophilic compartment. Described methods for detection of retinol and alpha-tocopherol are simple, sensitive, specific and precise. They are reliable, economic and fast. Only small amounts of serum are used for one analysis which is convenient for patients, too. Our methods can be recommended for routine use in laboratories of clinical biochemistry. Haemodialyzed patients, retinol serum level was higher than that in blood donors while alpha-tocopherol serum level did not differ. Both vitamin A and E serum levels were similar in alcoholics compared to controls.     

内置高导C/C材料的疏导式热防护结构防热效果

本文建立了内置高导C/C材料的疏导式热防护结构原理模型,通过实验的方法给出了高导C/C材料与耐热三维编织C/C材料间的接触热阻,并利用数值仿真针对影响结构热防护效果的若干关键参数进行了参数影响研究.研究结果表明:减小耐热层厚度是一种降低驻点温度的有效方法,但是必须同时考虑由此引起的强度问题;界面接触热阻对热防护效果影响很大,必须通过工艺处理降低界面热阻才能实现有效的热防护.     

A novel, synergistic interaction between 17 beta-estradiol and glutathione in the protection of neurons against beta-amyloid 25-35-induced toxicity in vitro

The present studies were undertaken to investigate the possibility of an interaction between 17 beta-estradiol (E2) and glutathione in protecting cells against the presence of beta-amyloid 25-35 (betaAP 25-35). We demonstrate that when evaluated individually, supraphysiological concentrations of either E2 (200 nM) or of reduced glutathione (GSH; 325 microM) can protect SK-N-SH human neuroblastoma cells from betaAP 25-35 (20 microM) toxicity. This dose of betaAP 25-35 was chosen based on the LD50 (28.9 microM) obtained in our earlier work. However, in the presence of 3.25 microM GSH, the neuroprotective EC50 of E2 was shifted from 126 +/- 89 nM to 0.033 +/- 0.031 nM, approximately 4000-fold. Similarly, in primary rat cortical neurons, the addition of GSH (3.25 microM) increased the potency of E2 against betaAP 25-35 (10 microM) toxicity, as evidenced by a shift in the EC50 values of E2 from 68 +/- 79 nM in the absence of GSH to 4 +/- 6 nM in its presence. The synergy between E2 and GSH was not antagonized by the addition of the estrogen receptor antagonist, ICI 182,780. Other thiol-containing compounds did not interact synergistically with E2, nor were any synergistic interactions observed between E2 and ascorbic acid or alpha-tocopherol. Based on these data, we propose an estrogen-receptor independent synergistic interaction between glutathione and E2 that dramatically increases the neuroprotective potency of the steroid and may provide insight for the development of new treatment strategies for neurodegenerative diseases.     

The synergistic effects of vitamin E and selenium in iron-overloaded mouse hearts

In the present study, we report that low concentrations of the glutamate ionotropic agonist kainate decreased the turnover of [3H]-phosphoinositides ([3H]-InsPs) induced by muscarinic receptors in the chick embryonic retina. When 100 microM carbachol was used, the estimated IC50 value for kainate was 0.2 microM and the maximal inhibition of approximately 50% was obtained with 1 microM or higher concentrations of the glutamatergic agonist. Our data also show that veratridine, a neurotoxin that increases the permeability of voltage-sensitive sodium channels, had no effect on [3H]-InsPs levels of the embryonic retina. However, 50 microM veratridine, but not 50 mM KCl, inhibited approximately 65% of the retinal response to carbachol. While carbachol increased [3H]-InsPs levels from 241.2 +/- 38.0 to 2044.5 +/- 299.9 cpm/mg protein, retinal response decreased to 861.6 +/- 113.9 cpm/mg protein when tissues were incubated with carbachol plus veratridine. These results suggest that the accumulation of phosphoinositides induced by activation of muscarinic receptors can be inhibited by the influx of Na+ ions triggered by activation of kainate receptors or opening of voltage-sensitive sodium channels in the chick embryonic retina.     

Determination of vitamin C in effervescent tablets containing other vitamins together with trace elements

A simple, rapid method is reported for the determination of vitamin C in effervescent tablets containing other vitamins and several trace elements such as Mg(II), Zn(II), Fe(II), Mn(II), Cu(II) and Mo(VI). The procedure was developed on the basis of the bromate ion-iodide ion-ascorbic acid clock reaction (Landolt reaction). Interference effects of air oxygen and metal ions and the role of pH are discussed in detail.     

Interaction of vitamins E and K: effect of high dietary vitamin E on phylloquinone activity in chicks

Age-standardised mortality rates are often used in epidemiologic studies to describe the dimension of social inequalities in mortality. This, however, conceals any age-dependence of social inequality. In an ecologic study, all causes and cause-specific mortality of all citizens of Bochum, FRG, who died 1988-1990, were evaluated using 13.171 death certificates. Data was aggregated on census tract level. The social status of a census tract was determined using 6 variables from the census 1987 describing the socio-economic situation in each census tract. Census tracts were grouped into quintiles according to their social status. Age and sex-specific mortality rates as well as rate ratios, using the quintile with the highest social status as reference, were calculated. Results for men (n = 6.288) indicate that social inequality is age-dependent for total mortality. Social differentials are especially marked for the age groups 35-64 years. For age group < 35 years and > 84 years no social differentiation in mortality is visible. Similar patterns are found with mortality from cardiovascular diseases (ICD-9: 390-459) and cancer (ICD-9: 140-208). Mortality from diseases related to health behaviour such as lung cancer or diseases associated with high alcohol intake are characterised by social inequalities above average in the middle age groups. For total mortality in women (n = 6.883) large social differentials are found for age groups 25-34 years and 45-54 years. Efforts to reduce social inequality on community level should especially be aimed at adolescents and young adults living in underprivileged areas.