Vitamin C and vitamin E antagonistically modulate human vascular endothelial and smooth muscle cell DNA synthesis and proliferation

Summary Background Vitamin C and E are suggested to play a preventive role in the pathogenesis of atherosclerosis. They reduce oxidation of low density lipoproteins (oxLDL), thereby protecting human vascular arterial endothelial and smooth muscle cells from oxLDL induced damages. Aims of the Study Since vascular arterial endothelial and smooth muscle cells are both involved in atherosclerotic plaque formation, we simultaneously examined the effect of vitamin C, E and oxLDL on their DNA synthesis and proliferation to further elucidate their joint role in this process. Methods Human umbilical arterial endothelial cells (HUAEC) and human arterial smooth muscle cells (HUASMC) were incubated with “preventive concentrations” of vitamin C (60μM) and E (30μM) and with LDL (60μg/ml) of increasing oxidation grade. Cell proliferation and DNA synthesis were determined by cell count and [³H]-thymidine uptake, respectively. Results Vitamin C alone or in combination with E increased significantly cell number and [³H]-thymidine uptake in HUAEC. The combination exhibited the strongest effect. In contrast, cell number and [³H]-thymidine uptake in HUASMC were significantly decreased in the presence of vitamin C, vitamin E or its combination. OxLDL (60 μg/ml) inhibited cell number and [³H]-thymidine uptake in HUAECs, the latter in an oxidation-grade dependent manner. In HUASMC oxLDL promoted a higher cell number and [³H]-thymidine uptake. If induced by minimally oxLDL, this reduc-tion or increase could be partially reversed by vitamin C alone or in combination with vitamin E. Conclusion Vitamin C and E, alone or in combination, modulate proliferation and DNA synthesis of human arterial endothelial and muscle cells and this modulation is antagonistic. Thus, vitamin C and E may act “preventive” on atherosclerotic plaque formation in two steps: first reendothelialisation is promoted, then HUASMC growth is inhibited. Received: 23 August 2001, Accepted: 8 January 2002     

Chronic vitamin E inadequacy and thermally treated oils affect the synthesis of hepatic metallothionein isoforms

Summary Background: Metallothionein (MT)^# synthesis can be stimulated in many organs not only by various metals such as cadmium, zinc, and copper, but also by many nonmetalic compounds or experimental conditions such as oxidative stress. The latter lead to the hypothesis that MT is induced in response to free radicals formed in tissues and lipid peroxidation. Aims of the study: Whether the relationship between lipid peroxidation amd MT synthesis is a common phenomenon also valid for lipid peroxidation induced by dietary factors such as chronic vitamin E inadequacy and autoxidation products of polyenoic fatty acids derived from thermally oxidized oil was investigated in the presence study. Methods: The relationship between the induction of metallothionein isoforms I and II (MT-I and MT-II) in response to diet-induced lipid peroxidation using a rat model system in which lipid peroxidation was examined in vivo by chronic vitamin E inadequacy or by administration of lipid peroxidation products from a thermally treated polyenoicrich oil with either basal (dietary zinc concentration: 48 mg/kd; experiment 1) or Zn-stimulated MT levels (dietary zinc concentration: 305 mg/kd; experiment 2) was studied. In both experiments, growing male rats were fed diet containing either a fresh or a thermally treated soybean oil with deficient of sufficient amounts of vitamin E (14 and 11 vs. 648 and 560 mg α-tocopherol equivalents per kg diet) over 40 days according to a bifactorial experimental design. Plasma and liver concentrations of tocopherols and hepatic levels of thiobarbituric acid-reacitve substances (TBARS) were measured by high performance liquid chromatography. MT isoform concentrations in rat liver were isolated and quantified by ion-exchange high performance liquid chromatography and atomic absorption spectrometry. Results: Irrespective of the zinc supply, rats receiving inadequate amounts of vitamin E with the diet had markedly lower plasma and liver concentrations of α-tocopherol and total tocopherols than vitamin E-sufficient rats. ANOVA also revealed an interaction between the diet factors vitamin E and oil on tocopherols in plasma and liver of rats from both experiments. In experiment 1, where rats received normal amounts of dietary zinc, ingestion of the thermally treated oil impaired the tocopherol status compared to the treatment with the fresh oil, although this effect was only obvious in the vitamin E-deficient groups. In experiment 2, where rats received excessive amounts of zinc, the thermally treated oil did not contribute to a reduction of the tocopherol status in plasma and liver. In both experiments a significant increase in TBARS level, indicative of lipid peroxidation, was observed in the liver at chronic vitamin E inadequacy, but no effect of the oil was observed. Here, we show that the dietary treatment had some effects on the synthesis of liver metallothionein isoforms. In groups, receiving normal amounts of zinc, there was a significant interaction between the dietary treatments on the levels of MT-I and MT-II in liver. Chronic vitamin E inadequacy which was accompanied by diminisched tocopherol levels in liver induced the synthesis of MT-I and MT-II. When vitamin E inadequacy was combined with the ingestion of a thermally treated polyenoic acid-rich oil hepatic levels of MT-I and MT-II remained low. In experiment 2, where rats were fed the high zinc diet, vitamin E inadequacy caused an increase of hepatic MT-I level just as in experiment 1, although this MT stimulating effect was irrespective of the oil. For MT-II there was a 43% increase in the vitamin E-deficient group fed the fresh oil compared to all the other groups, although this effect was not statistically significant. The liver MT isoform response to stress was similar in rats with basal MT levels and Zn-induced liver MT levels. The failing effect of the thermally treated oil on MT levels which were stimulated by vitamin E deficiency in experiment 2 was possibly due to the low oxidation grade of the thermally treated oil. Conclusion: The present results are strongly indicative of an apparent induction of MT isoform synthesis in response to an impaired antioxidant defence system in the lipid regions of liver cells induced by vitamin E inadequacy. In contrast, thermally treated polyenoic-rich oils with a certain oxidation grade seem to restrain the induction of MT isoform synthesis under the present experimental conditions. Received: 10 January 2000, Accepted: 27 April 2000     

维生素C、E对汞急性肾毒作用影响的实验研究

目的 探讨Vit C和Vit E对汞急性肾毒作用的影响。方法 Wistar大鼠随机分成6组：对照组,低、中、高剂量染汞组,Vit C、Vit E预处理组。染毒12h后收集12h尿样,采集血液,分离血清,切取肝脏、肾皮质样品。测定肝、肾皮质和尿中汞含量,尿 N-乙酰-β-D氨基葡萄糖苷酶(NAG)、碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)活性和尿蛋白、血清尿素氮(BUN)含量。结果高剂量染汞组肝、肾皮质和尿中汞含量显著高于对照组,且肾皮质中汞含量显著高于肝汞,高剂量染汞组尿NAG、ALP、EDH活性和尿蛋白、BUN含量显著高于对照组。Vit C和Vit E预处理组肝、肾皮质和尿中汞含量显著高于对照组,尿NAG、ALP活性和尿蛋白含量显著低于高剂量染汞组,LDH活性和BUN含量也低于高剂量染汞组,且Vit C预处理组与高剂量染汞组差异有显著性。结论Vit C和Vit E对汞急性肾毒作用有一定的拮抗作用。     

Effects of dietary vitamin E and high supplementation of vitamin C on plasma glucose and cholesterol levels

Weanling male Sprague Dawley rats were fed ad libitum a purified basal diet free of vitamins E and C. In Experiment I (4 weeks), 24 rats were divided into four groups with 2×2 factorial design. They were supplemented with 0 or 45 IU/kg diet of vitamin E, and O or 2.0 g/kg diet of vitamin C. In Experiment II (16 weeks), 36 rats were divided into six groups with 2×3 factorial design. Vitamin E was supplemented at the level of O or 45 IU/kg diet, and vitamin C was supplemented at the level of O, 1.5, or 3.0 g/kg diet, respectively. Plasma glucose level and cholesterol level were determined in both experiments. The plasma levels of glucose and cholesterol were significantly and negatively correlated. Plasma glucose level was significantly increased and plasma cholesterol level significantly decreased by the high supplementation of vitamin C with or without vitamin E in the diet. Vitamin E deficiency decreased plasma glucose level and increased plasma cholesterol level significantly with or without vitamin C supplementation. The groups with adequate level of vitamin E (45 IU/kg diet) and no vitamin C showed moderate plasma glucose and cholesterol levels.     

Role of glutamine on the de novo purine nucleotide synthesis in Caco-2 cells

Summary Background: The body's nucleotide pool derives from three potential sources: de novo synthesis, salvage of preformednucleosides/bases or the diet. The relative contributions of these pathways of assimilation are poorly understood in vivo. Dietary nucleotides have been suggested to have beneficial effects an the development and repair of the gastrointestinal tract. Tissues with a rapid turnover, such as the gut and the immune system cells, may utilise preformed nucleotides (coming from the diet), in situation in which there is a high demand of nucleotides for nucleic acid synthesis. Therefore, nucleotides could be onsidered as conditionally essential nutrients. Aim of the work and methods: -Development of a method to measure synthesis de novo of RNA-purine nucleotides in Caco-2 cells, relying an the incorporation of ¹⁴C-glycine into the purine ring of the nucleotide. To establish the fractional synthesis rate of RNA purine nucleotides in Caco-2 cells, grown in culture medium containing different concentrations of glutamine, in the presence or abscence of added nucleotides. To investigate the degree to which tissue ribonucleosides are derived from the culture medium or from de novo synthesis in the presence of different concentrations of glutamine, using undifferentiated Caco-2 cells, stressed or not by the addition of IL-1β to the medium. Results and conclusions:The presence of high levels of glutamine in the culture medium is essential for cell proliferation (estimated by measurement of the fractional synthesis rate of purine nucleotides) and the presence of nucleotides cannot replace the glutaminedependence of Caco-2 cell proliferation. The incorporation or exogenous purine nucleotides into RNA of Caco-2 cells is rather limited, and it becomes important when cells are stressed by glutamine deprivation. Stress by addition of interleukin-1β resulted in the maintenance or the increase in de novo synthesised RNA-purine nucleotides, even in the presence of exogenous nucleotides. However, the addition of interleukin-1β to the culture medium led to an enhanced salvage of preformed pyrimidine nucleotides for nucleic acid synthesis when glutamine was present in the medium at a concentration of 0.5 mmol/L. Received: 10 December 1998, Accepted: 8 March 2000     

黄绿青霉素对人血管内皮细胞凋亡和DNA损伤的作用

目的:观察黄绿青霉素(CIT)对血管内皮细胞凋亡和DNA损伤的作用.方法:体外原代培养人脐静脉内皮细胞,给予浓度分别为1umo1/L、2umol/L、5upmol/L、1Oumol/L的CIT毒素,处理时间为48h.光镜观察细胞生长形态,MMT法检测细胞活性,流式细胞仪检测细胞凋亡情况,单细胞凝胶电泳法分析CIT对内皮...     

芍药苷对过氧化氢损伤的人脐静脉内皮细胞的 保护作用

摘要:目的　探讨芍药苷对过氧化氢（H2O2）诱导人脐静脉血管内皮细胞（HUVEC）损伤的保护作用。方法　体外培养HUVEC,以200 μmol/L H2O2诱导人脐静脉血管内皮细胞损伤建立模型,同时以100、200、400 μmol/L的芍药苷分别干预,显微镜下观察细胞形态,用噻唑蓝（MTT）法检测HUVEC活力,微板法检测上清液中乳酸脱氢酶（LDH）的活性及一氧化氮（NO）的含量,酶联免疫吸附法（ELISA）法检测内皮素-1（ET-1）、组织型纤溶酶原激活物（tPA）、纤溶酶原激活物抑制因子（PAI-1）的含量。结果　与模型组比较,芍药苷中、高剂量组细胞活力显著升高,LDH活性显著减低、ET-1和PAI-1含量显著减少,NO和tPA显著升高（P＜0.05或P＜0.01）。结论　芍药苷对H2O2诱导的HUVEC损伤具有明显的保护作用。     

Dietary flavonoids protect human colonocyte DNA from oxidative attack in vitro

Summary Background & Aims: Epidemiological studies suggest that antioxidant polyphenols in the human diet may protect against diseases such as cancer. In this study we investigated the cytoprotective potential of the flavonoids, quercetin, myricetin, kaempferol and rutin against oxidative DNA damage in human colonocytes in vitro. Methods: Caco-2 cells, which display specialised enterocyte/colonocyte cell functions, were used as an in vitro model for human colonocytes. Hydrogen peroxide was employed as the oxidant. DNA damage (strand breakage, oxidised purines and oxidised pyrimidines) was determined using the alkaline single cell gel electrophoresis or comet assay. Cell growth and viability were measured. Results: Hydrogen peroxide caused a dose-dependent increase in DNA strand breakage in human colonocytes, presumably via oxygen free radical generation. Quercetin and myricetin protected Caco-2 cells against oxidative attack. In addition, quercetin decreased hydrogen peroxide-mediated inhibition of growth. Neither rutin nor kaempferol was effective. However, quercetin, while inhibiting DNA strand breakage, did not alter the levels of oxidised bases following peroxide treatment. The antifungal agent ketoconazole, prevented quercetin cytoprotection in Caco-2 cells, indicating that P450-mediated metabolism may alter the efficacy of the flavonoids against oxidative DNA damage. Conclusion: Flavonoids, particularly quercetin, the most abundant flavonoid in the human diet, are likely to be important in defending human colonocytes from oxidative attack. Received: 7 October 1998, Accepted: 5 November 1998     

人脐静脉内皮细胞的培养与鉴定

对血管内皮细胞体外培养的常规方法进行了改进 ,采用胰蛋白酶 胶原酶 (1∶1)混合酶液消化方式分离人脐静脉内皮细胞 ,简化完全培养液的组成成分 (不添加血管内皮细胞生长因子、肝素等辅助因子 ) ,机械刮擦法分离单层细胞进行传代培养。培养细胞用形态学、超微形态学和免疫组织化学染色法进行鉴定 ,证实培养的细胞是血管内皮细胞。     

Recovery of human lymphocytes from oxidative DNA damage; the apparent enhancement of DNA repair by carotenoids is probably simply an antioxidant effect

Summary Background: Many epidemiological studies have identified a protection against cancer associated with consumption of fruit and vegetables. One factor is this protection may be the enhancement of cellular DNA repair activity by micronutrients, such as carotenoids, found in these foods. Aims of the study: To measure the capacity of lymphocytes isolated from volunteers supplemented with β-carotene, lutein or lycopene to recover from DNA damage induced in vivo by treatment with H₂O₂. Methods: Healthy volunteers were given supplements of lutein (15 mg/day), lycopene (15 mg/day) and βcarotene (15 mg/day), each for 1 week, the supplementation periods being separated by 3-week wash-out periods. Blood samples were taken at the beginning and end of each supplementation, and at 1 week and 3 weeks during the wash-out period. Carotenoid levels were measured in plasma. Lymphocytes were isolated and frozen. Subsequently, they were treated with 100 μM H₂O₂ and incubated for up to 24 h; DNA damage was measured with the comet assay (single cell gel electrophoresis) after 0, 2, 4, 8, and 24 h. Results: Increases of 2- to 3-fold in mean plasma lutein and β-carotene concentrations were seen at the end of the respective supplementation periods; they returned virtually to basal levels after wash-out. Lycopene concentrations were less affected by supplementation, and were more variable. H₂O₂-induced DNA strand breaks were apparently only slowly rejoined by the lymphocytes. The rejoining of breaks in the first few hours appeared substantially faster in lymphocytes following supplementation with β-carotene, but no such effect was seen with lutein. In those individuals who showed increases in lycopene concentrations, the recovery was significantly faster. Lymphocytes that were not treated with H₂O₂ showed a transient increase in DNA breakage to about double the background level in 2 h, presumably as a result of exposure to atmospheric oxygen; this effect, too, was relieved by supplementation with lycopene or β-carotene. Conclusions: While certain carotenoids appear to enhance recovery from oxidative damage, this is probably in fact an antioxidant protective effect against additional damage induced by atmospheric oxygen, rather than a stimulation of DNA repair. Received: 6 December 1999, Accepted: 22 March 2000     

Dietary supplementation with different vitamin C doses: no effect on oxidative DNA damage in healthy people

Summary Background Antioxidants are believed to prevent many types of disease. Some previous studies suggest that dietary supplementation with vitamin C results in a decrease in the level of one of the markers of oxidative damage—8-oxoguanine in the DNA of peripheral blood mononuclear cells (PBMC). Aim of trial To investigate the effect of different dose levels of dietary supplementation with vitamin C on oxidative DNA damage. Methods A randomised double–blind placebo–controlled trial was carried out using three different levels (80, 200 and 400 mg) of dietary vitamin C supplementation in a healthy population of 160 volunteers; supplementation was for a period of 15 weeks followed by a 10 week washout period. Peripheral blood samples were obtained every 5 weeks from baseline to 25 weeks. Results An increase in PBMC vitamin C levels was not observed following supplementation in healthy volunteers. There was no effect found on 8–oxoguanine measured using HPLC with electrochemical detection for any of the three supplemented groups compared to placebo. 8–oxoadenine levels were below the limit of detection of the HPLC system used here. Conclusions Supplementation with vitamin C had little effect on cellular levels in this group of healthy individuals, suggesting their diets were replete in vitamin C. The dose range of vitamin C used did not affect oxidative damage in PBMC DNA.     

维生素E对体外氧化低密度脂蛋白诱导血管内皮细胞损伤的保护作用

为探讨维生素E(VE)对体外氧化低密度脂蛋白 (ox LDL)所致血管内皮细胞 (VEC)氧化损伤的保护作用。利用体外培养人脐静脉血管内皮细胞 ,建立了氧化损伤模型。将细胞分为 5组 :对照组、ox LDL组、VE L +ox LDL组 ,VE M +ox LDL组和VE H +ox LDL组。各剂量组首先在含有不同浓度的VE培养液中孵育 ,2 4小时后加入ox LDL进行氧化损伤 ,继续培养 2 4小时后收集细胞 ,进行有关指标测定。结果显示 ,ox LDL组MDA含量高于对照组和各VE组 (P <0 0 5) ;ox LDL组SOD活性低于对照组和各VE组 (P <0 0 5) ;ox LDL组、VE L +ox LDL组GSH Px活性低于其它各组 (P <0 0 5)。提示维生素E对ox LDL诱导的血管内皮细胞损伤有一定的保护作用     

The controversial efficacy of vitamin E for human male infertility

Vitamin E (VE) is major lipophilic chain-breaking antioxidant which protects tissue polyunsaturated fatty acids (PUFA) against peroxidation, a property that could be beneficial in the male reproductive physiology because the membranes of germ cells and spermatozoa are very sensitive to oxidation because of their high content of PUFA. Some of the available data on the efficacy of VE as an oral drug for male infertility or as an additive during in vitro manipulations of spermatozoa were reviewed here, observing that they are often contradictory, possibly because: (1) antioxidant therapy could be ineffective in certain studies not concentrated on men in whom oxidative stress is implicated as an infertility factor, and (2) the VE antioxidant therapy is a double-edged sword strictly depending on the dosage or the in vitro concentration of the vitamin. Thus, further laboratory and clinical studies with better-defined experimental conditions should be performed to establish the in vitro and in vivo efficacy of VE for human male infertility.     

大剂量维生素C、维生素E对高原肺心病急性发作期患者脂质过氧化损伤的保护作用研究

目的探讨大剂量维生素C、维生素E对高原肺心病急性发作期患者脂质过氧化损伤的保护作用。方法选择高原肺心病急性发作期患者126例,分为观察组和对照组,对照组患者应用常规治疗,观察组患者在此基础上应用VitC150～250mg/(kg.d)静脉滴注,VitE100～200mg/d口服,10d为1疗程。结果①观察组患者治疗显效38例,有效22例,无效4例,有效率93.75%。对照组患者治疗显效34例,有效16例,无效12例,有效率80.65%。观察组患者治疗有效率显著高于对照组(P﹤0.05)。②治疗后,两组患者血P-LPO水平均显著降低,P-β-CAR、WB-GSH、E-SOD及E-CAT均显著升高,与治疗前相比差异有统计学意义(P﹤0.05)。治疗后,观察组患者血P-β-CAR、WB-GSH、E-SOD及E-CAT水平均显著高于对照组(P﹤0.05)。结论大剂量维生素C、维生素E对高原肺心病急性发作期患者脂质过氧化损伤具有较好的保护作用。     

Addition of vitamin E to long-chain polyunsaturated fatty acid-enriched diets protects neonatal tissue lipids against peroxidation in rats

Summary Background: Tissue 10:4(n-6) and 22:6(n-3) status have been correlated with neonatal development and growth. Artificial formulas for neonates have been supplemented with long chain polyunsaturated fatty acids (LCP) from animal and marine sources which may enhance sensitivity of cellular membranes to oxidative damage. Diet-derived antioxidants like vitamin E play a key role in the protection of tissue lipids against oxidation. Aim of the study: We seek to determine the influence of dietary vitamin E on tissue sensitivity to oxidative stress in rats fed for 4 weeks on diets enriched in (n-3) and (n-6) long-chain polyunsaturated fatty acids. Methods: Weanling rats received 10% fat diets that provided 18:1(n-9), 18:2(n-6) and 18:3(n-3) in a similar ratio to that of rat milk (group A), supplemented with fish oil (groups B and B+E) and supplemented with (n-6) and (n-3) LCP from an animal phospholipid concentrate (groups C and C+E). Vitamin E (500 mg vitamin E/kg fat) was added to diets B+E and C+E. Tissue fatty acid content and the activities of catalase, superoxide dismutase, glutathione transferase und glutathione peroxidase in liver and brain were measured. Glutathione status, vitamin E and the production of thiobarbituric acid reactive substances (TBARs) after incubation of erythrocyte, liver and brain lipids with inducers of enzymatic or non-enzymatic lipid peroxidation was measured. Results: Group B registered significantly lower total superoxide dismutase acitvity than group B+. Catalase activity was significantly higher in group C than in group C+E. Hepatic total and reduced glutathione levels were decreased in vitamin E supplemented groups compared to unsupplemented ones. TBARs production in erythrocyte lipids was significantly higher in groups B and C compared to vitamin E supplemented groups B+E and C+E. Conclusions: This study shows that the addition of vitamin E protected erythrocyte and liver microsome lipids enriched in (n-3) and (n-6) LCP from lipid peroxidation during the postnatal development of rats. The protection was more effectively in group C+E than in group B+E. Received: 14 January 1999, Accepted: 14 June 1999     

氧化修饰低密度脂蛋白对血管内皮细胞氧化损伤的研究

目的　用氧化修饰低密度脂蛋白 (OX LDL)建立对血管内皮细胞的氧化损伤模型。方法　将人脐静脉内皮细胞暴露于OX LDL环境下 ,测定细胞活力及丙二醛含量。结果　当内皮细胞暴露于OX LDL不同剂量组 (10、5 0、10 0 μg ml) 2 4h后 ,其细胞活力显著降低 ,丙二醛含量增加 ,特别是OX LDL高浓度组最为明显。结论　OX LDL对内皮细胞有明显损伤作用 ,能促发动脉粥样硬化的形成。     

维生素C对缺氧诱导人滋养细胞凋亡的影响研究

目的:探讨外源性维生素C对缺氧诱导人滋养细胞凋亡的影响。方法:行实施人早孕期滋养细胞株TEV-1培养,经95%氮气处理30 min,行递增浓度的维生素C(0、1、5、50 ng/ml)继续孵育24 h后,各组细胞均应用噻唑兰(MTT)比色法、流式细胞术(FCM)法检测细胞增殖指数、凋亡率,同时利用黄嘌呤氧化酶法测定各组细胞超氧化物歧化酶(SOD)活性变化。结果:滋养细胞经缺氧诱导30 min后,与对照组相比,添加不同浓度组(1、5及50 ng/ml)维生素C对其增殖行为无明显影响。但维生素C具有增强滋养细胞SOD活性,减弱其凋亡程度的作用(P<0.05)。结论:维生素C能明显提高缺氧损伤滋养细胞的抗氧化能力,可能参与了妊娠的病理生理过程。     

自然流产者绒毛织中维生素A、E含量及流产影响因素分析

目的 了解孕早期妇女的自然流产状况与维生素A、E营养状况的关系,为指导孕妇健康膳食提供科学依据.方法 于2010年10月～2011年4月在广州市收集进行流产刮宫术的孕妇绒毛组织共258例(自然流产组63例,对照组195例).对研究对象进行问卷调查及24h膳食调查,并采用高效液相色谱法检测绒毛组织中的维生素A、E含量.结果 自然流产组与对照组的比较中,年龄、体质指数、婚姻状况、流产史、孕周的差异均具有统计学意义(均有P＜0.05);多因素Logistic回归分析显示,自然流产的危险因素为年龄(与≤22岁相比,23～岁组:OR=3.903,95％CI:1.533～9.937;≥29岁组:OR=2.896,95％CI:1.116 ～7.519)、流产史(OR=2.174,95％ CI:1.105 ～4.278)和孕周≥8周(OR=3.532,95％CI:1.813 ～6.883).自然流产组能量、蛋白质、脂肪、碳水化合物、维生素A、维生素E的摄入量与对照组比较,差异也无统计学意义.自然流产组绒毛组织中维生素A、E含量与对照组的比较,差异均无统计学意义(均有P＞0.05).结论 年龄、流产史是自然流产的危险因素;未见自然流产者膳食维生素A、E摄入量及绒毛组织中维生素A、E含量增加.     

Hyperhomocysteinemia,and low intakes of folic acid and vitamin B12 in urban North India

Summary Background and Aim An adverse coronary risk profile has been reported amongst rural-to-urban migrant population living in urban slums undergoing stressful socio-economic transition. These individuals are likely to have low intakes of folic acid and vitamin B12, which may have an adverse impact on serum levels of homocysteine (Hcy). To test this hypothesis, we studied serum levels of Hcy in subjects living in an urban slum of North India and healthy subjects from urban non-slum area. Methods Group I consisted of 46 subjects (22 males and 24 females) living in an urban slum, while group II consisted of healthy subjects (n = 26, 13 males and 13 females) living in the adjacent non-slum area. Anthropometric measurements, biochemical profile (fasting blood glucose, total cholesterol, serum triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol) and fasting serum levels of Hcy were measured. Dietary intakes of folic acid, vitamin B12, vitamin B1, and iron were calculated by the 24-hour dietary recall method. Serum levels of Hcy were correlated with dietary intakes of nutrients, anthropometry, and metabolic variables. Results Sex-adjusted serum levels of Hcy in mmol/L (Mean ± SD) were high, though statistically comparable, in both the groups (group I: 20.8 ± 5.9 and group II: 23.2 ± 5.9). Overall, higher than normal serum levels of Hcy (> 15 μmol/L) were recorded in 84 % of the subjects. A substantial proportion of subjects in both groups had daily nutrient intakes below that recommended for the Asian Indian population (folic acid: 93.4 % in group I and 96.7 % in group II, vitamin B12: 76.1 % in group I and 88.4 % in group II). However, between the two groups, average daily dietary intakes of both the nutrients were statistically comparable. As compared to non-vegetarians, vegetarians showed lower intakes of folic acid (p < 0.01) and vitamin B12 (p < 0.01) in both groups. On multivariate linear regression analysis with serum Hcy as the response variable and vegetarian/non-vegetarian status and sex (male/female) as predictor variables, higher serum levels of Hcy were observed in vegetarians vs non-vegetarians (β = 4.6, p < 0.05) and males vs females (β = 5.3, p < 0.01). Conclusions Low intakes of folic acid and vitamin B12, and hyperhomocysteinemia, in both the healthy population living in urban slums and adjacent urban non-slum areas, are important observations for the prevention of nutritional and cardiovascular diseases in the Indian subcontinent. Received: 30 October 2001, Accepted: 14 January 2002