Vitamins in human arteriosclerosis with emphasis on vitamin C and vitamin E

INTRODUCTION: This review focuses on the process of arteriosclerosis arising from oxidative stress on lipoproteins and the general failure of randomized human trials using vitamins to retard this process. REVIEW: As well as clinical trials, the paper reviews the mechanisms by which a variety of oxidants act. Antioxidants are discussed, emphasizing interactions of vitamins C and E with transition metals that can lead to prooxidation. There is a focus on interactions between supplemental or co-antioxidants that counterbalance prooxidant effects of one another. CONCLUSIONS: It is concluded that normal cellular supplementation mechanisms are poorly accessible in the arteriosclerotic plaque leading to a prooxidant environment in which the haphazard introduction of vitamins could potentially be hazardous. Continued investigations into basic and clinical redox interactions of the kind discussed in this review using new measuring techniques may lead to approaches whereby antioxidants can be introduced into tissue in controlled ways for reducing arteriosclerosis.     

Simultaneous liquid-chromatographic determination of vitamin K1 and vitamin E in serum

We describe a high-performance liquid chromatographic procedure for the simultaneous measurement of vitamins K1 and E in human serum. Delipidated human serum (free of vitamins K1 and E) was used to make standard solutions of these vitamins, and cetyl naphthoate and alpha-tocopheryl acetate were the internal standards for vitamin K1 and vitamin E, respectively. A simple, novel separation method utilizing liquid-liquid partition chromatography was used as a preparative "clean-up" procedure. Cetyl naphthoate and vitamin K1 (after post-column reduction) were detected by fluorescence, alpha-tocopheryl acetate and vitamin E by ultraviolet absorption. Sensitivity (detection limit) of the assay was 30 pg for vitamin K1 and 5 ng for vitamin E per injection. The method is specific, precise, and more rapid than previously described procedures. Within- and between-assay CVs were 8.1% and 12.9%, respectively, for vitamin K1; 3.5% and 6.0%, respectively, for vitamin E. Analytical recoveries of vitamins K1 and E were 80% and 93%, respectively, from serum and from delipidated serum (standards). The average neonatal serum concentration of vitamin K1 was 83 ng/L, 2.5 mg/L for vitamin E; for normolipidemic adults, the values were 343 ng/L and 7.9 mg/L, respectively, and for hyperlipidemic adults, 541 ng/L and 11.1 mg/L, respectively.     

The physiology of vitamin K nutriture and vitamin K-dependent protein function in atherosclerosis.

Recent advances in the discovery of new functions for vitamin K-dependent (VKD) proteins and in defining vitamin K nutriture have led to a substantial revision in our understanding of vitamin K physiology. The only unequivocal function for vitamin K is as a cofactor for the carboxylation of VKD proteins which renders them active. While vitamin K was originally associated only with hepatic VKD proteins that participate in hemostasis, VKD proteins are now known to be present in virtually every tissue and to be important to bone mineralization, arterial calcification, apoptosis, phagocytosis, growth control, chemotaxis, and signal transduction. The development of improved methods for analyzing vitamin K has shed considerable insight into the relative importance of different vitamin K forms in the diet and their contribution to hepatic vs. non-hepatic tissue. New assays that measure the extent of carboxylation in VKD proteins have revealed that while the current recommended daily allowance for vitamin K is sufficient for maintaining functional hemostasis, the undercarboxylation of at least one non-hemostatic protein is frequently observed in the general population. The advances in defining VKD protein function and vitamin K nutriture are described, as is the potential impact of VKD proteins on atherosclerosis. Many of the VKD proteins contribute to atherogenesis. Recent studies suggest involvement in arterial calcification, which may be influenced by dietary levels of vitamin K and by anticoagulant drugs such as warfarin that antagonize vitamin K action.     

维生素D及其受体在强直性脊柱炎患者中的表达及其临床意义

目的：研究As患者PBMC维生素D受体（VDR）mRNA的表达及血清25-羟维生素D,和1,25-二羟维生素D3的水平,探讨其与AS疾病活动性（BASDAI、CRP、ESR）的相关性。方法：选取26例AS患者（As组）和年龄、性别与之相匹配的13名健康志愿者（健康对照组）。采用SYBRGreenI实时荧光定量PCR检测两组受检者PBMC的VDRmRNA表达水平,应用ELISA法检测两组受检者血清25-羟维生素D3和1,25-二羟维生素D3水平,分析VDRmRNA表达水平、血清25-羟维生素D3和1,25-二羟维生素D3水平与临床相关指标（BASDAI、CRP、ESR）的关系。结果：As患者PBMC的VDRmRNA表达水平明显高于健康对照组（P〈0．01）,VDRmRNA表达水平与临床相关指标（BASDAI、CRP、ESR）无关（P〉0．05）。AS患者血清25．羟维生素D3、1,25-二羟维生素D3水平分别为（5．3±2．6）μg／L、（12．8±6．0）ng／L,明显低于健康对照组（14．7±3．5）μg/L、（32．6±18．5）ng／L（P均〈0．01）。AS患者血清1,25-二羟维生素D3的水平与BASDAI（r=-0．481,P〈0．05）、ESR（r=-0．535,P〈0．01）、CRP（r=-0．674,P〈0．01）均呈负相关。血清25-羟维生素D,水平与BASDAI、CRP、ESR无关（P〉0．05）。结论：As患者VDRmRNA表达水平升高,但与As的疾病活动无关。As患者血清1,25-二羟维生素D3水平下降,与疾病活动呈负相关,可作为AS疾病活动的指标之一。AS患者PBMC的VDR活化可能与1,25-二羟维生素D,的作用无关。     

Role of vitamin D-dependent and vitamin D-independent mechanisms in absorption of food calcium.

We measured net calcium absorption and the calcium content of the digestive glands secretions in people with widely different serum concentrations of 1,25 dihydroxy vitamin D (hereafter referred to a 1,25-D). Patients with end stage renal disease on hemodialysis served as a model of human 1,25-D deficiency; they were also studied when they had abnormally high serum 1,25-D concentrations as a result of short periods of treatment with exogenous 1,25-D. Normal subjects were studied for comparison. The amount of calcium secreted into the duodenum by the digestive glands was found to be trivial compared to the calcium content of normal or even low calcium meals; therefore, values for net and true net calcium absorption differed only slightly. There was a linear correlation between true net calcium absorption and serum 1,25-D concentration. By extrapolating the short distance to a zero value for serum 1,25-D, D-independent true net calcium absorption was estimated. By subtracting D independent from true net calcium absorption, values for D-dependent absorption were obtained. For a given level of meal calcium intake, D-dependent calcium absorption was found to be directly proportional to serum 1,25-D concentration. At any given value for serum 1,25-D, absorption via the D-dependent mechanism was approximately the same with a low (120 mg) calcium meal as it was when meal calcium intake was increased to 300 mg. We interpret this to mean that the D-dependent mechanism is saturated or nearly saturated by low calcium meals. The D-independent absorption/secretion mechanism resulted in secretion (a loss of body calcium in the feces) when intake was low (120 mg per meal) and absorption when intake was normal. All of the increment in calcium absorption that occurs when low or normal calcium meals are supplemented with extra calcium is mediated by the D-independent mechanism.     

维生素C在脓毒症中的应用进展

脓毒症是重症患者发病和死亡的主要原因。由于氧化应激时代谢消耗增加以及脱氢抗坏血酸再循环减少等原因,脓毒症患者常合并维生素C减少或缺乏。外源性补充维生素C,可能是脓毒症有效的辅助治疗措施。本文就维生素C在脓毒症中应用的作用机制、用法用量、潜在副作用、联合疗法及目前开展的临床研究等方面进行综述,旨在深化临床医师对维生素C在脓毒症治疗中的作用的认识。     

维生素D及其受体与毛发的关系

背景：越来越多的研究发现,维生素D及其受体与毛发有一定关系。目的：全面阐述维生素D及其受体与毛囊干细胞、毛发生长周期、信号转导以及脱发性疾病等的关系。方法：应用计算机以＂维生素D、维生素D受体、毛发、脱发、基因多态性＂或＂vitamin D,vitamin D receptor,hair,alopecia,gene polymorphism＂为检索词检索PubMed和CNKI数据库1990/2011-11发表的关于维生素D及其受体与毛发关系的文章,同一领域选择近期发表或发表在权威杂志上的文章。结果与结论：初检得到152篇文献,根据纳入排除标准选择30篇文章进行综述。目前研究显示,维生素D及其受体在毛发中扮演重要角色,其异常可导致脱发等疾病的产生,为预防和治疗脱发性疾病提供新的可能,并有望在未来广泛应用。     

Plasma vitamin D-binding globulin in vitamin D deficiency, pregnancy and chronic liver disease.

Plasma concentrations of vitamin D-binding globulin were measured by radial immunodiffusion in healthy subjects, pregnancy, and during oestrogen therapy. Subjects with disorders of vitamin D metabolism (dietary deficiency, malabsorption, anticonvulsant therapy, chronic liver disease) were also studied. Neither sex nor age influenced the plasma vitamin D-binding globulin concentration in healthy subjects, but there was a significant increase in concentration during pregnancy and oestrogen therapy. Elevated levels were found in vitamin D deficient elderly but not younger subjects, while levels in subjects with chronic liver disease were significantly reduced. Normal levels of vitamin D-binding globulin were present in hypervitaminosis D and no vitamin D-binding globulin was detected in human milk. No correlation was observed between plasma 25-hydroxycholecalciferol levels and plasma vitamin D-binding globulin concentrations.