维生素B_(12)片含量测定方法的改进

本实验采用避光条件下用水洗[1]去糖衣,在避光条件下自然干燥后,按《国家药品标准》维生素B12片测定含量的方法,对不同厂家5批的维生素B12片含量测定结果进行了t检验,P>0.05,结果表明此方法可用于维生素B12片的含量测定。     

耳穴压豆配合眼部直流电控维生素B_(12)导入治疗视疲劳

目的探讨耳穴压豆配合眼部直流电控维生素B12导入治疗视疲劳的疗效。方法将120例患者随机分为治疗组和对照组各60例。对照组在避免一切刺激因素,矫正屈光不正,注意饮食及用眼卫生,锻炼身体,治疗全身其它慢性病,借以提高机体素质的基础上给予珍珠明目滴眼液4次/d点双眼,口服复合维生素B片,2片/次,3次/d。治疗组在此基础上耳穴压豆配合电控维生素B12导入,1次/d。7d为一疗程,治疗2个疗程后,通过统计学分析两组病例的有效率。结果观察组治愈率40.0%,有效率94.0%;对照组治愈率38.3%,有效率75.0%。两组比较差异有显著性意义(P<0.05)。应用耳穴压豆配合电控维生素B12导入治疗视疲劳的有效率明显优于对照组。结论应用耳穴压豆配合电控维生素B12导入治疗视疲劳的疗效显著。     

妊娠妇女在不同孕期血清铁蛋白、叶酸和维生素B_(12)的检测及临床意义

目的检测妇女妊娠期血清铁蛋白、叶酸和维生素B12的含量,为预防和治疗妊娠贫血提供实验依据。方法用化学发光免疫分析方法检测妊娠妇女血清铁蛋白、叶酸和维生素B12的含量。结果血清铁蛋白、叶酸和维生素B12的含量随孕期增长而降低,早孕妇女与正常对照组比较,铁蛋白和叶酸明显低于对照组(P<0.05),维生素B12无统计学意义(P>0.05);中、晚孕期妇女血清铁蛋白、叶酸和维生素B12的含量与正常对照组比较,铁蛋白、叶酸和维生素B12均显著低于对照组(P<0.01)。结论测定妇女妊娠期血清铁蛋白、叶酸和维生素B12的含量,可以鉴别妇女妊娠期贫血的原因,预防和治疗孕妇贫血,并保障胎儿的正常生长发育。     

维生素B_2(核黄素)缺乏症(口角炎)与补充

1维生素B2 的由来中国营养学会近来公布的一项有关国民营养调查的结果显示 ,在国人最为缺乏的营养素排序中 ,维生素A(β-胡萝卜素)、维生素B2(核黄素)和钙剂分列前3名 ,其次为维生素C(抗坏血酸)、维生素B1(硫胺)和维生素B6(吡多辛)。儿童缺锌、妇女缺铁、中老年人缺乏维生素的状况较为严重。天然的维生素B2 存在于酵母、肝肾及肉类中 ,能参与人体正常的生物氧化过程 ,是一种主要用于治疗粘膜及皮肤炎症的水溶性维生素。1920年 ,伊迈特首次从酵母的提取液中发现了维生素B2。仅隔了12年 ,瓦瓦格又从酵母中提取得到了一种黄色酵素 ,后证明…     

维生素B1片专属性鉴别方法探究

目的:建立维生素B1片TLC鉴别方法.方法:以醋酸乙酯-甲醇-浓氨溶液(10:2:3)为展开剂,展开.结果:所得薄层色谱分离效果好.结论:该方法简便易行,可用于维生素B1片的鉴别.     

血清维生素B_(12)浓度与脑梗死的关系

目的探讨血清维生素B12浓度水平与脑梗死的关系及其临床意义。方法采用电化学发光免疫分析技术测定400例脑梗死患者和400例健康人血清维生素B12的水平。结果脑梗死患者血清维生素B12水平明显低于对照组(P<0.01)。并且若患者脑梗死病变程度越重,其血清中维生素B12水平则越低。重型与中型、重型与轻型脑梗死患者之间血清中维生素B12水平差别均有显著性统计学意义(P<0.01),中型与轻型的患者之间维生素B12水平差别无统计学意义(P>0.05)。结论血清维生素B12水平降低与脑梗死的发生有一定的相关性,应该予以监测。     

叶酸联合维生素B_(12)对高血压合并脑卒中伴轻度认知障碍患者相关指标的影响

目的:探讨叶酸联合维生素B12对高血压合并脑卒中伴轻度认知障碍患者相关指标的影响。方法:选择高血压合并脑卒中伴轻度认知障碍患者80例为观察组,另选择20名健康自愿者为健康对照组。观察组患者给予加强型匀浆膳300~500 ml,口服,每日3次+叶酸片5 mg,口服,每日3次+维生素B12片25μg,口服,每日3次。连续用药2个月,不能自行服用者鼻饲给予。观察所有患者治疗前后简易精神状态量表(MMSE)评分、叶酸、维生素B12、Hcy水平,并与健康对照组进行比较,记录所有患者的不良反应发生情况。结果:治疗后,观察组患者MMSE评分、叶酸、维生素B12水平均显著高于同组治疗前,但低于健康对照组;Hcy显著低于同组治疗前,但高于健康对照组,差异均有统计学意义(P<0.05)。观察组患者不良反应发生率为5.00%,均未见严重不良反应发生。结论:叶酸联合维生素B12可降低高血压合并脑卒中伴轻度认知障碍患者的认知障碍程度与Hcy水平,安全性较好。     

流动注射化学发光测维生素B_(12)

本文用镀锌粒作成还原柱在线还原维生素 B_(12),使其催化 H_2O_2氧化 Luminol 产生化学发光,实现 V_(B12)在线检测。方法的检出限为3.1×10~(-10)g/ml,RSD=2.0%(n=7,C=1×10~(-7)g/ml)。用于针剂、片剂 V_(B12)测定,结果满意。     

维生素B12片含量测定方法的改进

本实验采用避光条件下用水洗^[1]去糖衣，在避光条件下自然干燥后，按《国家药品标准》维生素B12片测定含量的方法，对不同厂家5批的维生素B12片含量测定结果进行了t检验，P〉0．05，结果表明此方法可用于维生素B12片的含量测定。     

维酶素片质量标准探讨

维酶素片是以黄豆渣为原料，经阿氏假囊酵母菌生物发酵后精制而成的一种复方制剂。其主要成份为维生素B2、维生素E和多种氨基酸。现行标准是《国家药品标准化学药品地方标准上升国家标准第九册》。该标准[性状]描述：本品为糖衣片，除去糖衣后显黄色或棕黄色。[鉴别]（1）是维生素B。的颜色反应；[鉴别]（2）是氨基酸的颜色反应。[含量测定]只对维生素B：的含量做了限定。但我们在2004年抽验了4个厂家的5批维酶素片。经检验发现，无论是从性状还是鉴别上都有很大差别，结果见表1：     

HPLC法测定复合维生素B片维生素B1、维生素B2、烟酰胺的含量及含量均匀度

目的：建立高效液相色谱法测定复合维生素B片维生素B1、维生素B2、烟酰胺的含量及含量均匀度。方法采用色谱柱：Diamonsil C18（250mm ×4.6mm,5μm）,流动相：0.005mol· L －1庚烷磺酸钠溶液（含0.5％冰醋酸和0.05％三乙胺）-甲醇（70∶30,V／V）;检测波长为261nm,流速为1.0mL· min －1,进样量：20μL。结果维生素 B1、维生素 B2、烟酰胺浓度分别在2.65～66.2μg· mL －1、1.19～30.15μg· mL－1、7.83～196.2μg· mL －1范围内与峰面积线性关系良好,平均回收率均大于98％,RSD均小于1.0％。结论本方法简单、精确、可靠,可作为合维生素B片的质量控制方法。     

血浆同型半胱氨酸与脑分水岭梗死的关系探讨

目的 探讨同型半胱氨酸(Hcy)与脑分水岭梗死(CWI)的关系.方法 58例CWI患者(观察组)和56例健康者(对照组),采用荧光偏振免疫分析法检测两组及CWI各亚组的Hcy、叶酸和维生素B12水平.结果 CWI患者Hcy水平明显高于对照组,维生素B12及叶酸水平则明显低于对照组,差异均有统计学意义(t=2.013、2.842、3.051,均P＜0.05);CWI患者不同亚组之间血浆Hcy、叶酸和维生素B12水平差异均无统计学意义(均P＞0.05).结论 高血浆Hcy可能是CWI发生的重要原因之一.     

早产儿血清铁蛋白和叶酸与维生素B12水平的变化及其临床意义

目的 探讨早产儿血清铁蛋白、叶酸、维生素B12(贫血3项)的变化情况,以便及早采取干预措施,预防和治疗早产儿贫血.方法 完全随机选取住院的早产儿30例作为观察组,正常新生儿30例为对照组.采用电发光分析仪,分别对2组对象进行贫血3项检测和比较.结果 早产儿出生时血清铁蛋白为(159.2±83.2)μg/L,低于对照组的(334.4±150.5)μg/L,差异有统计学意义(P＜0.05);维生素B12(383.5±236.4)ng/L与对照组(502.4±168.8)ng/L比较差异亦有统计学意义(P＜0.01).2周后检测,早产儿叶酸与出生时比较有明显下降[(17.1±2.2)μg/L比(13.1±3.9)μg/L,P＜0.01],维生素B12(248.8±205.4)ng/L也有明显下降(P＜0.05);红细胞总数、血红蛋白以及红细胞平均压积亦明显下降(P＜0.05).结论 早产儿出生后体内血清铁蛋白和维生素B12处于低水平;叶酸、维生素B12水平随着日龄的增加逐渐减低.

Abstract：

Objective To investigate the level changes of serum ferritin, folacin and vitamin B12 in prematurity. Methods Thirty prematurities and 30 healthy newborn babies were were enrolled in this study. Serum ferritin, folacin and vitamin B12 were measured by using electroluminescence analyzer. Results The serum ferritin and vitamin B12 of prematurity were lower than those of normal newborn babies [( 159.2 ± 83.2) μg/L vs (334.4 ±150.5 ) μg/L, P ＜ 0.05; ( 383.5 ± 236.4 ) ng/L vs (502.4 ± 168.8 ) ng/L, P ＜ 0. 01]. Serum ferritin and vitamin B12 of prematurity decreased after 2 weeks[(17. 1 ±2.2)μg/L vs (13.1 ±3.9) μg/L, P＜0.01;(383.5 ±236.4)ng/L vs (248.8 ±205.4)ng/L, P ＜0.05]. Conclusions After birth, serum ferritin and vitamin B12 of prematurity are at a low level. Folacin and vitamin Bi2 decrease with the increase of age.     

Long-term use of proton pump inhibitors and vitamin B12 status in elderly individuals

Background  Some studies have shown that short-term use of proton pump inhibitors decreases the absorption of vitamin B12, but the results of studies into long-term proton pump inhibitor use and vitamin B12 deficiency are inconsistent.
Aim  To investigate whether long-term proton pump inhibitor use is associated with an abnormal vitamin B12 status in elderly individuals.
Methods  One hundred and twenty-five long-term (>3, years) proton pump inhibitor users aged 65, years and above were recruited from general practices. Their 125 partners (who did not use proton pump inhibitors) served as the reference group. Vitamin B12 status was determined by serum levels of vitamin B12 and homocysteine, and mean corpuscular volume.
Results  No differences in mean vitamin B12 levels were observed between the long-term proton pump inhibitor users and their partners [345 (s.d. 126), p m vs. 339 (s.d. 133), p m , P, = , 0.73], even after adjustment for age, gender, Helicobacter pylori status and C-reactive protein levels ( P, = , 0.87). Four proton pump inhibitor users and three partners had vitamin B12 levels <150, p m (3% vs. 2%, P, = , 1.00). No differences between the groups were observed in homocysteine levels and mean corpuscular volume.
Conclusions  No association between long-term proton pump inhibitor use and vitamin B12 status was observed. Regular testing for low vitamin B12 levels in elderly patients on long-term treatment with proton pump inhibitors is therefore not recommended.     

维生素B12与腔隙性脑梗塞后抑郁的关联研究

目的 探讨血清维生素B12与腔隙性脑梗塞后抑郁之间关系。方法 2009年6月—2012年6月腔隙性脑梗塞患者共829例,使用汉密尔顿抑郁量表将患者分为两组：无抑郁组和抑郁组,比较两组间血清维生素B12浓度和维生素B12缺乏者的比例。在抑郁组内对汉密尔顿抑郁量表评分和血清维生素B12浓度进行曲线拟合。结果 无抑郁组患者750例,血清维生素B12平均浓度为(172.5±20.4)pmol·L^-1,其中维生素B12缺乏者212例。抑郁组79例,血清维生素B12平均浓度为(139.1±18.2)pmol·L^-1,其中维生素B12缺乏者53例。两组间维生素B12浓度和缺乏比例均存在显著差异(P<0.000 1)。通过对汉密尔顿抑郁量表评分随血清维生素B12浓度变化的曲线拟合得知,倒数曲线拟合度较好。结论 腔隙性脑梗塞后抑郁与维生素B12缺乏存在相关性。     

Effect of CYP2C19 polymorphism on serum levels of vitamin B12 in patients on long-term omeprazole treatment

BACKGROUND: The S-mephenytoin hydroxylase is a polymorphic cytochrome P450 (CYP) enzyme, identified as CYP2C19, which catalyses the metabolism of omeprazole and some other drugs. AIM: To determine whether long-term treatment with omeprazole affects serum vitamin B12 levels, and if so to what extent it depends on CYP2C19 activity. METHODS: Serum vitamin B12 levels (pmol/L) were assessed in 179 patients. Genotyping for wild-type (wt) and mutated (mut) CYP2C19 alleles was performed by allele-specific PCR amplification. RESULTS: One-hundred and eleven of the patients received one dose of 20 mg omeprazole. No difference in B12 levels were found between heterozygous (wt/mut) (n = 23) and homozygous (wt/wt) (n = 85) patients (mean +/- s.d., 350 +/- 82 vs. 315 +/- 87 pmol/L, respectively). Three patients were mut/mut, with serum vitamin B12 levels of 303 +/- 50 pmol/L. In the 68 patients on long-term (>1 year) therapy with 20 mg omeprazole daily, serum vitamin B12 levels were lower in the heterozygous (wt/mut) (n = 19) compared to homozygous wt/wt (n = 49) (246 +/- 71 vs. 305 +/- 98 pmol/L, P = 0. 01, respectively). In one patient (mut/mut) who was studied both after a single dose and after long-term (15 months) treatment with omeprazole, serum vitamin B12 decreased from 360 to 178 pmol/L. In the wt/mut, but not in the wt/wt group, serum vitamin B12 levels were significantly lower in patients on long-term therapy compared with those receiving one dose (246 +/- 71 vs. 350 +/- 82 pmol/L, P < 0.0001, respectively). CONCLUSIONS: CYP2C19 polymorphism significantly affected serum vitamin B12 levels in patients on long-term therapy with omeprazole. In the future, genotyping of CYP2C19 may be useful for patients in need of long-term treatment with omeprazole or other proton pump inhibitors.     

Vitamin B12b increases the cytotoxicity of short-time exposure to ascorbic acid, inducing oxidative burst and iron-dependent DNA damage

It has been found previously that hydroxycobalamine (vitamin B12b) amplifies significantly the cytotoxic effect of ascorbic acid (vitamin C) added to cells for small a, Cyrillic long period of time (48 h). However, according to pharmacokinetics, the concentration of vitamin C in vivo decreases to a physiological value within a short period of time (2-3 h) after the injection. Therefore, in this study we examined the cytotoxic effect of a short-time (up to 2 h) exposure of human larynx carcinoma HEp-2 cells to a combination of vitamins B12b and C (B12b+C). The kinetics of the B12b+C-caused extracellular oxidative burst in this time interval was also explored. Vitamin B12b combined with ascorbic acid provoked a rapid accumulation of extracellular hydrogen peroxide followed by intracellular oxidative stress, DNA single-strand breaks, and the initiation of apoptosis. The chelators of iron phenanthroline and desferrioxamine prevented B12b+C-induced DNA single-strand breaks and cell death but not the accumulation of H2O2 in culture medium. The nonthiol antioxidants pyruvate and catalase were effective in preventing the prooxidant and cytotoxic effects of B12b+C. Thiols, when added simultaneously with the combined vitamins, inhibited these effects only partially (N-acetylcysteine, GSH) or even amplified them (dithiothreitol). The results obtained point to the determining role of oxidative burst and iron-dependent DNA damage in the cytotoxic effect of short-time exposure to B12b+C combination.     

Trichloroethylene induced vitamin B(12) and folate deficiency leads to increased formic acid excretion in the rat

Exposure of rats to trichloroethylene induces a sustained excretion of large amounts of formic acid in urine. Both of the major metabolites, trichloroethanol and trichloroacetic acid, were found to induce this response, but not the minor metabolite S-(1, 2-dichlorovinyl) cysteine. Other polychlorinated solvents, including carbon tetrachloride and chloroform, also increased urinary formate excretion. Addition of folic acid either to diet or drinking water modulated the response indicating that these rats were folate deficient. Two markers of vitamin B(12) deficiency, methylmalonic acid and 5-methyltetrahydrofolate, were also markedly increased in urine and plasma respectively. The increase in 5-methyltetrahydrofolate is consistent with a folate deficiency caused by an inhibition of the vitamin B(12) dependent methionine salvage pathway. Since both vitamin B(12) and chemicals containing polychlorinated carbon atoms readily form free radicals, it is suggested that trichloroacetic acid and trichloroethanol interact with vitamin B(12) through a free radical mechanism inducing a B(12) deficiency and, as a consequence, a folate deficiency. As a result of the folate deficiency, excess formic acid, which is normally utilised through this pathway, is excreted in urine.     

Evaluation of vitamin B12 effects on DNA damage induced by paclitaxel

Abstract

Paclitaxel (PAC) is an anticancer drug that has been shown to generate free radicals leading to irreversible cell injury. Vitamin B12 has antioxidative properties and can protect DNA from free radicals. In this study, we examined the possible genotoxic effect of PAC on DNA as well as the possible protective effect of vitamin B12 on DNA damage induced by paclitaxel. Sister chromatid exchanges (SCEs), chromosomal aberrations (CAs) and 8-hydroxy-2’-deoxyguanosine (8-OHdG) levels were measured in cultured human blood lymphocytes treated with PAC (10?µM) and/or vitamin B12 (2.7?mg/mL). Our results showed that PAC significantly increased the frequencies of SCEs (p?<?0.001) and CAs (p?<?0.001) in human blood lymphocytes, as compared to controls. These DNA damages, caused by PAC drug, were prevented by pretreatment of cells with vitamin B12. In addition, we showed that PAC induced an increase in 8-OHdG, a marker of oxidative DNA damage, and that this increase was prevented by vitamin B12. Vitamin B12 seems to protect against genotoxicity induced by PAC in human blood lymphocytes.     

Vitamins and minerals: their role in nail health and disease

Nail health and appearance are global concerns. We investigated the use of biotin vitamin E, alpha-tocopherol, vitamin C (ascorbic acid), vitamin A, retinoids, retinol, retinal, silicon, zinc, iron, copper, selenium, and vitamin B12 (Cyanocobalamin) in nail health and disease. The evidence that we adduce in this paper suggests that: 1) proper nail care seems to help maintain nail health; 2) no evidence supports the use of vitamin supplementation with vitamin E, vitamin C (ascorbic acid), vitamin A, retinoids, retinol, retinal, silicon, zinc, iron, copper, selenium, or vitamin B12 (Cyanocobalamin) for improving the nail health of well-nourished patients or improving the appearance of nails affected by pathologic disease; and 3) brittle nail syndrome appears to abate with supplementation with a 2.5-mg dose of biotin daily or a 10-mg dose of silicon daily, a useful form of which is choline-stabilized orthosilicic acid.