尿钒的自然排泄速度及CaNa2DETA驱钒效果

通过观察钒作业工人尿钒自然排泄速(?)及Ca-Na_2EDTA 驱钒效果,可以间接分析钒在体内的蓄积情况,并对防治钒中毒具有重要意义.现将初步观察结果报道如下.方法和结果1.钒作业工人尿钒含量     

尿钒作为炼钒工人生物监测指标的探测

本文报导了对87名炼钒男性工人在离开作业后尿钒排泄情况的研究,观察了不同接触水平下工人尿钒排泄的异同。结果显示,钒作业者离岗后5天,尿中钒浓度仍较对照组高,为对照的2～4倍,但不同接触水平的工人的尿钒值差别已不显著。表明不同接触水平下,尿钒的排泄特点基本相似,从而提示尿钒可作为近期接触的指标,采尿样时间最好在当天班末或次日上班前,这样能比较真实地反映工人的接触情况。     

钒化合物的降血糖作用

迄今为止，已发现三种无机钒对糖尿鼠具有降血糖作用，其机理为钒化合物，作用于胰岛素受体或胰岛素受体或胰岛素受体后。钒化合物有一定程序的毒性，须研制低毒，高效的钒化合物用于糖尿的治疗。     

钒与人体健康

钒的生物学重要性受到人们的广泛重视 ,主要介绍钒的生物学作用以及它对人类健康的影响     

钒:一种具有非典型生物学意义的元素

过渡元素钒的生物学表现引起很大矛盾—从毒性到必要性。作为微量营养素,钒的重要性还有待明确地被生物学家和生物医学家所接受,尽管有毒性分析这种元素不同的生物学作用似乎很有兴趣。钒化物已被证明与人类一些疾病的发病机制有关,也与维持正常的机体功能有关。钒盐干扰诸如不同的三磷酸腺苷酶、蛋白激酶、核糖核酸酶和磷酸酶等酶系统的基本排列。钒缺乏可导致包括甲状腺、葡萄糖和脂类代谢等的一些生理学功能障碍,因为一些基因是通过这种元素或它的化合物调节的,这些基因包括肿瘤坏死因子α-、白细胞介素-8、激活蛋白-1、ras、C-raf-1、细胞分裂素活化蛋白激酶、p53、核因子-kB等。所有这些接近于形成一种认识,即钒是药理学和营养学意义上的一种元素,但这一点通过它在糖尿病中逐渐增加的治疗作用上表现出来。钒也是一种新出现的有效的抗致癌物的代表。通过对钒的一般生物化学功能的分析,全面总结了与钒生物学有关的进展。     

钒化合物对作业工人肺功能的影响

随着国民经济的发展,钒及其化合物的生产与使用也日益普遍,近年来钒的毒性及对工人健康的影响也已逐渐为人们所重视。钒及其化合物在工业生产中主要以尘和烟的形式污染车间环境,经呼吸道和肺进入人体而产生一系列毒作用。为了进一步了解其对工人肺功能的影响和为职业性慢性钒中毒早期诊断提供依据,对102名接钒工人肺功能状态进行了测定,报告如下。     

钒与糖尿病

本文简述了钒的代谢、功能、毒性、影响因素，着重回顾了近１０多年来关于钒治疗糖尿病的机理研究，指出了钒与胰岛素的异同性，强调了钒与磷酸代谢的密切关系。     

钒化合物对工人肺功能影响的研究

本文对上海某冶炼厂80名钒作业工人进行了肺功能检查,前后共二次,间隔9个月。结果接触钒组与对照组相比,MMEF的下降两次均有统计学意义;前后两次肺功能比较无明显差异;工人当天上班前后的肺功能观察结果表明,钒化合物无类似二异氰酸甲苯对肺功能有即时影响的作用。     

钒的摄取,吸收,体内分布及其作用

钒为人体的必需微量元素。本文就钒的摄取、吸收途径，体内各组织器官的分布，以及钒的生理和药理作用作了简单综述，对各自的影响因素及其涉及的有关机理也作了讨论。     

钒在糖尿病

本文了简述了钒的代谢，功能，毒性，影响因素，着重回顾了近１０多年来关于钒治疗糖尿病的机理研究，指出了钒在胰岛素的异同性，强调了钒在磷酸代谢的密切关系。     

Serum and urinary vanadium of workers processing vanadium pentoxide

Summary Serum and urinary vanadium concentrations were investigated in eight men exposed to vanadium pentoxide dust. The creatinine-adjusted urinary vanadium concentrations were found to correlate with serum vanadium concentrations (r=0.81), but not with the vanadium contents of factory air. The urinary vanadium excretion decreased significantly with the time the workers spent out of exposure. At the beginning of their summer holidays the serum vanadium concentration of the workers was 393 ± 223 (S.D.) nmol/l and the urinary excretion of vanadium 73 ± 50 nmol/mmol of creatinine. Three days after exposure the urinary excretion of vanadium was 46 ± 24 nmol/mmol of creatinine. On the 16th day of their holidays vanadium could be detected in the serum (225 ± 83 nmol/1) and in the urine (48 ± 26 nmol/mmol of creatinine) of the workers. Eight family members of the exposed had less vanadium in urine (32 ± 17 nmol/mmol of creatinine). These results suggest that most of the absorbed vanadium is excreted in the urine within one day after a long-term moderate exposure to vanadium dust.     

A survey of exposure to and urinary excretion of vanadium and response to heat stress in boiler cleaners working in Scotland

Between July and November 1991, 24/31 boiler cleaners working on six oil‐fired boilers of varying sizes provided periodic samples of urine which was analysed for its vanadium content. Eight of these men also had their heart rate and body temperature monitored The dust, its vanadium and nickel content and thermal aspects of the workplace environment were assessed using standard occupational hygiene techniques. Urinary excretion of vanadium depended on length of exposure, method of cleaning and vanadium content of the ash. Thus high amounts (270.1 μg l^‐1, median 77.4 μg l^‐1) were observed during ‘dry’ cleaning, when eight hour time weighted average dust and vanadium levels of up to 357 and 88.7 mg m^‐3 respectively were found when the ash had a vanadium content of 15%. Nickel comprised 4.64%. Although ‘wet’ methods produced much lower levels, extremely high short term exposures could still occur ‐ 210 mg m^‐3 and 15.2 mg m^‐3 for dust and vanadium during a 10 min period ‐ emphasising the need for adequate personal protective equipment. Even under conditions of heat stress, core temperatures always stayed within safe limits, and maximum predicted heart rates were rarely exceeded ‐ the greatest excursion in any of those monitored was for only 2.8% of the working day.     

Vanadium in Ambient Air: Concentrations in Lung Tissue from Autopsies of Mexico City Residents in the 1960s and 1990s

Vanadium concentrations in lung tissue were determined by atomic absorption spectrometry from autopsy specimens taken from residents of Mexico City during the 1960s and 1990s (20 males and 19 females, and 30 males and 18 females, respectively). Samples from the 1990s had significantly increased mean vanadium concentrations (mean ± standard deviation: 1.36 ± 0.08), compared with those from the 1960s (1.04 ± 0.05). Concentrations were not correlated with gender, smoking habit, age, cause of death, or occupation. These findings suggest that vanadium in ambient air is increasing and it represents a potential health hazard for Mexico City residents. Air pollution monitoring efforts should include vanadium concentrations in suspended particles to follow-up the findings reported herein. Researchers need to acquire a better knowledge of the levels of airborne vanadium exposure at which risk to human health occurs.     

钒的职业危害效应研究

目的调查钒职业危害效应性质及其表征,探讨发生、发展规律与特点。方法以暴露明确、时间长而稳定、规模较大的某钒制品企业职业人群为研究对象,从人群医保重慢病病史和职业健康监护两个层面进行调查与分析。结果暴露人群医保重慢病发病强度低于总体人群(即暴露人群所在公司参加医保的全体职员),以高血压病、糖尿病、甲状腺疾病和恶性肿瘤较为明显;职业环境中90%以上暴露者出现眼鼻咽刺激反应;长期职业暴露会降低接触人员的积极情绪、运动协调能力、运动速度和稳定性,损害短期视觉记忆力,增加消极情绪;并可提高血清HDL-C和PLT水平,降低TCHO、ALT、TBIL、BUN水平;引起肺通气功能下降,血压升高和心电图阳性指标增加,以及胆结石和脂肪肝的检出率较高。结论钒职业危害主要是对眼和上呼吸道刺激作用,同时也作用和影响脂肪代谢过程、神经行为功能和心血管、肺、肝、肾等器官功能。     

2-(2-喹啉偶氮)-1,3-二羟基苯固相萃取分光光度法测定环境样品中钒的研究

根据新试剂 2 (2 喹啉偶氮 ) 1,3 二羟基苯 (QADHB)与钒的显色反应及C1 8固相萃取小柱对显色络合物的固相萃取 ,建立了一种测定环境样品中痕量钒的新方法 ,在pH 3 5的柠檬酸 -氢氧化钠缓冲介质中 ,溴化十六烷基三甲基铵 (CTMAB)存在下 ,QADHB与钒反应生成 2∶1稳定络合物 ,该络合物可用C1 8固相萃取小柱富集 ,小柱上富集的络合物用乙醇 (内含 2 %乙酸 )洗脱后用分光光度法测定 ,在富集后的测定液中 ,络合物最大吸收波长为 5 5 2nm ,摩尔吸光系数ε=8 2 9ⅹ 10 4 L·moL- 1 ·cm- 1 ,钒含量在 0～ 1 0 μg ml内符合比尔定律。方法用于几种环境样品中钒的分析 ,结果令人满意     

Effects of vanadium on immunologic functions

Exposure of mice to vanadium caused a dose-related but nonsignificant decrease in the antibody-forming cells in the spleen of animals challenged with sheep erythrocytes. Delayed hypersensitivity reaction was not affected in similarly sensitized animals. Serum immunoglobulins were also not altered by the vanadium treatment. Splenic lymphocytes obtained at 1, 4, 8, and 13 wk of exposure to 0, 1, 10, and 50 mg of vanadium per liter of drinking water showed an increased DNA synthesis related to vanadium treatment when cultured in the presence of phytohemagglutinin and pokeweed mitogen but not with bacterial lipopolysaccharide. Addition of vanadium to splenic cultures in vitro caused a marked enhancement of lymphocyte transformation at low concentrations, whereas a decreased cellular proliferation was observed at high concentrations of vanadium.     

Vanadium, Vitamin C And Depression

A clinical trial has shown that subjects suffering from mania and depression improved when treated with a low vanadium diet or with ascorbic acid.     

Inverse Association of Plasma Vanadium Concentrations with Gestational Diabetes Mellitus

Vanadium compounds were identified to be beneficial for the control of glucose homeostasis. We aimed to explore the association of plasma vanadium (V) with gestational diabetes mellitus (GDM). We performed a case-control study including 252 newly diagnosed GDM cases and 252 controls matched by age, parity, and gestational age. Fasting blood samples were collected from each participant at GDM screening (≥24 weeks of gestation). The plasma concentrations of V were determined utilizing inductively coupled plasma mass spectrometry. Plasma V levels were significantly lower in the GDM group than those in the control group (p < 0.001). The adjusted OR (95% CI) of GDM comparing the highest V tertile with the lowest tertile was 0.35 (0.20–0.61). According to the cubic spline model, the relation between plasma V and odds of GDM was potentially nonlinear (p < 0.001). Moreover, plasma V was negatively correlated with 1-h post-glucose load, 2-h post-glucose load, and lipid metabolism indices (all p < 0.05). The present study indicates an inverse association of plasma V with GDM. Further prospective cohort studies are required to validate our results.     

Lung clearance, translocation, and acute toxicity of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium oxides following deposition in rat lung

Young adult rats were exposed via inhalation or intratracheal instillation to oxides of arsenic, beryllium, cadmium, cobalt, lead, selenium, vanadium, and ytterbium. Serial necropsies were performed to assess the metal content in organs at times up to several weeks after exposure. The lung clearance varied widely for these compounds, and the times to remove 50% of the initial burden ranged from 18 min for vanadium to 400 days for beryllium. Arsenic, cadmium, lead, selenium, and vanadium were initially soluble in lung, but a small fraction (1-20%) remained there over the long term. Extrapulmonary tissues often accumulated substantial amounts of the soluble oxides, and whole-body retention was often greater for compounds that were more soluble in lung. Arsenic, selenium, and vanadium translocated to carcass and bone. Arsenic, cadmium, lead, and selenium accumulated in the liver, and the kidney retained cadmium and lead. Beryllium, cobalt and ytterbium did not deposit at any extrapulmonary site in significant amounts. In general, the aqueous solubility of these compounds was a poor predictor for behavior in vivo because of their interaction with metabolic processes. Of the metal oxides tested for acute lethality following pulmonary deposition, cadmium was most toxic, followed by selenium, vanadium, and arsenic.