Vanadium pentoxide appears as a yellow to red crystalline powder. Slightly soluble in water and denser than water. Contact may cause severe irritation to skin, eyes, and mucous membranes. May be toxic by ingestion, inhalation and skin absorption.
Within tissues in organisms, V3+ and V4+ predominate because of largely reducing conditions; in plasma, however, which is high in oxygen, V5+ is formed.
Vanadium is absorbed mainly via inhalation, though small amounts can be absorbed through the skin and gastrointestional tract. It is rapidly distributed in the plasma, mainly to the kidney, liver, lungs, heart, bone, where it tends to accumulate. With the help of cytochrome P-450 enzymes, it can interconvert between its two oxidation states, vanadyl (V+4) and vanadate (V+5). Both states of vanadium can reversibly bind to transferrin protein in the blood and then be taken up into erythrocytes. Vanadium is excreted mainly in the urine. (L837)
IDENTIFICATION AND USE: Vanadium pentoxide is yellow to red crystalline powder forming finely divided particulate dispersed in air. Vanadium pentoxide is used in ceramics and as a catalyst as well as in the production of superconductive magnets. Vanadium pentoxide is also used as a catalyst in dye mordants, paint and varnish drying, glass and ink manufacture, pesticides, and photographic chemicals. HUMAN EXPOSURE AND TOXICITY: It is a confirmed animal carcinogen with unknown relevance to humans. The main signs and symptoms of intoxication caused by single iv doses of the order of 100 mg vanadium pentoxide included nausea, vomiting, salivation, and lacrimation, disappearance of pulse, and cylindrical casts and albumin in the urine. Men exposed to vanadium pentoxide while cleaning oil-fired burners or gas-fired turbines had symptoms consisting of cough, wheezing, rhinitis, sneezing, nosebleeds, sore throat, fatigue, nervousness, eye irritation, hoarseness, and chest pain. Workers exposed to vanadium pentoxide for only a few days may develop irritation of the conjunctivae, rhinitis, dryness of the throat, hoarseness, bronchitis with coughing and wheezing, dyspnea, and pneumonitis. A green-black discoloration of the tongue sometimes occurs. Inhalation of vanadium pentoxide for 1-5 yr produced asthma in 3 of 20 workers. In human leukocytes V(2)O(5) causes oxidation of DNA bases, affects DNA repair, and induces formation of micronucleus, nucleoplasmic bridges, and nuclear buds, suggesting that the workers are at increased risk for cancer and other diseases that are related to DNA instability. It is also induced single-strand DNA breaks in human lymphocytes. Vanadium workers are more susceptible to colds and other respiratory illnesses than others. Exposure to vanadium may impair the lung resistance to respiratory infection. ANIMAL STUDIES: Rabbits were exposed to vanadium pentoxide dust at concentrations of 77, 109, 205, and 525 mg/cu m for 7, 4, 4, and 1 hours, respectively. On autopsy, the animals exhibited chronic inflammatory changes in the nasal and tracheal mucosa, slight emphysema of the lungs, bronchopneumonic patches, pyelonephritis, and hepatitis. In rats 1 hr exposures to vanadium pentoxide pulverized dust at 80 mg/cu m caused acute intoxication. Acute inhalation toxicity in rats was characterized by an irritation of the respiratory mucosa and nasal discharge that sometimes contained blood. Autopsy showed severe congestion and small hemorrhages in all internal organs, signs of increased intracranial pressure, and fatty degeneration of the liver. In the lungs, there was capillary congestion, edema, bronchitis, and focal interstitial pneumonia. Administration of 10 mg/kg bw to mice causes hindlimb paralysis, increased reflex excitability, and GI tract upsets. Gross pathology examination revealed congestion and capillary stasis in the visceral organs. Rats and mice were exposed via inhalation six hours/day, five days/week for three months at 0, 1, 2, 4, 8, or 16 mg/cu m. In male mice vanadium accumulates in the testes starting with the initial inhalation (24 hr). In general, vanadium was capable of significantly decreasing the percentage of gamma-tubulin in all analyzed testicular cells (Sertoli, Leydig, and germ cells) starting with the first week of treatment. There was a statistically significant decrease in the number of implantation sites, live fetuses, and fetal weight among the progeny of the exposed mice compared to controls. There was a statistically significant increase in resorptions and dead fetuses among the females mated with exposed males compared to those mated to controls. In other study, there was a statistically significant decrease in skeletal ossification among the fetuses of mice exposed on day eight. In addition, 6 of 106 exposed fetuses and one of the controls had broken spinal cords. Inhalation of vanadium pentoxide clearly increases the incidence of alveolar/bronchiolar neoplasms in male and female mice at all concentrations tested (1, 2, or 4 mg/cu m). V(2)O(5) exposure was a pulmonary carcinogen in male rats and male and female mice. Salmonella typhimurium mutagenicity test protocol conducted with multiple strains of S. typhimurium with and without metabolic activation enzymes and cofactors were negative. However, REC assay suggested that vanadium pentoxide caused DNA damage at 0.5 umol (91 ug/mL). The selective immunotoxic effects (depression of phagocytosis, splenotoxicity enlargement of spleen, elevation of peripheral blood leukocytes, and T-and B-cell activation) were observed in rats given vanadium pentoxide in drinking water for 6 months, and mice given vanadium pentoxide in water 5 days a week for 6 weeks. ECOTOXICITY STUDIES: The 96-hr LC50 of vanadium pentoxide to adult American flagfish (J. floridae) was 11.2 mg/L in very hard water. Larvae showed 28-day LC50 of 1.13 and 1.88 mg/L of vanadium with larger larvae being more resistant.
Vanadium damages alveolar macrophages by decreasing the macrophage membrane integrity, thus impairing the cells' phagocytotic ability and viability. The pentavalent form of vanadium, vanadate, is a potent inhibitor of the Ca+-ATPase and Na+,K+-ATPase of plasma membranes, which decreases intracellular ATP concentration. Vanadium is also believed to induce the production of reactive oxygen species. This may damage DNA and also cause oxidative stress, which can damage the reproductive system. Vanadium also inhibits protein tyrosine phosphatases, producing insulin-like effects. (L837, A247, A248, A249, A250, A251)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌性证据
A3; 对动物已确认的致癌物,对人类的相关性未知。/五氧化二钒,以V表示,可吸入颗粒物/
A3; Confirmed animal carcinogen with unknown relevance to humans. /Vanadium pentoxide, as V, inhalable particulate matter/
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
国际癌症研究机构致癌物:五氧化二钒
IARC Carcinogenic Agent:Vanadium pentoxide
来源:International Agency for Research on Cancer (IARC)
毒理性
致癌物分类
国际癌症研究机构(IARC)致癌物分类:2B组:可能对人类致癌
IARC Carcinogenic Classes:Group 2B: Possibly carcinogenic to humans
来源:International Agency for Research on Cancer (IARC)
Median serum vanadium concentrations in /vanadium pentoxide/-exposed factory workers were 5.38 ug/L (range 2.18-46.3 ug/L), compared to 2.54 ug/L (range 1.01-12.5 ug/L) in unexposed controls.
/A study/ found that 40% of endotracheally instilled (48)V2O5 (40 ug V/animal of 0.3 mg V/kg) was eliminated from the lungs within 1 hr of dosing, 90% had been cleared from the lung by day 3, and 40% had been excreted, primarily in the urine.
Lung deposition and clearance of inhaled vanadium pentoxide was ... studied over a period of 18 months in rats and mice. Female F-344 rats and B6C3F1 mice were exposed six hours/day, five days/week for up to 18 months at concentrations of 0, 0.5, 1, or 2 mg vanadium pentoxide/cu m (rats) and 0, 1, 2, or 4 (mice). Lung weights, vanadium lung burdens, and blood vanadium concentrations were determined periodically. Modeling of the data produced the significant outcome that lung burden data for both species followed a time-dependent decline in the deposition rates in the middle and high exposure groups but not in the low exposure group. Total lung doses were not proportional to exposure concentrations and for each species, by the end of 18 months, the overall lung doses in the lower two exposure concentrations were almost identical.
Studies of (48)V2O5 on rats demonstrate that it is absorbed in the gastrointestinal tract and via intratracheal instillation. It is distributed to all major organs sampled (except the brain) including blood, lungs, bone, kidneys, spleen, liver, testes, heart, intestines, stomach, trachea, and muscle. Both urinary excretion and fecal elimination were observed, with urine accounting for about twice as much of the elimination as feces.
1.周国泰,化学危险品安全技术全书,化学工业出版社,1997 2.国家环保局有毒化学品管理办公室、北京化工研究院合编,化学品毒性法规环境数据手册,中国环境科学出版社.1992 3.Canadian Centre for Occupational Health and Safety,CHEMINFO Database.1998 4.Canadian Centre for Occupational Health and Safety, RTECS Database, 1989
A liquid-phase synthesis of inorganic phosphor materials at a moderate temperature was proposed by using immiscible liquid–liquid biphasic systems. A self-activated Ba2V2O7 phosphor was actually synthesized from vanadiumalkoxide dissolved in an organic solution and barium acetate in an aqueous solution. A mild hydrolysis reaction of the alkoxide started at the organic–inorganic interface, and an intermediate
提出了通过使用不混溶的液-液两相体系在中等温度下液相合成无机磷光体的方法。实际上,自溶解在有机溶液中的烷氧基钒和水溶液中的乙酸钡合成了自活化的Ba 2 V 2 O 7磷光体。在有机-无机界面开始醇盐的温和的水解反应,以及中间化合物,钡(VO 3)2 ·H 2 O,最初形成。然后由Ba(VO 3)2 ·H 2转化而获得Ba 2 V 2 O 7粉末。O在水溶液中促进。通过类似的化学反应,在表面改性的石英玻璃基板上获得了Ba 2 V 2 O 7膜。检查诸如基材的表面状态,有机溶剂的种类和水溶液的体积等因素以改善膜沉积行为。所得的Ba 2 V 2 O 7材料在以二聚体形式存在的VO 4 3–单元中,由于电荷转移跃迁,在紫外光照射下显示出宽带可见光致发光。
Process for the ring expansion of penicillins to cephalosporin compounds
申请人:Fujisawa Pharmaceutical Co., Ltd.
公开号:US03993646A1
公开(公告)日:1976-11-23
A process for producing a 2-cephem or 3-cephem derivative compound of the formula: ##SPC1## Wherein R.sub.1 represents a substituted or unsubstituted amino radical and R.sub.4 represents hydrogen or a radical selected from the group consisting of carboxy, protected carboxy, ester, acid amide, acid anhydride, acid halide, acid azide and carboxy salt, and the dotted line indicates the alternate bond structure providing 3-cephem or 2-cephem, which comprises: Reacting a halogenated derivative selected from the group consisting of a halogenated penam derivative having the formula: ##SPC2## A halogenated cepham derivative of the formula: ##SPC3## Wherein X represents a halogen atom, R.sub.3 represents a radical selected from the group consisting of carboxy, protected carboxy, ester, acid amide, acid anhydride, acid halide, acid azide and carboxy salt, and R.sub.1 is as defined above, or mixtures thereof with a dehydrohalogenoic acid reagent.
Halogenated penam derivatives and the preparation thereof
申请人:Fujisawa Pharmaceutical Co., Ltd.
公开号:US04009159A1
公开(公告)日:1977-02-22
A penam derivative having the formula: ##STR1## wherein X represents a halogen atom, and wherein R.sub.1 represents an amino or acylamino, and R.sub.3 represents a radical selected from the group consisting of carboxy, ester, acid amide, acid anhydride, acid halide, and acid azide.
From Plates to Spheres: Tuning the Vanadyl Phosphate Morphology by Intercalation of Nitrosyl Oxide
作者:José C. V. de Miranda、Deyse de S. Dantas、João E. T. S. Dantas、Francisco C. Pereira、Robson F. de Farias
DOI:10.1080/15533174.2013.799490
日期:2014.10.21
matrix VOPO4.2H2O was used to the intercalation of nitrosyl (NO) ligand. The vanadylphosphate matrix, as well as the prepared intercalated compound (VOPO4.NO.H2O), were characterized by infrared spectroscopy, thermogravimetry, X-ray difractometry, and SEM microscopy. The X-ray diffraction patterns shown that the VOPO4.NO.H2O synthesis occurs with a decrease in the lamellar distance in comparison with
Catalytic Oxidation of 1,2-Dichlorobenzene over Supported Transition Metal Oxides
作者:Sundaram Krishnamoorthy、Juan A. Rivas、Michael D. Amiridis
DOI:10.1006/jcat.2000.2895
日期:2000.7
The catalyticoxidation of 1,2-dichlorobenzene has been systematically investigated over a series of transitionmetaloxides (i.e., Cr2O3, V2O5, MoO3, Fe2O3, and Co3O4) supported on TiO2 and Al2O3. The activity of the different catalysts for this reaction depends on the nature of the transitionmetaloxide used, with Cr2O3-and V2O5-based catalysts being the most active ones. With the exception of the
已经系统地研究了负载在TiO上的一系列过渡金属氧化物(即Cr 2 O 3,V 2 O 5,MoO 3,Fe 2 O 3和Co 3 O 4)对1,2-二氯苯的催化氧化作用。2和Al 2 O 3。用于该反应的不同催化剂的活性取决于所用的过渡金属氧化物的性质,其中Cr 2 O 3和V 2 O 5基催化剂是最活跃的催化剂。除氧化钴催化剂外,TiO 2负载的体系比相应的Al 2 O 3负载的体系更具活性,表明该反应中金属氧化物与负载的相互作用非常重要。在水的存在下进行的实验表明,对基于V 2 O 5和Cr 2 O 3的催化剂具有抑制作用,并且对Co 3 O 4 / TiO 2具有促进作用。Fe 2 O 3-和MoO 3的催化剂不受水的影响。表面物质和水之间竞争吸附被怀疑是用于抑制的缘故,而促进效果可以归因于水与表面Cl为基准的反应- 。现场FTIR研究表明,在反应条件下研究的所有催化剂表面均存在羧酸