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 oxytrichloride is lemon-yellow liquid. It is used as catalyst in olefin polymerization, (ethylene-propylene rubber) and organovanadium synthesis. HUMAN EXPOSURE AND TOXICITY: Genotoxic effects were not found for vanadyl chloride at a concentration of 5X10-5 M on human peripheral white blood cells. ANIMAL STUDIES: The influence of vanadium oxytrichloride on drug action in male rats was investigated. Following the addition of vanadyl trichloride (2.5X10-6 to 2.5X10-3 M) to rat liver supernatant fractions, significant inhibition of drug metabolism was evident only at concn greater than 2.5X10-4 M. Following in vivo vanadium admin (2 mg vanadium/kg, ip, for 2 days), duration of pentobarbital hypnosis measured 48 hr later was not significantly prolonged.
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
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
Breathing high levels of vanadium affects the lungs, throat, and eyes. Ingestion of vanadium may cause kidney and liver damage, birth defects, or death. (L837)
... /A study was/ performed in rats ... to determine the ... distribution /of vanadium/ in organs and subcellular particles ... /but it has/ the shortcomings resulting from observations made after a single administration ... . The chief ... information ... relates to distribution of (48)vanadium as the pentavalent vanadium oxytrichloride in subcellular fractions of the liver; although supernatant contained 57% of the isotope 10 min after administration with the remainder equally divided among the microsomal, mitochondrial, and nuclear fractions, at 8 days (48)vanadium had migrated mainly into the nuclear fractions and mitochondria about equally to the total extent of 80%, with the isotope now being equally distributed between microsomes and supernatant of 10% each.
(48)Vanadium oxytrichloride was administered intratracheally to juvenile male Wistar rats. All major tissues were analyzed for (48)vanadium content. Over half was removed from lung within 15 min of exposure, vanadium isotope translocated to all organs except brain. The peak uptake for most organs occurred between 4 and 24 hr after injection with kidney maintaining largest fraction. Bones accumulated large fractions, testes small fraction. Excretion occurred by urine and fecal routes. Three percent of the burden remained after 63 days.
Male Wistar rats were given vanadyl trichloride (48VOCl3) ip in doses of V ranging from 0.1 to 8 mg/kg and their tissues were collected 1 and 5 d after the injection. V was distributed in the order bone greater then kidney greater then liver greater than spleen greater than intestines greater than stomach greater than muscle greater than testis greater than lung greater than brain. Residues of V in tissues declined rapidly between 24 hr and 5 d after administration. The tissue:blood ratios of V were greater than unity for bone, kidney, liver, and spleen and near unity for all other organs except the brain. Brain levels of V were found to be considerably lower than blood in all cases. V residues were linearly related to dose in most organs when the dose was below 2 mg/kg. At 8 mg/kg, however, liver and kidney showed consistently higher amounts than would be expected from the linear relationship at the low doses. Subcellular distribution of V in liver and kidney indicated that it was associated with nuclei, mitochondria, microsomes, and primarily with high-molecular-weight proteins in the soluble fraction of liver. The results suggest that the distribution pattern of V is dependent on exposure level.
The distribution of vanadium among the tissues of the body studied using intravenously injected V(3+), intratracheally injected vanadium chloride or vanadium oxytrichloride, and oral doses of vanadyl sulfate or orthovanadate. The relative levels of V in organs and tissues differed according to the route of administration; however, differences in the distribution of different compounds administered by the same route were small, indicating that the vanadium may be converted to a common oxidation state in vivo. ... Rats injected with V(5+) later contained V(4+) in their tissues. In general, kidney, liver, and bone accumulated the highest levels of vanadium. The tissues that retained vanadium the longest were bone, kidney, testicle, and lung. Reported preliminary results for vanadium levels in fluids and hard tissues from humans. Vanadium appears to concentrate in bone and hair.
A process for producing vitamin A esters, vitamin A aldehyde and vitamin A acid esters from esters of 3,7-dimethyl-9-(1-hydroxy-2,2,6-trimethylcyclohexyl)-nona-2,4,6-trien-8-yn -1-ol and 3,7-dimethyl-9-(1-hydroxy-2,2,6-trimethylcyclohexyL)-nona-2,4,6-trien-8-yn oic acid including intermediates in this process.
Novel phenylsiloxy vanadium oxide catalyst where the phenyl moiety is substituted with an electron withdrawing group, said catalyst being used to convert secondary and tertiary acetylenic carbinols to the corresponding .alpha.,.beta.-unsubstituted carbonyl compounds.
Process for converting secondary and tertiary acetylenic carbinols to the corresponding alpha,beta-unsaturated carbonyl compounds by rearranging the carbinol with (trilower alkyl-, tricycloalkyl-, triaryl- or triarylalkyl-siloxy)-vanadium oxide catalyst in the presence of a silanol where either the vanadium oxide or the silanol contains a phenyl group substituted with at least one electron withdrawing group.
