Vanadyl sulfate

163

162.890610

248-652-7

2931

DTXSID4021428

2825309000

106

-0.37600

Blue Solid

3.0 g/cm3 (20ºC)

105°C

330ºC at 760 mmHg

H2O: soluble

Divalent and trivalent vanadium compounds are reducing agents and require storage under an inert atmosphere to avoid oxidation. /Divalent and trivalent vanadium compounds/

Abdominal cavity-mouse LD50: 114 mg/kg

Non-combustible; toxic vanadium and sulfur oxide fumes are produced in the fire

Blue crystals, soluble in water /Vanadyl sulfate dihydrate/|Divalent sulfate is violet VSO4.7H2O /Divalent vanadyl sulfate/|Ethereal blue solid; readily soluble in water /Vanadyl sulfate pentahydrate/|Within tissues in organisms, V3+ and V4+ predominate because of largely reducing conditions; in plasma, however, which is high in oxygen, V5+ is formed.

Very soluble in water.

Non-Redox-Active Inorganic Compounds

VANADYL SULFATE has weak oxidizing or reducing powers. Redox reactions can however still occur.

II

6.1

UN 2931/9152

22-36/38

26-36/37/39

Treasury is ventilated, low temperature and dry; stored and transported separately from acids and food

Stable. Incompatible with strong oxidizing agents.

P201, P202, P234, P260, P261, P264, P270, P271, P273, P280, P281, P301+P310, P301+P312, P302+P352, P304+P340, P305+P351+P338, P308+P313, P312, P314, P321, P330, P332+P313, P337+P313, P362, P390, P391, P403+P233, P404, P405, P501

H290

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product. /Vanadium(IV) oxide sulfate hydrate/|Waste material contaminated with vanadium shall be disposed of in a manner not hazardous to employees. The disposal method must conform with applicable local, state, and federal regulations and must not constitute a hazard to the surrounding population or environment. /Vanadium/|The following wastewater treatment technologies have been investigated for vanadium: Concentration process: chemical precipitation. /Vanadium/

Incompatible materials: Strong oxidizing agents /Vanadium(IV) oxide sulfate hydrate/|Sulfates react with aluminum, magnesium. Incompatible with strong oxidizers.|Lithium, chlorine trifluoride. /Vanadium dust, Vanadium fume/

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways. (ERG, 2016)

|Danger|H290 (40.52%): May be corrosive to metals [Warning Corrosive to Metals]|P201, P202, P234, P260, P261, P264, P270, P271, P273, P280, P281, P301+P310, P301+P312, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P310, P312, P314, P321, P330, P332+P313, P337+P313, P362, P363, P390, P391, P403+P233, P404, P405, and P501|Aggregated GHS information provided by 117 companies from 14 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P301+P312, P330, and P501

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2016)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. (ERG, 2016)|Eye/face protection: Safety glasses with side-shields conforming to EN166 Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /Vanadium(IV) oxide sulfate hydrate/|Skin protection: Handle with gloves. /Vanadium(IV) oxide sulfate hydrate/|Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /Vanadium(IV) oxide sulfate hydrate/|Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /Vanadium(IV) oxide sulfate hydrate/|For more Personal Protective Equipment (PPE) (Complete) data for VANADYL SULFATE (15 total), please visit the HSDB record page.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /Vanadium(IV) oxide sulfate hydrate/|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary. /Vanadium(IV) oxide sulfate hydrate/|Extinguish fire using an agent suitable for type of surrounding fire. Use water spray to reduce vapors. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water spray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position.|If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty). Use water in flooding quantities as fog. Use "alcohol" foam, dry chemical, or carbon dioxide. Keep run-off water out of sewers and water sources.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment, and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist, or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Do not let product enter drains. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /Vanadium(IV) oxide sulfate hydrate/|Evacuate persons not wearing protective equipment from area of spill or leak until cleanup is complete. Remove all ignition sources. Collect powdered material in the most convenient and safe manner and deposit in sealed containers. Ventilate area after cleanup is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.|Environmental considerations: Water spill: Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates. /Vanadium compound, N.O.S./|Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with plastic sheet to prevent dissolving in rain or fire fighting water. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. /Vanadium compound, N.O.S./

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Avoid breathing dust. Environmental precautions: Do not let product enter drains.|Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed. /Vanadium(IV) oxide sulfate hydrate/|Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of the workday. /Vanadium(IV) oxide sulfate hydrate/|Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /Vanadium(IV) oxide sulfate hydrate/|For more Preventive Measures (Complete) data for VANADYL SULFATE (13 total), please visit the HSDB record page.

/GUIDE 151 SUBSTANCES - TOXIC (Non-combustible)/ Fire or Explosion: Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways.|/GUIDE 151 SUBSTANCES - TOXIC (Non-combustible)/ Health: Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.|/GUIDE 151 SUBSTANCES - TOXIC (Non-combustible)/ Public Safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.|/GUIDE 151 SUBSTANCES - TOXIC (Non-combustible)/ Protective Clothing: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.|For more DOT Emergency Guidelines (Complete) data for VANADYL SULFATE (8 total), please visit the HSDB record page.

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./|The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. Vanadyl sulfate is included on the dangerous goods list.|The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. Vanadyl sulfate is included on the dangerous goods list.

Contact can irritate the skin. Exposure can irritate the eyes, nose, throat, and lungs with cough and phlegm.|Vanadium compounds act chiefly as an irritant to the conjunctiva and respiratory tract. /Vanadium compounds/|... Extensive evidence exists that vanadium dust (usually the pentoxide) is severely irritating to the mucous membranes of the eyes, nose, throat, and respiratory tract. /Vanadium dust/|Vanadium is a primary irritant to the ... skin. /Vanadium/|Potential symptoms of overexposure to dust or fumes are irritation of eyes, skin, throat ... . /Vanadium dust and fumes/

Recommended Exposure Limit: 15 Minute Ceiling value: 0.05 mg V/cu m. /Vanadium dust; The REL applies to all vanadium compounds except vanadium metal and vanadium carbide./

The major hazards encountered in the use and handling of vanadyl sulfate stem from its toxicologic properties. Toxic primarily via inhalation and dermal contact, exposure to this blue, crystalline powder may occur from vanadium ore extraction, from its use as a mordant in dyeing and printing textiles, in the manufacture of colored glass, in pottery glaze, in aniline black, as a reducing agent, and from the cleaning of oil-fired boilers, combustion chambers, gas turbines, and firebrick linings. Effects from exposure may include headache, eye irritation, dermatitis, rhinitis, tracheitis, bronchitis, pulmonary edema, and peripheral vasoconstriction of lungs, spleen, kidneys, and intestines. Engineering controls should be used to limit vanadyl sulfate exposure. In activities and situations where over-exposure may occur, wear protective clothing to prevent skin contact, and a self-contained breathing apparatus. Safety showers and eyewash fountains should be located in areas where exposures are likely. If contact should occur, flush exposed skin and eyes with copious amounts of tepid water for at least 15 minutes. Remove contaminated clothing at the work site. While vanadyl sulfate does not ignite readily, it may burn with the production of irritating or poisonous gases (e.g., sulfur oxides). Also, containers may explode violently in the heat of a fire. For fires involving vanadyl sulfate, extinguish with dry chemical, CO2, Halon, water spray, fog, or standard foam. Fight fire from a maximum distance, and dike fire control water to prevent material from entering water sources and sewers. Vanadyl sulfate should be stored in tightly closed containers (e.g., glass bottles or kegs), away from moisture, heat, sparks, or flames. Large spills of vanadyl sulfate on land should be contained in pits or other holding areas (liquid solutions diked to prevent runoff; solids covered with a plastic sheet). Small spills should be placed in a covered container (liquid solutions first taken up with sand or a noncombustible absorbent), and placed into containers for later disposal. Large spills in water should be neutralized with agricultural lime, crushed limestone, or sodium bicarbonate, and allowed to aerate.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1000 lb or 454 kg. The toll free number of the NRC is (800) 424-8802. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV.D.3.b).

highly toxic

IDENTIFICATION AND USE: Vanadyl sulfate is a pale blue powder. It is used as mordant in dyeing and printing textiles; manufacture of colored glass; for blue and green glazes on pottery. It's other uses include catalyst; aniline black preparation; reducing agent. Vanadyl sulfate has been tested as an experimental therapy in diabetes. HUMAN EXPOSURE AND TOXICITY: The treatment group (11 males; 4 females) was orally administered vanadyl sulfate 0.5 mg/kg bw/day for 12 weeks, and a control group (12 males; 4 females) received placebo capsules. At the end of the study, there were no significant differences between the groups in terms of body weight, blood pressure, standard hematological indices, blood viscosity, or standard blood biochemistry measurements. Vanadyl sulfate was positive in human lymphocyte micronucleus assay. Vanadyl sulfate induced DNA damage in human normal lymphocytes and in HeLa cells. ANIMAL STUDIES: Vanadyl sulfate pentahydrate were administered to rats and mice. The clinical and physical signs appearing after the intoxication include irregular respiration, diarrhea, ataxia, and paralysis of the hind legs. Chronic exposure of rats to vanadium sulfate, initially through maternal milk and later in the drinking water, resulted after 10 weeks in a significant increase in malondialdehyde formation by kidney but not by other tissues. In both acute and chronic studies in rats and mice, no significant increase in lipid peroxidation by vanadium treatment was detected in brain, heart, lung, spleen, or liver. Treatment of male rats with different dose levels of vanadyl sulfate in drinking water corresponding to 34, 54, and 90 mg/kg bw/day over 52 weeks did not indicate severe signs of systemic toxicity. Peroral administration to male rats of VOSO4, 31 mg V/kg body weight/day for 60 days, caused a decrease in reproductive organ weight, sperm count, and motility, as well as atrophy of the seminiferous tubules. Rats were exposed to 10 mg V/kg body weight/day as VOSO4 in drinking water during late gestation and lactation until postnatal day 100. Decreases in survival were observed and behavioral effects recorded in surviving offspring. A significant increase in early resorptions and decrease in fetal growth was observed in the offspring of mice administered VOSO4 by gavage on gestation days 6-15 in doses from 7.5 mg V/kg body weight/day. Cleft palate was increased at 15 and 30 mg Va/kg body weight/day. Micrognathia and delayed ossification was increased at all dose levels. In vivo, VOSO4 induced chromosomal aberrations and aneuploidy-related endpoints (hypoploidy and hyperploidy) in mice bone marrow after a single intragastric dose of 100 mg VOSO4/kg (31 mg V/kg). Vanadyl sulfate induced no convertants or revertants in the D7 strain of S. cerevisiae at dose levels between 420 and 1000 mmol/L in both the presence and absence of metabolic activation. Also, no mutagenic activity was detected in hamster V79 cells at dose levels between 0 and 7.5 mmol/L in both the presence and absence of metabolic activation.

Bis(maltolato)oxovanadium(IV) (BMOV), and its ethylmaltol analog, bis(ethylmaltolato)oxovanadium(IV) (BEOV), are candidate insulin-enhancing agents for the treatment of type 2 diabetes mellitus; in mid-2008, BEOV advanced to phase II clinical testing. The interactions of BMOV and its inorganic congener, vanadyl sulfate (VOSO(4)), with human serum apo-transferrin (hTf) were investigated using differential scanning calorimetry (DSC). Addition of BMOV or VOSO(4) to apo-hTf resulted in an increase in thermal stability of both the C- and N-lobes of transferrin as a result of binding to either vanadyl compound. A series of DSC thermograms of hTf solutions containing different molar ratios of BMOV and VOSO(4) were used to determine binding constants; at 25 degrees C the binding constants of BMOV to the C- and N-lobes of apo-hTf were found to be 3 (+/- 1)x10+5 and 1.8 (+/- 0.7)x10+5/M, respectively. The corresponding values for VOSO(4) were 1.7 (+/- 0.3)x10+5 and 7 (+/- 2)x10+4/M. The results show that the vanadium species initially presented as either BMOV or VOSO(4) had similar affinities for human serum transferrin due to oxidation of solvated vanadyl(IV) prior to complexation to transferrin. Binding of metavanadate (VO(3)(-)) was confirmed by DSC and isothermal titration calorimetry (ITC) experiments of the interaction between sodium metavanadate (NaVO(3)) and hTf.|We sought to determine the ultrastructure of pancreatic islet beta cells of streptozotocin-induced diabetic rats treated with oral vanadyl sulfate. Diabetes was induced in male Wistar rats by intravenous injection of 40 mg/kg streptozotocin. The same volume of normal saline was injected in sham animals. Animals were divided into treated and control groups. Vanadyl sulfate was added to the drinking water of the treated animals at a concentration of 1 mg/mL up to three months. Two months after vanadyl sulfate withdrawal animals were killed. Ultrastructure of islet beta cells were studied by transmission electron microscope. In diabetic treated rats plasma glucose and fluid intake returned to normal levels within three months while control animals remained diabetic. Well granulated cytoplasm, well developed endoplasmic reticulum, increase in the number of immature granules in the cytoplasm with no clear signs of cell injury were found in the islet beta cells of diabetic treated rats. Lymphocyte filteration, nuclear picnosis, cytoplasmic vacuolization were found frequently in the islet beta cells of untreated diabetic rats. In conclusion as was evident in thin sections of panceatic islet beta cells of treated diabetic rats in this study, vanadyl sulfate through preserving islet beta cells structure and ultrastructure contributes in reversing diabetic signs and symptoms in streptozotocin induced diabetic rats.|Streptozotocin- and galactose-induced diabetic rats are protected against nephrotoxic effects of cisplatin. While the mechanism remains to be defined, protection is associated with a decrease in the accumulation of platinum in renal cortical tissues of streptozotocin-diabetic versus non-diabetic rats. A physiological abnormality common to streptozotocin and galactosemic models of diabetes is hyperglycemia, suggesting that elevated sugars are involved in mediating protection of diabetic kidney against cisplatin nephrotoxicity. The current study focused on the effect of normalization of hyperglycemia by vanadyl sulfate trihydrate on the initiation of protection and accumulation of platinum in kidneys of streptozotocin-diabetic rats. Streptozotocin-diabetic rats were treated with 0.75 mg/mL of vanadyl sulfate trihydrate in drinking water to normalize streptozotocin-induced hyperglycemia. Vanadyl sulfate treatment normalized plasma glucose and glycosylated hemoglobin levels in streptozotocin-diabetic rats to values observed for non-diabetic rats. Intraperitoneal administration of cisplatin (5 mg/kg bw) increased blood urea nitrogen by a factor >2.5 over baseline in both untreated and vanadyl-treated non-diabetic groups. Cisplatin-induced increases in blood urea nitrogen were 1.6 times baseline in both untreated and vanadyl-treated streptozotocin-diabetic rats. Renal platinum accumulation was significantly lower in streptozotocin-diabetic versus non-diabetic rats regardless of vanadyl sulfate treatment. Renal vanadium levels in all groups of diabetic rats were not significantly different from each other. These results indicate that normalization of plasma glucose levels with vanadyl sulfate in streptozotocin-diabetic rats did not reverse protection of streptozotocin-diabetic kidney against cisplatin nephrotoxicity. /Trihydrate/|In the present study the antitumor effects of a new vanadium complex with cysteine in relation to identical doses of vanadyl sulfate and cysteine, in tumor bearing rats are investigated. Male Wistar rats were injected with benzo(a)pyrene and divided into 4 groups of 21 rats each. Control group was treated only with BaP. The first group (TR-1) was treated by vanadyl sulfate /orally/ at daily doses of 0.5 mg of V/kg bw/day. The second (TR-2) by cysteine at doses of 4.5 mg/kg bw/day and the third group (TR-3), by the complex V(III)-cysteine at daily doses of V 0.5 mg/kg bw (containing cysteine at concentrations of 4.5 mg/bw). Treatment was started when tumors were developed (evidenced from a palpable mass at the site of BaP injection) and went on until death. Toxicological tests were performed in 27 rats divided into a control group and two test groups; T-1 administered with vanadyl sulfate at daily doses of 18.5 mg V/kg bw and T-2 group with V(III)-cysteine complex at daily doses of 18.5 V/kg bw, for 9 weeks. Mean survival time, death rate, tumor growth rate, the carcinogenic potency of BaP, and the anticarcinogenic potency in relation to histological findings in each treatment group were calculated in each group in order to evaluate the antitumor effects of the substances used. Vanadyl sulfate, cysteine and V(III)-cysteine exerted antitumor effects on leiomyosarcoma bearing Wistar rats. However, V(III)-complex exerted much more potent effects than the other treatments, significantly prolonging mean survival time, retarding tumor growth rate, and decreasing the carcinogenic potency of BaP in the TR-3 group, in comparison to the control and the TR-1 and TR-2 groups. Moreover V(III)-cysteine complex resulted in complete remission of 4 (19.7%) of the tumor bearing rats. Blood, urine, biochemical routine tests as well as autopsy did not reveal any toxic effects either of vanadyl sulfate or V(III)-cysteine complex. Vanadyl sulfate, cysteine and V(III)-cysteine complex exerted antitumor effects in tumor bearing rats. The V(III)-cysteine complex, however, exerts much more potent effects, as evident from the results of the present study. These beneficial effects of the above complex, in combination with its low toxicity provide evidence suggest its possible application in the treatment of human malignant diseases.|... Two vanadium compounds, VOSO4 and V2O5, and fly ash from an oil-fueled power plant were dissolved or suspended in culture medium over a range of concentrations and epithelia were exposed for 1 hr/day, for 9 consecutive days. At intervals during this period, alterations in cilia-beating frequency, cytology, and histology were documented by light microscopy. Explants treated with VOSO4 either decreased ciliary activity or produced ciliostasis depending upon the concentration and length of exposure. Early morphological alterations consisted of vacuolization of both nuclei and cytoplasm. After multiple exposures, cytology of VOSO4-treated respiratory mucosa was markedly affected. Similar changes were observed in cultures exposed to V2O5; however, the cytotoxicity appeared earlier and was more pronounced.

LC50 Mouse inhalation 0.125 mg/L/4 hrs|LC50 Rat inhalation <1.0 mg/L/4 hrs|LD50 Rat (male) oral 467.2 mg/kg bw|LD50 Rat (male) oral 448 mg/kg bw|For more Non-Human Toxicity Values (Complete) data for VANADYL SULFATE (11 total), please visit the HSDB record page.

Anhydrous vanadyl sulfate occurs in the mineral pauflerite which is a mineral of fumarolic origin (often in the vicinity of volcanoes)(1). Hydrated forms of vanadyl sulfate, also rare occurrence in nature minerals, include hexahydrate (stanleyite), pentahydrates (minasragrite, orthominasragrite and anorthominasragrite) and trihydrate (bobjonesite)(2,3).

The best food sources of vanadium are mushrooms, shellfish, black pepper, parsley, dill weed, beer, wine, grain and grain products, and artificially sweetened drinks. Vanadium exists in several forms, including vanadyl sulfate and vanadate. Vanadyl sulfate is most commonly found in nutritional supplements(1).

According to the 2012 TSCA Inventory Update Reporting data, 1 reporting facility estimates the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of vanadyl sulfate in the United States may be as low as <10 workers and as high as <10 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 106 workers (0 of these are female) were potentially exposed to vanadyl sulfate in the US(1). Occupational exposure to vanadyl sulfate may occur through inhalation and dermal contact with this compound at workplaces where vanadyl sulfate is produced or used(2). The general population may be exposed to vanadyl via ingestion of food and nutritional supplements containing vanadyl sulfate(3).|... Inhalation; possibly, though to a lesser extent, from ingestion of the pentoxide, sulfate or mixed vanadium dust. The exposure has usually occurred during the cleaning of oil fired burners or gas turbines, but has also been noticed in the extraction process of vanadium from vanadium containing ores; one of the earliest of these observations was ... /published in 1911, but the/ conclusions have not been universally confirmed ...

/EXPL THER/ Diabetes mellitus manifests itself in a wide variety of complications and the symptoms of the disease are multifactorial. The present study was carried out to investigate the effects of vanadyl sulfate on biochemical parameters, enzyme activities and brain lipid peroxidation, glutathione and nonenzymatic glycosylation of normal- and streptozotocin-diabetic rats. Streptozotocin (STZ) was administered as a single dose (65 mg/kg) to induce diabetes. A dose of 100 mg/kg vanadyl sulfate was orally administered daily to STZ-diabetic and normal rats, separately until the end of the experiment, at day 60. In STZ-diabetic group, blood glucose, serum sialic and uric acid levels, serum catalase (CAT) and lactate dehydrogenase (LDH) activities, brain lipid peroxidation (LPO), and nonenzymatic glycosylation (NEG) increased, while brain glutathione (GSH) level and body weight decreased. In the diabetic group given vanadyl sulfate, blood glucose, serum sialic and uric acid levels, serum CAT and LDH activities and brain LPO and NEG levels decreased, but brain GSH and body weight increased. The present study showed that vanadyl sulfate exerted antioxidant effects and consequently may prevent brain damage caused by streptozotocin-induced diabetes.|/EXPL THER/ The aim of this study was to investigate the protective effects of vanadyl sulfate on aorta tissue of normal and streptozotocin (STZ)-induced diabetic rats, morphologically, and biochemically. The animals were made diabetic by an intraperitoneal injection of streptozotocin (65 mg/kg) and vanadyl sulfate (100 mg/kg) that was given every day for 60 days by gavage technique to rats. Under the light and transmission electron microscopes, hypertrophy of the vessel wall, focal disruption in the elastic lamellae, an increase in thickness of total aortic wall, tunica intima, subendothelial space and adventitial layer, and a disorganization in smooth muscular cells of the tunica media were observed in diabetic animals. The aorta lipid peroxidation (LPO) levels were significantly increased and the aorta glutathione (GSH) levels were significantly reduced in STZ diabetic rats. In diabetic rats administered vanadyl sulfate for 60 days, aorta LPO levels significantly decreased and the aorta GSH level significantly increased. In conclusion, in vivo treatment with vanadyl sulfate of diabetic rats prevented the morphological and biochemical changes observed in thoracic aorta of diabetic animals.|/EXPL THER/ Vanadyl sulfate (VS) and taurine are two promising agents in the treatment of diabetes related to their antihyperglycemic, antihyperlipidemic, and hyperinsulinemic effects. Data about the effects of VS on the oxidant-antioxidant system is limited and controversial. However, taurine is a well-documented antioxidant agent and our aim was to investigate the effects of VS, taurine and VS, and taurine combination on the oxidative-antioxidative systems in streptozotocin-nicotinamide (STZ-NA) diabetic rats. Nicotinamide (230 mg/kg, ip) and streptozotocin (65 mg/kg, ip) were administered. VS (0.75 mg/mL) and taurine (1%) were added to drinking water for 5 weeks. Rats were divided as control (C), diabetes (D), diabetes+VS (D+VS), diabetes+taurine (D+T), diabetes+VS, and taurine (D+VST). Plasma and tissue malondialdehyde (MDA) levels were measured by high-performance liquid chromatography and spectrophotometry, respectively. Paraoxonase and arylesterase activities were measured by spectrophotometric methods and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined using commercial kits. VS, taurine, and VS and taurine combination treatments reduced the enhanced blood glucose, serum total cholesterol and triglyceride, tissue MDA and plasma MDA (except in the D+VS group) levels and increased the reduced serum insulin level, serum paraoxonase and arylesterase activities, GSH-Px activity and SOD activity (except in the D+VS group). The findings of the present study suggest that VS and taurine exert beneficial effects on the blood glucose and lipid levels in STZ-NA diabetic rats. However, VS might exert prooxidative or antioxidative effects in various components of the body and taurine and VS combination might be an alternative for sole VS administration.|/EXPL THER/ In recent years, the role of free radical damage consequent to oxidative stress is widely discussed in diabetic complications. In this aspect, the protection of cell integrity by trace elements is a topic to be investigated. Vanadium is a trace element believed to be important for normal cell function and development. The aim of the present study was to investigate the effect of vanadyl sulfate supplementation on the antioxidant system in the muscle tissue of diabetic rats. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg body weight) to male Swiss albino rats. The rats were randomly divided into 4 groups: Group I, control; Group II, vanadyl sulfate control; Group III, STZ-diabetic untreated; Group IV, STZ-diabetic treated with vanadyl sulfate. Vanadyl sulfate (100 mg/kg) was given daily by gavage for 60 days. At the last day of the experiment, rats were killed, muscle tissues were taken, homogenized in cold saline to make a 10% (w/v) homogenate. Body weights and blood glucose levels were estimated at 0, 30 and 60th days. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), as well as carbonic anhydrase (CA), myeloperoxidase (MPO) activities and protein carbonyl content (PCC) were determined in muscle tissue. Vanadyl sulfate administration improved the loss in body weight due to STZ-induced diabetes and decreased the rise in blood glucose levels. It was shown that vanadium supplementation to diabetic rats significantly decrease serum antioxidant enzyme levels, which were significantly raised by diabetes in muscle tissue showing that this trace element could be used as preventive for diabetic complications.|For more Therapeutic Uses (Complete) data for VANADYL SULFATE (7 total), please visit the HSDB record page.

Substances which lower blood glucose levels. (See all compounds classified as Hypoglycemic Agents.)

The study used higher doses of vanadyl sulfate (equivalent to 7.56 and 15.12 mg V/kg), which are within the same dose range as doses used for demonstrating its anti-diabetic activity. Absolute bioavailability, calculated as ratio of vanadium AUC ext after oral or iv administration, were similar between doses (15.7% and 16.4%), indicating that for pharmacologically active doses vanadyl sulfate actual bioavailability is relatively high and not dose-dependent.|Dietary vanadium as vanadyl sulfate is retained in rat tissues: heart >spleen >thyroid >lung >kidney; about 10% of the injected dose is retained in the tissues in experimental animals. Bone retains about 50% of it, presumably because vanadates are isomorphic with phosphates.|Rats absorbed an average of 0.5% of orally administered vanadyl sulfate.|Plants of garlic (Allium sativum) were germinated at 30 °C in a 5 mM calcium sulfate aqueous solution for 4 days. Plants were then suspended in vanadyl oxide sulfate aqueous solutions (concentration range 1.6x10-4 to 5.0x10-3 M, volume: 50 mL and initial pH approx 3-4). After timed incubations, varying from 10 min to 8 days, plant samples were removed from solution and washed. Their roots, cloves, and leaves were cut and immediately subjected to ESR spectroscopy. Examination of the ESR parameters allowed exclusion of the presence of VO(H2O)5 +2 species and indicated that the ions were almost totally bound to ligands having low molecular weights. ... Most of adsorbed VO+2 ions accumulated in the root as soluble low molecular weight complexes of o-diphenolic compounds. However, with increasing concentration, immobilized oxovanadium(IV) ions, possibly associated with acid polysaccharide components, were also detected. When plants were exposed to solutions containing VO+2 and EDTA (ligand-to-metal molar ratio= 1:1) spectra of roots showed only the isotropic signals of the soluble VO(EDTA) complex, and they are mobile enough to be extensively translocated to the tops. /Vanadyl oxide sulfate aqueous solution/|For more Absorption, Distribution and Excretion (Complete) data for VANADYL SULFATE (8 total), please visit the HSDB record page.

Within tissues in organisms, V3+ and V4+ predominate because of largely reducing conditions; in plasma, however, which is high in oxygen, V5+ is formed.

The half-life for vanadium elimination from the kidney of Wistar rats fed vanadyl sulfate trihydrate (0.75 mg/mL) in drinking water for 3 weeks was found to be 11.7 days. It is supported by another study in which the half-lives were determined of vanadium elimination from various organs of male Sprague-Dawley rats treated with sodium orthovanadate or vanadyl sulfate at concentrations ranging from 1.6-160 umol V/kg bw/day for a week. The values varied greatly among organs; the liver and kidney have the shortest (about 3-4 days) and the testis the longest (about 14-16 days) half-lives. Almost all the tissues showed a slightly longer vanadium half-life in the group of rats fed sodium orthovanadate compared to those receiving vanadyl sulfate.|Experiments were conducted to determine the distribution and effects of selected vanadium (V) salts in male rats following continuous ingestion. Wistar rats were continuously fed drinking water ad. Lib. containing 5 and 50 ppm V as vanadyl sulfate and sodium orthovanadate for a 3-month period. At the end of the 3rd, 6th, 9th, and 12th week, blood, kidney, liver, bone, muscle, and digestive tract were collected and analyzed for V utilizing flame atomic absorption spectrophotometry. In addition, the decline of vanadium residues in tissues after 6 weeks of continuous exposure was studied in selected groups. At the 5 and 50 ppm levels, V had no significant effect on body weights or hematocrit values. In the tissues of animals given 5 ppm of V salt, the V contents were essentially the same as those in controls. The tissues of animals given 50 ppm of V salt showed increased levels of vanadium. Kidney had the highest concentration, followed by bone, liver, and muscle. In general, the tissue concentrations of V in animals given 50 ppm as sodium orthovanadate were higher than those exposed to similar levels as vanadyl sulfate. The V concentration in kidney of the animals given 50 ppm sodium orthovanadate continued to rise until the 9th week of sampling, whereas the V content of other tissues analyzed for the treated animals plateaued from the 3rd week. The concentration of V in tissues after cessation of exposure declined rapidly except in the bone. After 6 weeks of the depletion phase the concentration of vanadium in animals given vanadyl sulfate returned to control values except in bone and kidneys. The animals exposed to sodium orthovanadate contained relatively high concentrations of V even after a 6-week depletion phase.

Vanadium salts such as vanadyl sulfate (VS), potent inhibitors of protein tyrosine phosphatases, have been shown to mimic, augment, and prolong insulin's action. However, the molecular mechanism of responses to these salts is not clear. In the present studies, we examined if VS-induced effects on insulin action are associated with enhancement or augmentation in the activation state of key components of the insulin signaling pathway. Treatment of insulin receptor-overexpressing cells with insulin or VS resulted in a time-dependent transient increase in phosphorylation and activation of extracellular signal-regulated kinases 1 and 2 (ERK 1/2) that peaked at about 5 min, then declined rapidly to about baseline within 30 min. However, when the cells were treated with VS before stimulation with insulin, sustained ERK 1/2 phosphorylation and activation were observed well beyond 60 min. VS treatment also prolonged the insulin-stimulated activation of phosphatidylinositol 3-kinase (PI3-K), which was associated with sustained interaction between insulin receptor substrate-1 (IRS-1) and the p(85 alpha) subunit of phosphatidylinositol 3-kinase (PI3-K) in response to insulin. These data indicate that prolongation of insulin-stimulated ERK 1/2 and PI3-K activation by VS is due to a more stable complex formation of IRS-1 with the p(85 alpha) subunit which may, in turn, be responsible for its ability to enhance and extend the biological effects of insulin.

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution. (ERG, 2016)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim calm and warm. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. (ERG, 2016)

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ Vanadyl sulfate is apparently used by some weight-training athletes in an attempt to improve performance, as it has been claimed to lower blood cholesterol levels. A double-blind trial ... investigated the effects of administration of vanadyl sulfate on hematological indices, blood viscosity, and biochemistry in weight-training athletes. The treatment group (11 males; 4 females) was orally administered 0.5 mg/kg bw/day for 12 weeks, and a control group (12 males; 4 females) received placebo capsules. At the end of the study, there were no significant differences between the groups in terms of body weight, blood pressure, standard hematological indices, blood viscosity, or standard blood biochemistry measurements.|/GENOTOXICITY/ ... Vanadyl sulfate /was/ not found to increase the frequency of structural chromosome aberrations /in human leukocytes/, whereas a significant increase in numerical aberrations, micronuclei, and satellite associations was found. Fluorescence in situ hybridization (FISH) applied to the human lymphocyte micronucleus assay, by means of an alphoid centromere-specific DNA probe, confirmed the aneuploidogenic potentiality of vanadium.|/GENOTOXICITY/ It /was/ concluded that vanadium oxide sulphate induced micronuclei in cultured human peripheral blood lymphocytes and human lymphoblastoid TK6 cells when tested for 3+21 hours and for 24+24 hours in the absence of S9. Vanadium oxide sulphate did not induce micronuclei in cultured human peripheral blood lymphocytes when tested up to toxic concentrations for 3+21 hours in the presence of S9.|/GENOTOXICITY/ The genotoxicity of four vanadium compounds, sodium metavanadate (NaVO3), ammonium metavanadate (NH4VO3), sodium ortovanadate (Na3VO4) and vanadyl sulfate (SVO5), was evaluated in human lymphocyte cultures using structural and numerical chromosome aberrations, micronuclei, sister-chromatid exchanges and satellite chromosome associations as endpoints. These compounds were not found to increase the frequency of structural chromosome aberrations whereas a significant increase in numerical aberrations, micronuclei and satellite associations was found. Since these results could have been related to a possible mechanism of the action of vanadium as a mitotic spindle poison, the fluorescence in situ hybridization (FISH) technique was applied to the human lymphocyte micronucleus assay, by means of an alphoid centromere-specific DNA probe. The four vanadium salts showed a micronucleus percentage with positive signal (presence of centromere and thus of whole chromosome(s)) that was always higher than 68% at all doses tested. That confirmed the aneuploidogenic potentiality of vanadium.|For more Human Toxicity Excerpts (Complete) data for VANADYL SULFATE (8 total), please visit the HSDB record page.

oxosulfatovanadium(IV)

Under environmental conditions, vanadium may exist in oxidation states +3, +4, and +5. V3+ and V4+ act as cations, but V5+, the most common form in the aquatic environment, reacts both as a cation and anionically as an analogue of phosphate. /Vanadium ions/