Chromic nitrate

400.15

237.904510

236-921-1

C6H0RE016B

2720

TSCA listed

DTXSID8065531

Dark purple to black

2834298000

189

Dark purple to black Crystalline Chunks

1.00 g/mL at 20 °C

60 °C(lit.)

> 100ºC (212 °F) (decomp.)

Soluble

1Pa at 20℃

mouse,LD50,intraperitoneal,110mg/kg (110mg/kg),Sangyo Igaku. Japanese Journal of Industrial Health. Vol. 20, Pg. 590, 1978.

Supports combustion, emits spicy and irritating smoke containing chromium and nitrogen oxides

III

5.1

UN 2720 5.1/PG 3

2

O,Xi,C

17-26-36-45-36/37/39-23

GB6300000

O,Xi,C

Color Code—Yellow: Reactive Hazard; Store in alocation separate from other materials, especially flammables and combustibles. Color Code—Blue: HealthHazard/Poison: Store in a secure poison location. Prior toworking with this chemical you should be trained on itsproper handling and storage. Chromium nitrate must bestored to avoid contact with strong reducing agents, fuels,and ether since violent reactions occur. Store in tightlyclosed containers in a cool, well-ventilated area away fromflammable and combustible materials. A regulated, markedarea should be established where this chemical is handled,used, or stored in compliance with OSHA Standard1910.1045. See OSHA Standard 1910.104 and NFPA 43ACode for the Storage of Liquid and Solid Oxidizers fordetailed handling and storage regulations.

Mixed with reducing agent, sulfur, phosphorus, etc., heated, impacted, friction can be explosive

P210, P220, P221, P261, P264, P271, P272, P273, P280, P283, P302+P352, P304+P312, P304+P340, P305+P351+P338, P306+P360, P312, P321, P332+P313, P333+P313, P337+P313, P362, P363, P370+P378, P371+P380+P375, P391, P403+P233, P405, P501

May ignite organic materials on contact; may be explosive when shocked or heated; powerful oxidizer. Very toxic.

This chemical is a strong oxidizer. Contact with reducing agents; fuels, ethers, and other flammable and combustible materials cause a fire and explosion hazard. Violent reaction with many compounds, including reducing agents; alcohols, chemically active metals; combustible materials, strong acids, alkaline earth sulfides, aluminum carbides, aluminum, amines, calcium sulfide, carbides, chlorine trifluoride, glycerin, hydrides, hydrochloric acid, hydrogen peroxide, hydrogen sulfide, hydroxylamine, magnesium, metal powders, metal sulfides, molybdenum, phenylhydrazine, phosphorous red/friction, phosphorous trichloride, silicon, sulfides, sulfur, sulfur Chromium Nitrate 845 dioxide, sulfur/friction, sulfuric acid, tungsten, hydrogen trisulfide

UN 2720 (CHROMIUM NITRATE)

|Danger|H271 (21.46%): May cause fire or explosion; strong Oxidizer [Danger Oxidizing liquids; Oxidizing solids]|P210, P220, P221, P261, P264, P271, P272, P273, P280, P283, P302+P352, P304+P312, P304+P340, P305+P351+P338, P306+P360, P312, P321, P332+P313, P333+P313, P337+P313, P362, P363, P370+P378, P371+P380+P375, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 302 companies from 18 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

moderately toxic

Oral LD50 for Cr (VI) is 135 - 175 mg/kg in mouse and 46 - 113 mg/kg in rat. Oral LD50 for Cr (III) in rat is >2000 mg/kg. LD50 of chromium (III) oxide in rats is reported to be > 5g/kg. Other LD50 values reported for rats include: 3.5 g/kg (CI 3.19-3.79 g/kg) for chromium sulphate; 11.3 g/kg for chromium (III) acetate; 3.3 g/kg for chromium nitrate; and 1.5 g/kg for chromium nitrate nonahydrate. Acute overdose of chromium is rare and seriously detrimental effects of hexavalent chromium are primarily the result of chronic low-level exposure. In case of overdose with minimal toxicity following acute ingestion, treatment should be symptomatic and supportive. There is no known antidote for chromium toxicity. Hexavalent chromium is a Class A carcinogen by the inhalation route of exposure and Class D by the oral route. The oral lethal dose in humans has been estimated to be 1-3 g of Cr (VI); oral toxicity most likely involves gastrointestinal bleeding rather than systemic toxicity. Chronic exposure may cause damage to the following organs: kidneys, lungs, liver, upper respiratory tract [MSDS]. Soluble chromium VI compounds are human carcinogens. Hexavalent chromium compounds were mutagenic in bacteria assays and caused chromosome aberrations in mammalian cells. There have been associations of increased frequencies of chromosome aberrations in lymphocytes from chromate production workers. In human cells _in vitro_, Cr (VI) caused chromosomal aberrations, sister chromatid exchanges and oxidative DNA damage.

In the blood, 95% of chromium (III) is bound to large molecular mass proteins, such as transferrin, while a small proportion associates with low molecular mass oligopeptides. Serum chromium is bound to transferrin in the beta globulin fraction.

Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms.

Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.

Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form. Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed. Vitamin C and the vitamin B niacin is reported to enhance chromium absorption. Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids. Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration. Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF).|Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile. Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter.|Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form. Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone.|Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day. The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day.

The metabolism of Cr (VI) involves reduction by small molecules and enzyme systems to generate Cr (III) and reactive intermediates. During this process, free radicals can be generated, which is thought to induce damage of cellular components and cause toxicity of chromium. The metabolites bind to cellular constituents.

The elimination half-life of hexavalent chromium is 15 to 41 hours.

Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein. As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells. Chromium attenuates the activity of PTP-1B _in vitro,_ which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling. Transient upregulation of AMPK by chromium also leads to increased glucose uptake.

chromic nitrate

All other chemical product and preparation manufacturing|Nitric acid, chromium(3+) salt (3:1): ACTIVE