Physicochemical Properties
| Molecular Formula | O2SI |
| Molecular Weight | 60.0843 |
| Exact Mass | 59.966 |
| CAS # | 68855-54-9 |
| Related CAS # | 31392-49-1 |
| PubChem CID | 24261 |
| Appearance |
Amorphous powder Transparent to gray powder (Note: Amorphous silica is the non-crystalline form of O2Si). ... solid Silica gel is a coherent, rigid, continuous three-dimensional network of spherical particles of colloidal microporous silica. Transparent crystals |
| Density | 0.47 g/cm3 (loose weight)(lit.) |
| Melting Point | >450℃ |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 0 |
| Heavy Atom Count | 3 |
| Complexity | 18.3 |
| Defined Atom Stereocenter Count | 0 |
| SMILES | O=[Si]=O |
| InChi Key | VYPSYNLAJGMNEJ-UHFFFAOYSA-N |
| InChi Code | InChI=1S/O2Si/c1-3-2 |
| Chemical Name | dioxosilane |
| HS Tariff Code | 2934.99.9001 |
| Storage |
Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion ...Rats /were exposed/ by inhalation to... silica (particle size 0.5 to 5 m) in the form of Belgian glass sand for periods ranging from 0.5 to 40 hr. The initial deposition of silica was highest in the tracheobronchial ciliated air passages; it also was seen throughout the acini, where the extent of deposition decreased as the respiratory airways proceeded distally. The distribution of particles was not uniform between the different acini, and, 2 to 3 months following cessation of exposure, aggregates were formed, primarily in the proximal alveolar ducts but also in the distal portion of the acini. Inhalation studies with rats... indicate that the long-term clearance of quartz after inhalation is slow and biphasic, whereas amorphous silica dusts are cleared more rapidly. The absolute amount of silica dust eliminated increased with lung burden, but the efficiency of the elimination was either constant or decreased with time. ...The half-life lung clearance of rats exposed via inhalation to an amorphous silica suspension (Ludox ) at concentrations up to 150 mg/cu m was about 50 days. A study /in (1983)/, showed that the total silica content in the lungs of guinea pigs exposed by inhalation for up to 2 years to a cristobalite sample or to amorphous silica (at dust concentrations of 150 mg/cu m or 100 mg/cu m , respectively) increased linearly over 21 months, without evidence that lung retention rates changed with time. ...The maximum lung content of cristobalite was only 68 mg/lung, whereas that of amorphous silica was 120 mg/lung. The total amount of accumulated silica varied inversely with the degree of pulmonary damage. /It was/ suggested that silica dust producing cell damage may be more efficiently cleared from the lung than are the less toxic amorphous forms. However, this difference also could be due to different rates of deposition for the two dust forms. The cristobalite sample, which was 45% cristobalite and 55% diatomaceous earth, was significantly coarser (and less likely to deposit in the lungs) than the amorphous silica, which contained 100% diatomaceous earth. Also, tissue changes induced by cristobalite could have altered particle deposition. In a long-term inhalation study with guinea pigs, ...the amount of silica retained as a result of 8-hr/day exposures to amorphous silica (Hi-Sil 233) /was compared/ with that retained during inhalation of quartz dust for a comparable 12-month period. Guinea pigs that inhaled quartz dust at a concentration of 106 mg/cu m retained between 500 and 600 mg of silica, whereas <10 mg of dust was retained in those that inhaled 126 mg/cu m of amorphous silica. After 12 months of exposure, the relative silica content (silica mass/lung mass) decreased in guinea pigs exposed to quartz dust, but continued to increase slowly in the animals exposed to the amorphous silica. This difference was explained by an increasing nonsiliceous materials content (e.g., collagen, minerals) in the lungs of the quartz-exposed animals associated with the progressive deposition of fibrous tissue in the lungs. Six months after cessation of exposure, the silica content of the lungs of Hi-Sil 233-exposed animals was similar to that of untreated controls. This lack of accumulation may be due, in large part, to the higher solubility of amorphous silica compared to quartz... . By comparison, the elimination of silica from the quartz-exposed guinea pigs was negligible, and the silicotic lesions continued to progress during this elimination phase. For more Absorption, Distribution and Excretion (Complete) data for AMORPHOUS SILICA (6 total), please visit the HSDB record page. Rats were exposed for 6 hr/day, on 5 days/week, for up to 13 weeks to 3 mg/cu m crystalline... Lung burdens were 819... ug for crystalline... Deposition of particles in the respiratory bronchioles and proximal alveoli results in slow clearance, interaction with macrophages and a greater likelihood of lung injury. This contrasts with deposition on the conducting airways where the majority of the particles are cleared by the mucociliary escalator. Therefore, quartz particles with an aerodynamic diameter below 10 um are likely to be the most harmful to humans. There are few data on human lung quartz-dust burdens that allow conclusions to be drawn about deposition or clearance. However, quartz is found in the bronchoalveolar macrophages and sputum of silicotic patients. Also, at autopsy, there is wide variation in the masses and proportions of quartz retained in the lung. For example... 25-264 mg /were reported/ per single lung at autopsy in hard-rock miners with 14-36 years of exposure; these miners had variable amounts of pathological response but there was not a good correlation between lung crystalline quartz content and pathological score. The well-documented effect of smoking on clearance is a further confounding factor in drawing conclusions about clearance kinetics in humans. The physico-chemical changes in quartz that result from residence in the lung could be an important factor in determining the continuing toxicity of quartz to the lung following deposition. As a response to the rejection of the 'mechanical model' of silicosis, which had propounded that any particle with 'sharp or jagged edges' might injure tissue, a solubility theory of silicosis was proposed. The solubility theory was based on the release from silica of silicic acid, which was considered to be a 'protoplasmic poison.' In fact very little dissolution occurs; for example, 9 mg SiO2 (0.45%) was released from 2 g crystalline silica placed in ascitic fluid for two weeks. Current theories no longer consider that the dissolution of quartz contributes substantially to its clearance or to changes in its biological activity. Indeed there is evidence of enrichment of crystalline silica in lungs of individuals exposed to hard rock compared to the dust in the air they breathed, suggesting that crystalline silica is less-efficiently cleared, either by dissolution or mechanical clearance, than the non-silica mineral components of the dust... biopersistence was assessed in occupationally exposed subjects by counting silica particles in bronchoalveolar lavage (BAL) fluid after varying periods of time since their last occupational exposure. Crystalline silica was found to be among the most biopersistent of non-fibrous mineral particles. For more Absorption, Distribution and Excretion (Complete) data for CRYSTALLINE SILICA (17 total), please visit the HSDB record page. |
| Toxicity/Toxicokinetics |
Toxicity Summary IDENTIFICATION: Quartz is a frequently occurring solid component of most natural mineral dusts. HUMAN EXPOSURE: Human exposures to quartz occur most often during occupational activities that involve the movement of earth, disturbance of silica containing products (masonry, concrete), or use or manufacture of silica containing products. Environmental exposure to ambient quartz dust can occur during natural, industrial and agricultural activities. Respirable quartz dust particles can be inhaled and deposited in the lung. There are many epidemiological studies of occupational cohorts exposed to respirable quartz dust. Silicosis, lung cancer and pulmonary tuberculosis are associated with occupational exposure to quartz dust. Statistically significant increases in deaths or cases of bronchitis, emphysema, chronic obstructive pulmonary disease, autoimmune related diseases (scleroderma, rheumatoid arthritis, systemic lupus erythematosus) and renal diseases have been reported. Silicosis is the critical effect for hazard identification and risk assessment. There are sufficient epidemiological data to allow the risk of silicosis to be quantitatively estimated, but not to permit accurate estimations of risks for other health effects. ANIMAL STUDIES: Quartz dust induces cellular inflammation in vivo. Short term experimental studies of rats have found that intratracheal instillation of quartz particles leads to the formation of discrete silicotic nodules in rats, mice and hamsters. Inhalation of aerosolized quartz particles impairs alveolar macrophage clearance functions and leads to progressive lesions and pneumonitis. Oxidative stress (formation of hydroxyl radicals, reactive oxygen species, or reactive nitrogen species) has been observed in rats after intratracheal instillation or inhalation of quartz. Many experimental in vitro studies have found the surface characteristics of the crystalline silica particle influence its fibrogenic activity and a number of features related to its cytotoxicity. Long term inhalation studies of rats and mice have shown that quartz particles produce cellular proliferation, nodule formation, suppressed immune functions and alveolar proteinosis. Experimental studies of rats reported the occurrence of adenocarcinomas and squamous cell carcinomas after the inhalation or intratracheal instillation of quartz. Pulmonary tumors were not observed in experiments with hamsters or mice. Quartz did not test positively in standard bacterial mutagenesis assays. In experimental studies of particles, results may vary depending on the test material, concentration administered and species tested. The experiments with quartz particles involved specimens from various sources, using various doses, particle sizes and species. Data on the reproductive and developmental effects of quartz in laboratory animals are not available. The adverse effects of quartz in aquatic organisms and terrestrial mammals have not been studied. Interactions Another form of amorphous silica, precipitated amorphous silica, /may/ form layers around quartz particles, which may facilitate the toxic action of quartz. Ameliorating effects of /poly-2-vinylpyridine-N-oxide/ PVNO were observed for pulmonary damage from colloidal SiO2 13 lead chromate-based pigments were assayed for mutagenicity and toxicity using Salmonella typhimurium TA100 with and without S9, both in the presence and absence of the chelating agent, nitrilotriacetic acid (NTA). In general, the use of NTA to solubilize the compounds resulted in /enhanced/ mutagenicity and/or toxicity ... . Encapsulation of pigments with amorphous silica rendered these pigments non-mutagenic and non-toxic, indicating that the active moieties were biologically unavailable to the bacteria. Lazaroid (U-75412E) scavenges .OH radicals generated by crystalline silica-mediated reaction from H2O2 and inhibits lipid peroxidation in macrophages induced by these particles. Occupational studies have found that the major source of co-morbidity with silicosis is infection by Mycobacterium tuberculosis (TB). Non-Human Toxicity Values LD50 Rat oral >22,500 mg/kg LD50 Mouse oral >15,000 mg/kg LD50 Rat iv 500 mg/kg bw /Quartz (10-200 um)/ |
| Additional Infomation |
Therapeutic Uses /Exptl Ther/ Previous in vitro studies showing that bioactive glasses support the growth and maturation of rat osteoblast-like cells and promote the expression and maintenance of the osteoblastic phenotype have suggested that there is both a solution-mediated and a surface-controlled effect on cell activity. This study investigated the behavior of human primary osteoblast-like cells cultured in contact with three different bioactive glasses and compared them with amorphous silica (SiO2) used in the form of granules. Osteoblasts synthesize collagen type I, which is subsequently mineralized. Immunoblot and biochemical studies showed increased collagen release from osteoblast-like cells cultured in contact with bioactive glasses over that of controls. Among the three bioactive glasses, 45S5 is the highest inducer of osteoblast-like cell collagen release; moreover, mRNA for type I collagen was stimulated approximately three- to fivefold after 45S5 treatment. 77S bioactive glass similarly increased type I collagen synthesis even though alkaline phosphatase was not higher. These results suggest that 45S5 Bioglass not only induces osteogenic differentiation of human primary osteoblast-like cells, but can also increase collagen synthesis and release. The newly formulated bioactive gel-glass 77S seems to have potential applications for tissue engineering, inducing increased collagen synthesis. |
Solubility Data
| Solubility (In Vitro) | May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples |
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples. Injection Formulations (e.g. IP/IV/IM/SC) Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] *Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline) Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline) Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline) Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil) Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Oral Formulations Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). Oral Formulation 3: Dissolved in PEG400 Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose Oral Formulation 6: Mixing with food powders Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 16.6445 mL | 83.2224 mL | 166.4447 mL | |
| 5 mM | 3.3289 mL | 16.6445 mL | 33.2889 mL | |
| 10 mM | 1.6644 mL | 8.3222 mL | 16.6445 mL |