1. Na(2)s(2)o(5)
2. Sodium Disulfite
3. Sodium Metabisulfite, 35s2-labeled Cpd
4. Sodium Pyrosulfite
1. 7681-57-4
2. Sodium Pyrosulfite
3. Sodium Disulfite
4. Disodium Pyrosulfite
5. Sodium Metabisulphite
6. Disodium Disulphite
7. Disodium Disulfite
8. Disodium Metabisulfite
9. Sodium Pyrosulphite
10. Sodium Bisulfite Anhydrous
11. Na2s2o5
12. Disodium Pentaoxodisulfate
13. Mfcd00167602
14. 4von5fns3c
15. Sodium Metabisulfite [nf]
16. Ins No.223
17. Sodium Metabisulfite (e 223)
18. Ins-223
19. Nsc-158277
20. Nsc-227243
21. Natrii Disulfis
22. Campden Tablets
23. E-223
24. Sodium Metabisulfite (nf)
25. Natrium Pyrosulfit
26. Natriummetabisulfit
27. Natrium Metabisulfurosum
28. Ccris 3951
29. Hsdb 378
30. Sodium Pyrosulfite (na2s2o5)
31. Sodium Metabisulfite (na2-s2o5)
32. Einecs 231-673-0
33. Unii-4von5fns3c
34. Ai3-51684
35. Disodiumdisulphite
36. Sodium Metasulfite
37. Sodiummetabisulphite
38. Sodium Metabisuifite
39. Sodium Metabisuiphite
40. Sodium Meta Bisulfite
41. Sodium Meta-bisulfite
42. Ec 231-673-0
43. Disodium Pyrosulphite
44. Sodium Pyrosulfite (jp17)
45. Chembl2016976
46. Dtxsid0029684
47. Sodium Pyrosulfite [jan]
48. Sodium Metabisulfite [ii]
49. Sodium Metabisulfite [mi]
50. Chebi:114786
51. Sodium Metabisulfite [fcc]
52. Sodium Metabisulfite [hsdb]
53. Sodium Metabisulfite [inci]
54. Sodium Metabisulfite, So2 58.5%
55. Sodium Metabisulfite [vandf]
56. Sodium Metabisulfite [mart.]
57. Sodium Metabisulfite A.c.s. Reagent
58. Sodium Metabisulfite [usp-rs]
59. Sodium Metabisulfite [who-dd]
60. Akos015950722
61. Disulfurous Acid, Sodium Salt (1:2)
62. Nsc 158277
63. Nsc 227243
64. E223
65. Sodium Metabisulfite [ep Monograph]
66. Ft-0645096
67. Disodium Oxido(oxo)-kappa(4)-sulfanesulfonate
68. D02054
69. Q284549
| Molecular Weight | 190.11 g/mol |
|---|---|
| Molecular Formula | Na2O5S2 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 6 |
| Rotatable Bond Count | 0 |
| Exact Mass | 189.89825401 g/mol |
| Monoisotopic Mass | 189.89825401 g/mol |
| Topological Polar Surface Area | 125 Ų |
| Heavy Atom Count | 9 |
| Formal Charge | 0 |
| Complexity | 136 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 3 |
Exptl Use: Conversion of Cr (VI) to Cr (III) via sodium metabisulfite or sodium dithionite prevents Cr dermatitis in sensitive individuals.
PMID:6216046 Wall LM; Contact Dermatitis 8 (5): 291-3 (1982)
Bronchoconstrictor Agents
Agents causing the narrowing of the lumen of a bronchus or bronchiole. (See all compounds classified as Bronchoconstrictor Agents.)
A method to estimate the total and regional deposition of disodium disulfite after aerosol inhalation was developed. Original particle sizes between 0.1 and 10 um were used. The particle size changes with the humidity of the environment because of the hygroscopic properties of the disulfite. It shows high deposition values of about 1/1000 of the inhaled particle mass/sq cm in the nasal region, values of about 1/100,000/sq cm in the tracheobronchial airways and a mean surface deposition in the pulmonary region which is a factor of 10,000 smaller than in the nose. The findings correspond to pathological effects found in animal inhalation studies.
European Chemicals Bureau; IUCLID Dataset for Sodium Metabisulfite (7681-57-4), p.82 (2000 CD-ROM edition). Available from, as of July 25, 2011: https://esis.jrc.ec.europa.eu/
Sulfites are generated in the human body by processing of the sulfur-containing amino acids, cysteine and methionine. Endogenous sulfite is maintained at a low, steady-state concentration by a mitochondrial enzyme, sulfite oxidase, that promotes the oxidation of sulfite to sulfate that is excreted in the urine. Sulfites can also be metabolized to thiosulfates (enzymatic reaction of sulfite with 3-mercaptopyruvate) or S-sulfonate compounds (nonenzymatic reaction with disulfide bonds). Thiosulfate and S-sulfonate were detected at very low concentrations in the urine of normal humans or rats, but were excreted in large amounts by those deficient in sulfite oxidase. /Sulfites/
Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite,and Potassium Metabisulfite. International Journal of Toxicology 22 (S2): 63-88 (2003).
Sulfite that enters the body via ingestion, inhalation, or injection is metabolized by sulfite oxidase to sulfate. Oral dose studies using dogs and rats and intravenous (IV) dose studies using rabbits, rats, and rhesus monkeys, demonstrated rapid metabolic clearance. In all species
Cosmetic Ingredient Expert Review Panel; Final Report on the Safety Assessment of Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite,and Potassium Metabisulfite. International Journal of Toxicology 22 (S2): 63-88 (2003).
Sulfite is a potentially toxic molecule that might enter the body via ingestion, inhalation, or injection. For cellular detoxification, mammalians rely on sulfite oxidase to convert sulfite to sulfate. The purpose of this research was to determine the effect of sulfite on zinc, iron, and copper levels in rat liver and kidney tissues. Forty normal and sulfite oxidase-deficient male albino rats were divided into four groups that included untreated controls (group C), a sulfite-supplemented group that received 70 mg sodium metabisulfite per kilogram per day (group S), a sulfite oxidase-deficient group (group D), and a sulfite oxidase-deficient group that was also given 70 mg sodium metabisulfite per kilogram per day (group DS). The iron and zinc levels in the liver and kidney in groups S and DS were not affected by sulfite treatment compared to their respective controls (groups C and D). Sulfite exposure led to an increase of kidney copper content in the S group when compared to untreated controls. The kidney copper levels were significantly increased in the unexposed deficient rats, but it was not different than that of the deficient rats that were given oral sulfite treatment. These results suggest that kidney copper levels might be affected by exogenous or endogenous sulfite.
Kucukatay V et al; Biol Trace Elem Res 114 (1-3): 185-195 (2006)
The mechanism of disodium disulfite induced bronchoconstriction was investigated in isolated human trachea preparations. Incubation of the trachea preparations with disodium disulfite at 10 uM induced depolarization combined with increased muscle tension. The effect was suppressed in the presence of a H1-receptor antagonist (pyrilamine maleate or cromolyn sodium). According to the author disodium disulfite increases the availability of endogenous histamine to the airway smooth muscle cells.
European Chemicals Bureau; IUCLID Dataset for Sodium Metabisulfite (7681-57-4), p.82 (2000 CD-ROM edition). Available from, as of July 25, 2011: https://esis.jrc.ec.europa.eu/
The effect of disodium disulfite solution on the trachea of anesthetized sheep was tested in vivo. Air supply was ensured by a tracheal cannula and a part of the trachea was filled with the solution at concentrations of 1, 20 and 100 mM. Disodium disulfite significantly increased arterial and venous blood flow, significantly reduced the potential difference to the tracheal lumen and significantly enhanced the permeability from tracheal lumen to venous blood for a low molecular weight hydrophilic tracer. Additionally the substance produced epithelial damage as confirmed histologically. The changes were not blocked by frusemide or flurbiprofen. The mechanism of the effects of disodium disulfite is uncertain but is consistent with the known actions of S02.
European Chemicals Bureau; IUCLID Dataset for Sodium Metabisulfite (7681-57-4), p.84 (2000 CD-ROM edition). Available from, as of July 25, 2011: https://esis.jrc.ec.europa.eu/
The mechanism of bisulfite induced bronchoconstriction was investigated in allergic sheep. Lung resistance was measured after application of disodium disulfite at concentrations of 25, 50 or 100 mg/mL for 30 breaths intratracheal with or without pretreatment with different drugs. Pretreatment with the anticholinergic agent ipratropium bromide or the antiasthma drug nedocromil sodium blocked the bronchoconstriction whereas the histamine H1-receptor antagonist chlorpheniramine was ineffective. According to the author in allergic sheep inhaled disodium disulfite causes bronchoconstriction that does not involve histamine release but appears to involve stimulation of bradykinin B2-receptors with subsequent activation of cholinergic mechanisms.
European Chemicals Bureau; IUCLID Dataset for Sodium Metabisulfite (7681-57-4), p.81 (2000 CD-ROM edition). Available from, as of July 25, 2011: https://esis.jrc.ec.europa.eu/
For more Mechanism of Action (Complete) data for SODIUM METABISULFITE (7 total), please visit the HSDB record page.
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