Absorption, Distribution and Excretion
We developed a method for estimating the total and regional deposition of sodium bisulfite after inhalation of aerosols. The original particle size used ranged from 0.1 to 10 micrometers. Due to the hygroscopic nature of sodium bisulfite, its particle size varies with ambient humidity. Results showed that the deposition in the nasal region was approximately 1/1000 of the mass of the inhaled particles per square centimeter, the deposition in the tracheobronchial region was approximately 1/100,000 of the mass per square centimeter, and the average surface deposition in the lung region was 10,000 times smaller than that in the nasal region. These findings are consistent with the pathological effects observed in animal inhalation studies. Metabolism/Metabolites Sulfites are produced in the human body by the metabolism of the sulfur-containing amino acids cysteine and methionine. Endogenous sulfites are maintained at a low steady-state concentration by the mitochondrial enzyme sulfite oxidase. This enzyme promotes the oxidation of sulfites to sulfates, which are then excreted in the urine. Sulfites can also be metabolized to thiosulfates (an enzymatic reaction of sulfite with 3-mercaptopyruvate) or S-sulfonates (a non-enzymatic reaction with disulfide bonds). In normal humans and rats, the concentrations of thiosulfates and S-sulfonates in urine are extremely low, but excretion is high in individuals lacking sulfite oxidase. Sulfites ingested, inhaled, or injected sulfites are metabolized to sulfates by sulfite oxidase. Oral dose studies in dogs and rats, and intravenous dose studies in rabbits, rats, and rhesus monkeys, have shown rapid sulfite metabolism and clearance. In all species, ≤10% of the administered dose is excreted unchanged in the urine. One difference between exogenous and endogenous sulfite metabolism kinetics is that hepatic oxidation of exogenous sulfites (at least in rats) is diffusion-limited. The liver metabolizes a constant proportion of the sulfites it receives, but a limited amount of sulfites enters the systemic circulation via the liver.

Interactions
Sodium metabisulfite (Na₂S₂O₅) is a substance used as an antioxidant and antibacterial agent in various pharmaceuticals and as a preservative in many food preparations. In addition to its antioxidant activity, sulfites can be oxidized to sulfite radicals (SO₃⁻), thereby initiating lipid peroxidation. This study aimed to elucidate the effects of subchronic intake of Na₂S₂O₅ (520 mg/kg/day) on the activity of hepatic and renal antioxidant enzymes and lipid peroxidation in albino rats. Simultaneously, this study also tested the antioxidant effect of L-carnitine in Na₂S₂O₅-treated rats. All rats involved in the study underwent monitoring of plasma uric acid levels. Compared with the control group, the malondialdehyde (MDA) level in rats treated with Na₂S₂O₅ was significantly increased. Kidney MDA values were 2.21±0.21 nmol/mg protein and 1.22±0.35 nmol/mg protein, respectively, while liver MDA values were 79.85±19.5 nmol/mg protein and 31.36±5.0 nmol/mg protein, respectively. Compared with the control group, the selenium-glutathione peroxidase (GPx) activity in rats treated with Na₂S₂O₅ was also significantly increased. Kidney GPx values were 38.22±2.21 U/g protein and 8.09±0.76 U/g protein, respectively, while liver GPx values were 31.11±6.37 U/g protein and 11.70±1.02 U/g protein, respectively. In this study, plasma uric acid levels were also increased in rats treated with Na₂S₂O₅. No protective effect of L-carnitine against lipid peroxidation was observed in the liver and kidneys of rats treated with Na2S2O5. The data provided confirm the pro-oxidative activity of sulfites and suggest that increased glutathione peroxidase (GPx) activity and plasma uric acid levels may partially mitigate sulfite-induced oxidative damage to kidneys and hepatocytes. Sodium metabisulfite is incompatible with chloramphenicol due to its more complex reaction. Sodium metabisulfite can also inactivate cisplatin in solution. Sodium metabisulfite reacts with sympathomimetic drugs and other o- or p-hydroxybenzyl alcohol derivatives to form sulfonic acid derivatives with almost no pharmacological activity. The drugs most susceptible to this inactivation are adrenaline and its derivatives. This experiment aims to examine the effects of wet preservation of triticale, primarily contaminated with deoxynivalenol (DON), using sodium metabisulfite (Na2S2O5, SBS) on growth performance, liver function, clinical biochemical plasma parameters, and organ histopathology in piglets. Therefore, uncontaminated control rye and DON-contaminated rye were added to piglet diets, and then subjected to either untreated (CON, FUS) or SBS-treated (CON-SBS, FUS-SBS) diets for 28 days from weaning. After SBS treatment, the dietary concentrations of DON and its derivative DON sulfonate (DONS) were: CON group 0.156 mg/kg, CON-SBS group 0.084 mg/kg, FUS group 2.312 mg/kg, and FUS-SBS group 0.275 mg/kg; the DONS concentration was below 0.05 mg/kg. Compared with the other three groups, feeding with the FUS diet significantly reduced feed intake, which was reflected in a significant interaction between the rye source and SBS treatment (p = 0.014), and live weight gain and feed conversion ratio were not affected throughout the 28-day trial period. Feeding contaminated diets significantly reduced total plasma protein concentrations, while SBS treatment simultaneously increased them (total plasma protein concentrations in piglets fed CON, CON-SBS, FUS, and FUS-SBS diets were 45.4, 49.5, 40.7, and 46.5 g/L, respectively). Liver function was assessed using the C-methoxyacetophenone breath test (MBT), a method for evaluating cytochrome P450 1A2 activity. MBT results are expressed as cumulative dose recovery (cPDR360) after 360 minutes, showing that SBS treatment had a slight stimulatory effect on liver function (p = 0.052) (cPDR360 for piglets fed CON, CON-SBS, FUS, and FUS-SBS diets were 37.5%, 39.4%, 37.4%, and 55.1%, respectively). Liver weight and histopathological scores showed weak correlations with MBT results. Further histopathological examination of the kidneys, pancreas, and heart revealed no therapeutic effect. The conclusion is that SBS treatment of contaminated rye restored the growth performance of piglets to the level of those fed the control diet, with minimal effects on liver function, clinical plasma chemical parameters (except protein concentration), and organ histopathology.

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Non-human toxicity values
Rat dermal LD50 > 2000 mg/kg
Hamster intravenous LD50 95 mg/kg body weight
Rabbit intravenous LD50 65 mg/kg body weight
Mouse intravenous LD50 130 mg/kg body weight
For more non-human toxicity values (complete data) for sodium metabisulfite (13 in total), please visit the HSDB record page.

[1]. Pharmaceutical excipients - quality, regulatory and biopharmaceutical considerations. Eur J Pharm Sci. 2016 May 25;87:88-99.

Therapeutic Uses

Experimental Uses: Conversion of Cr(VI) to Cr(III) via sodium metabisulfite or sodium dithionite may prevent chromodermatitis in sensitive individuals.

NA2O5S2

190.11

189.898

7681-57-4

18403-71-9 (unspecified hydrochloride salt)

656671

White to off-white solid powder

1.48

150 °C

0.272

0

6

0

9

136

0

HRZFUMHJMZEROT-UHFFFAOYSA-L

InChI=1S/2Na.H2O5S2/c;;1-6(2)7(3,4)5/h;;(H,1,2)(H,3,4,5)/q2*+1;/p-2

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O: 100 mg/mL (526.01 mM)
DMSO: 4 mg/mL (21.04 mM)

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.

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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).

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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)

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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).

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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

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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.

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 (Please use freshly prepared in vivo formulations for optimal results.)