For life science-related study, nitriletriacetic acid trisodium salt is a biochemical reagent that can be utilized as an organic substance or biological material.

Absorption, Distribution and Excretion
TRISODIUM AMINOTRIACETATE WAS WELL ABSORBED IN RATS AND DOGS, & EXCRETED UNCHANGED IN URINE. THE AMT (8 UG/G BONE), WHICH WAS INCORPORATED INTO RAT SKELETON IN COMBINATION WITH CA2+ REPRESENTED ONLY 0.007% OF THE 24 HR TURNOVER OF CALCIUM IN THAT TISSUE, AND WAS CONSIDERED UNLIKELY TO AFFECT DEVELOPMENT ADVERSELY.
RATS WERE GIVEN TRISODIUM NITRILOTRIACETATE AT DIETARY LEVELS OF 0.05, 0.1, 0.3, 0.5, 0.75, OR 2% FOR 42 & 30 DAYS. NITRILOTRIACETATE DID NOT ACCUMULATE IN BLADDER TISSUES TO ANY GREATER EXTENT THAN IN HEART AND LIVER, EVEN WHEN URINARY NTA LEVELS WERE EQUAL TO OR GREATER THAN 200 TIMES THOSE IN PLASMA.
In a whole body autoradiographic study, 0.93 Mg (1-(14)C-acetate) NTA, trisodium salt was administered intravenously to NMRI albino mice and the same amount orally to C57BI mice; heavy accumulation of radioactivity occurred in the skeleton, which persisted for 48 h, the longest interval studied.

Toxicity Data
LC50 (rat) > 5,000 mg/m3/4h

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Interactions
The development of renal tumors was examined in rats given 1000 ppm N-ethyl-N-hydroxyethylnitrosamine (NEELA) and then 30,000, 10,000 or 3,000 ppm of trisodium nitrilotriacetate monohydrate (Na3 X NTA X H20) in their food. The incidences of renal tumors in rats treated with N-ethyl-N-hydroxyethylnitrosamine for 2 wk and then 30,000, 10,000 and 3,000 ppm trisodium nitrilotriacetate monohydrate for 30 wk were 100, 86 and 22%, respectively, while they were 16 and 0% in rats treated with N-ethyl-N-hydroxyethylnitrosamine or 30,000 ppm trisodium nitrilotracetate monohydrate at 30,000 or 10,000, but not 3,000 ppm, also incr the size and number of renal tumors in rats treated with N-ethyl-N-hydroxyethylnitrosamine and trisodium nitrilotriacetate monohydrate 30,000 ppm, but not 10,000 or 3,000 ppm also induced hydronephrosis in rats irrespective of whether they were treated with N-ethyl-N-hydroxyethylnitrosamine. Thus, trisodium nitrilotriacetate monohydrate has a dose-related effect on the kidney. /Trisodium nitrilotriacetate monohydrate/
ORAL ADMIN OF TRISODIUM NITRILOTRIACETATE (0.01, 0.10, OR 1% WT/VOL IN DRINKING WATER) DID NOT ENHANCE THE PATHOLOGICAL EFFECTS OF LEAD ON THE RAT RENAL SYSTEM; HOWEVER, RATS GIVEN 0.01 OR 0.10% WITH OR WITHOUT LEAD WERE HYPERGLYCEMIC.
The effects of the renal tumor promoters; beta-cyclodextrin, DL-serine, basic lead acetate, trisodium nitrilotriacetate monohydrate & potassium bromate, & diethylene glycol as a negative control, on early stage of renal carcinogenesis were investigated in unilaterally nephrectomized male Wistar rats after N-ethyl-N-hydroxyethylnitrosamine admin. Wistar male rats were fed 1000 ppm N-ethyl-N-hydroxyethylnitrosamine diet for 2 wk & the left kidney was removed at week 3, then the animals were divided into 7 groups of 15 rats each. These groups received the following treatments: 1000 ppm lead acetate, 10000 ppm trisodium nitrilotriacetatemonohydrate or 500 ppm potassium bromate diet for 18 wk from wk 3; 45 mg/100 g bw/day of beta-cyclodextrin injected sc for 7 days; 100 mg/100 g bw of DL-Serine injected sc biweekly for 6 weeks; 5% diethylene glycol in drinking water as a negative control for two days. Five rats in each group were killed at wk 8, 12 & 20 & their kidneys were examined histologically. At wk 20, the avg numbers of adenomatous hyperplasias seen as preneoplastic lesions in the beta-C, DL-Serine, lead acetate, trisodium nitrilotriacetate monohydrate or potassium bromate groups were significantly higher than those in the diethylene glycol or control groups. Thus within a relatively short period of 20 wk, promoting effects of chemicals can be detected as a significant incr of adenomatous hyperplasias in this model. /Trisodium nitrilotriacetate monohydrate/
The dose-dependent effect of trisodium nitrilotriacetate monohydrate as a promoter in two stage carcinogenesis in the urinary bladder of male Wistar rats was investigated. Carcinogenesis was initiated by administration of 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine in the drinking water for 4 weeks, then trisodium nitrilotriacetate monohydrate was given at 1%, 0.5% and 0.3% in the diet for 28 weeks, and rats were killed in week 32. The incidences and numbers of preneoplastic lesions (papillary or nodular hyperplasia, PN hyperplasia) in rats treated with 0.3% to 1% trisodium nitrilotriacetate monohydrate increased progressively with increasing concentration of trisodium nitrilotriacetate monohydrate. The incidences of papillomas in rats treated with 1% and 0.5% trisodium nitrilotriacetate monohydrate in the diet and the incidence of transitional cell carcinoma of the urinary bladder in the rats treated with 1% trisodium nitrilotriacetate monohydrate (P< 0.05) were significantly higher than those in rats treated with N-butyl-N-(4-hydroxybutyl)nitrosamine only. Administration of various doses of trisodium nitrilotriacetate monohydrate without N-butyl-N-(-hydroxybutyl)nitrosamine did not cause any histological changes (papillary or nodular hyperplasia, papilloma or transitional cell carcinoma) in the urinary bladder. These findings showed that trisodium nitrilotriacetate monohydrate is a potent promoter of urinary bladder carcinogenesis initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine in rats, and that its effect is dose-dependent. /Trisodium nitrilotriacetate monohydrate/
For more Interactions (Complete) data for TRISODIUM NITRILOTRIACETATE (9 total), please visit the HSDB record page.

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Non-Human Toxicity Values
LC50 Mouse ip 680 mg/kg bw
LD50 Mouse ip 300 mg/kg bw
LD50 Rat ip 254-444 mg/kg bw
LC50 Rat inhalation >5 mg/L /4 hr
For more Non-Human Toxicity Values (Complete) data for TRISODIUM NITRILOTRIACETATE (15 total), please visit the HSDB record page.

Sodium nitrilotriacetate is an organic sodium salt composed of sodium and nitrilotriacetate ions in a 3:1 ratio. It has a role as a carcinogenic agent and a nephrotoxic agent. It contains a nitrilotriacetate(3-).
A derivative of acetic acid, N(CH2COOH)3. It is a complexing (sequestering) agent that forms stable complexes with Zn2+. (From Miall's Dictionary of Chemistry, 5th ed.)

C6H6NNA3O6

257.08

256.988

5064-31-3

Nitrilotriacetic acid;139-13-9;Nitrilotriacetic acid disodium salt;15467-20-6

21152

White to off-white solid powder

0.56

498.2ºC at 760mmHg

69-71 °C(lit.)

255.1ºC

0

7

3

16

171

0

DZCAZXAJPZCSCU-UHFFFAOYSA-K

InChI=1S/C6H9NO6.3Na/c8-4(9)1-7(2-5(10)11)3-6(12)13;;;/h1-3H2,(H,8,9)(H,10,11)(H,12,13);;;/q;3*+1/p-3

trisodium;2-[bis(carboxylatomethyl)amino]acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

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

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.)