2. Immunology/Inflammation NF-κB Metabolic Enzyme/Protease
  3. Reactive Oxygen Species (ROS) SOD
  4. MiADMSA

MiADMSA  (Synonyms: Monoisoamyl meso-2,3-dimercaptosuccinic acid)

Cat. No.: HY-177995
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MiADMSA (Monoisoamyl meso-2,3-dimercaptosuccinic acid) is an orally active thiol chelator that can effectively remove heavy metals such as arsenic and lead from the body of animals. Arsenic binds with two vicinal sulfhydryl groups available in MiADMSA leading to marked reduction in body arsenic burden and also marked reduction in various oxidative stress parameters and antioxidant enzymes like-ROS, nitrite, TBARS, GSH, SOD and catalase. MiADMSA attenuates urinary bladder carcinogenesis, protects against oxidative stress, ameliorates copper-induced histopathology, reverses neurotoxicity, and is safe in animals. MiADMSA can be used in studies of bladder cancer, arsenic, and lead-induced developmental neurotoxicity.

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MiADMSA

MiADMSA Chemical Structure

CAS No. : 142609-62-9

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MiADMSA Related Antibodies

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Description

MiADMSA (Monoisoamyl meso-2,3-dimercaptosuccinic acid) is an orally active thiol chelator that can effectively remove heavy metals such as arsenic and lead from the body of animals. Arsenic binds with two vicinal sulfhydryl groups available in MiADMSA leading to marked reduction in body arsenic burden and also marked reduction in various oxidative stress parameters and antioxidant enzymes like-ROS, nitrite, TBARS, GSH, SOD and catalase. MiADMSA attenuates urinary bladder carcinogenesis, protects against oxidative stress, ameliorates copper-induced histopathology, reverses neurotoxicity, and is safe in animals. MiADMSA can be used in studies of bladder cancer, arsenic, and lead-induced developmental neurotoxicity[1][2][3][4][5][6].

In Vitro

MiADMSA (50-200 nM; 6 h pre-incubation, 24 h exposure, repeated 7 days) reverses increased cell viability induced by 100 nM sodium arsenite or DMA in NBT-II and T-24 cells[1].
MiADMSA (100 nM; 7 days) reduces arsenic/DMA-induced oxidative stress by lowering ROS and restoring GSH in NBT-II and T-24 cells[1].
MiADMSA (100 nM; 7 days) reduces pro-oncogenic biomarker (MMP-9, survivin) levels induced by 100 nM sodium arsenite or DMA in NBT-II and T-24 cells[1].
MiADMSA (100 nM; 7 days) reduces the increased clonogenic potential and cell migration induced by 100 nM sodium arsenite or DMA in NBT-II cells[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

MiADMSA Related Antibodies

Cell Viability Assay[1]

Cell Line: NBT-II (rat bladder carcinoma), T-24 (human bladder carcinoma Grade-III)
Concentration: 50 nM, 100 nM, 200 nM (6 h pre-incubation with MiADMSA)
Incubation Time: 6 h (pre-incubation with MiADMSA), 24 h (exposure to sodium arsenite/DMA), repeated for 7 days
Result: Significantly reduced the increased cell viability induced by 100 nM sodium arsenite or DMA in NBT-II and T-24 cells, with 100 nM being more effective than 50 nM or 200 nM.

ELISA Assay[1]

Cell Line: NBT-II, T-24
Concentration: 100 nM
Incubation Time: 7 days
Result: Significantly decreased MMP-9 and survivin levels increased by 100 nM sodium arsenite or DMA in NBT-II and T-24 cells.

Cell Migration Assay[1]

Cell Line: NBT-II, T-24
Concentration: 100 nM
Incubation Time: 7 days (wound closure monitored at 24 h)
Result: Controlled increased cell migration induced by 100 nM sodium arsenite or DMA in NBT-II and T-24 cells.
In Vivo

MiADMSA (50 mg/kg; p.o.; 5 consecutive days per course for 3 courses with 1-week gaps between courses) reduces arsenic-induced bladder carcinogenesis in male Sprague-Dawley rats exposed to sodium arsenite or Dimethylarsinic acid (DMA)[1].
MiADMSA (50 mg/kg; p.o.; 5 days a week; for 4 weeks) reverses most arsenic-induced neurotoxic effects in male Wistar rats (arsenic-exposed)[2].
MiADMSA (50-100 mg/kg; oral or i.p.; once daily; 5 days) reverses chronic arsenic toxicity in male Wistar rats (80-90 g) challenged with arsenic (with a body arsenic burden reduction of 75% for 50 mg/kg oral)[3].
MiADMSA (75 mg/kg; orally; two courses of 5 days each with a 7-day rest period between courses) abrogates chronic copper-induced hepatic and immunological changes in male Sprague-Dawley rats (chronic copper sulfate exposure)[4].
MiADMSA (25-100 mg/kg; i.p.; daily; 7 days) modulates antioxidant and prooxidant markers and affects essential metal levels in male Wistar rats (young, adult, old)[5].
MiADMSA (50 mg/kg; orally via gavage; once daily; 3 consecutive days) mitigates arsenic- and lead-induced oxidative stress and apoptotic markers in Wistar rats (male pups from exposed pregnant rats challenged with sodium meta-arsenite and/or lead acetate)[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley rats (male, 80-100 g, ~5-6 weeks old) bearing bladder carcinogenesis[1]
Dosage: 50 mg/kg
Administration: p.o.; 5 consecutive days per course for 3 courses with 1-week gaps between courses
Result: Significantly reduced bladder tissue arsenic concentration in both sodium arsenite and DMA-exposed rats. Normalized oxidative/nitrosative stress markers (reduced ROS, TBARS, nitrite levels; restored GSH levels, SOD, and catalase activities) in serum and bladder tissues. Decreased 8-OHdG levels in serum and bladder tissues. Reduced pro-oncogenic biomarker levels (MMP-9, survivin) in serum and bladder tissues.
Animal Model: Wistar rats (male, 8 weeks old, 90 ± 10 g, exposed to sodium arsenite)[2]
Dosage: 50 mg/kg
Administration: p.o.; 5 days a week; for 4 weeks
Result: Improved arsenic-reduced neuronal cell proliferation/survival from 60% to 80-85% of normal; reduced arsenic-induced 3-fold ROS increase and 2-fold intracellular calcium increase (60-65% recovery for calcium); increased mitochondrial membrane potential from 4.67 to 7.45 (590:530 nm ratio); reversed arsenic-inhibited electron transport chain complex activities (65-75% recovery for complexes I-III, 15-20% for complex II, 40-50% for complex IV); restored arsenic-reduced ATP levels (over 50% recovery) and Mn-SOD activity (35-45% recovery); reduced arsenic-induced cytosolic cytochrome c translocation, 4-fold bax/bcl₂ ratio increase (to 1.7-fold), and caspase 3 activity (40-45% recovery); mobilized arsenic from brain (significant reduction in brain arsenic levels) and increased urinary arsenic excretion 4-fold; did not reduce arsenic-induced DNA damage.
Animal Model: Wistar rats (male, 80-90 g, exposed to 25-ppm arsenic as sodium arsenite in drinking water for 6 months)[3]
Dosage: 50 mg/kg (oral); 100 mg/kg (oral); 50 mg/kg (i.p.); 100 mg/kg (i.p.)
Administration: oral; once daily; 5 days; i.p.; once daily; 5 days
Result: Provided 45% protection against oxidative stress and 75% reduction in body arsenic burden with 50 mg/kg oral. Showed similar efficacy with 100 mg/kg oral. Provided 25% protection against oxidative stress and 40% reduction in body arsenic burden with 50 mg/kg i.p.
Showed similar efficacy with 100 mg/kg i.p. Reversed arsenic-induced decreases in blood ALAD activity (35-45% recovery), hemoglobin concentration, and GSH levels more effectively with oral administration. Replenished hepatic GSH, reduced hepatic GSSG and TBARS levels, and reduced arsenic burden in blood, liver, and kidneys by 70-75% with oral (vs. 40–50% with i.p.).
Produced the least hepatotoxicity and maximal recovery from arsenic-induced liver damage (minimal hepatic lesions vs. moderate lesions with higher doses or i.p.) with 50 mg/kg oral.
Animal Model: Sprague-Dawley (male, 80-100 g, chronic copper sulfate exposure)[4]
Dosage: 75 mg/kg
Administration: orally; two courses of 5 days each with a 7-day rest period between courses
Result: Reduced liver copper levels, restored serum ceruloplasmin activity to near-normal, reduced serum ALT levels from 70.78 U/L to 52.42 U/L, decreased hepatic ROS, nitrite, and MDA (TBARS) levels, restored hepatic SOD and catalase activities, normalized hepatic pro-inflammatory cytokines (IL-1β, IL-6) and anti-inflammatory cytokine (IL-4) levels, reduced hepatic caspase-3 expression, restored serum IgE and IgM levels to near-normal, and ameliorated copper-induced hepatic histopathological changes and collagen deposition.
Animal Model: Wistar rats (male, young:21 days old 40-50g; adult:8 months old 250-300g; old:16 months old 480-500g)[5]
Dosage: 25, 50, 100 mg/kg
Administration: i.p.; daily; 7 days
Result: Increased δ-aminolevulinic acid dehydratase (ALAD) activity in a dose-dependent manner in young rats at all doses and in adult/old rats at 50, 100 mg/kg; Increased zinc protoporphyrin (ZPP) levels in a dose-dependent manner across all age groups; Decreased superoxide dismutase (SOD) activity in old rats at all doses, young rats at 50, 100 mg/kg, and adult rats at 100 mg/kg; Increased blood glutathione (GSH) in young rats at 50, 100 mg/kg; Decreased hemoglobin (Hb) in old rats at 100 mg/kg; Increased hepatic metallothioneine (MT) in a dose-dependent manner across all age groups; Increased renal MT in a dose-dependent manner in young/adult rats at all doses and in old rats at 100 mg/kg; Increased liver catalase activity in young/old rats at 50, 100 mg/kg and in adult rats at 100 mg/kg; Increased liver thiobarbituric acid reactive substances (TBARS) in young rats at 50, 100 mg/kg and in old rats at all doses; Increased liver GSH in young rats at 50, 100 mg/kg; Decreased liver oxidized glutathione (GSSG) in young rats at 50, 100 mg/kg; Decreased brain SOD activity in adult/old rats at all doses and in young rats at 100 mg/kg; Increased brain catalase activity in young rats at all doses, adult rats at 50, 100 mg/kg, and old rats at all doses; Increased brain TBARS in young rats at 50, 100 mg/kg, adult rats at 100 mg/kg, and old rats at 50, 100 mg/kg; Decreased brain GSH in young rats at 100 mg/kg and in old rats at 50, 100 mg/kg; Decreased brain GSSG in young rats at all doses, adult rats at 50, 100 mg/kg, and old rats at 50, 100 mg/kg; Decreased blood zinc in young rats at all doses and in adult/old rats at 50, 100 mg/kg; Decreased blood copper in young/old rats at all doses and in adult rats at 50, 100 mg/kg; Decreased renal copper in all age groups at 50, 100 mg/kg.
Animal Model: Wistar rats (90 days old, 140 ± 10 g, male pups from exposed pregnant rats, challenged with sodium meta-arsenite and/or lead acetate)[6]
Dosage: 50 mg/kg
Administration: orally via gavage; once daily; 3 consecutive days
Result: Significantly reversed arsenic- and/or lead-induced decreases in antioxidant enzyme activities (manganese-superoxide dismutase, copper/zinc-superoxide dismutase, catalase, glutathione peroxidase) in all brain regions across all age points. Markedly reduced malondialdehyde levels, arsenic and lead content, and mRNA expression levels of caspase-3 and caspase-9 in all brain regions. Showed higher recovery in individual metal exposure groups than in the combined metal exposure group, though enzyme activities, malondialdehyde levels, and caspase expression did not reach control values.
Molecular Weight

252.34

Formula

C9H16O4S2
CAS No.
SMILES

[C@H](C(OCCC(C)C)=O)([C@@H](C(O)=O)S)S
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Storage

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Purity & Documentation
References
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MiADMSA Related Classifications

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

MiADMSA142609-62-9Monoisoamyl meso-2,3-dimercaptosuccinic acidReactive Oxygen Species (ROS)SODSuperoxide Dismutase8-OHdGGSHROSMMP-9survivincatalaseTBARSmigrationclonogenic potentialInhibitorinhibitorinhibit

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