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  4. MiADMSA

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

目录号: HY-177995
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MiADMSA (Monoisoamyl meso-2,3-dimercaptosuccinic acid) 是一种口服有效的硫醇螯合剂，能够有效从动物体内清除砷和铅等重金属。砷与 MiADMSA 中两个相邻的巯基结合，导致体内砷负荷显著降低，同时各种氧化应激参数和抗氧化酶 (如 ROS、亚硝酸盐、TBARS、GSH、SOD 和过氧化氢酶) 也显著降低。MiADMSA 能减轻膀胱癌的发生，保护机体免受氧化应激损伤，改善铜诱导的组织病理学改变，逆转神经毒性，并在动物体内安全。MiADMSA 可用于膀胱癌、砷和铅诱导的发育神经毒性研究。

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MiADMSA

MiADMSA Chemical Structure

CAS No. : 142609-62-9

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MiADMSA 相关抗体

Top Publications Citing Use of Products

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

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].

体外研究
(In Vitro)

MiADMSA (50-200 nM；预孵育 6 小时，暴露 24 小时，重复 7 天) 可逆转 100 nM 亚砷酸钠或 DMA 在 NBT-II 和 T-24 细胞中诱导的细胞活力增加[1]。
MiADMSA (100 nM；7 天) 可通过降低 NBT-II 和 T-24 细胞中的活性氧 (ROS) 水平并恢复谷胱甘肽 (GSH) 水平，减轻砷/二甲基胂酸 (DMA) 诱导的氧化应激[1]。
MiADMSA (100 nM；7 天) 可降低 100 nM 亚砷酸钠或 DMA 在 NBT-II 和 T-24 细胞中诱导的促癌生物标志物 (MMP-9、survivin) 水平[1]。
MiADMSA (100 nM；7 天) 可降低 100 nM 亚砷酸钠或 DMA 在 NBT-II 细胞中诱导的克隆形成潜能和细胞迁移的增加 [1]。

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

MiADMSA 相关抗体:

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.
体内研究
(In Vivo)

MiADMSA (50 mg/kg；口服；每个疗程连续给药 5 天，共 3 个疗程，疗程间隔 1 周) 可减轻亚砷酸钠或 DMA 暴露对雄性 Sprague-Dawley 大鼠的砷诱导膀胱致癌作用 [1]。
MiADMSA (50 mg/kg；口服；每周 5 天；持续 4 周) 可逆转砷暴露雄性 Wistar 大鼠中大多数砷诱导的神经毒性效应[2]。
MiADMSA (50-100 mg/kg；口服或者腹腔注射；每日一次；5 天) 可逆转砷暴露雄性 Wistar 大鼠 (80-90 g) 的慢性砷毒性 (50 mg/kg 口服剂量可使体内砷负荷降低 75%) [3]。
MiADMSA (75 mg/kg；口服；两个疗程各 5 天，疗程间休息 7 天) 可消除慢性硫酸铜暴露的雄性 Sprague-Dawley 大鼠中慢性铜诱导的肝脏及免疫学改变[4]。
MiADMSA (25-100 mg/kg；腹腔注射；每日；7 天) 可调节雄性 Wistar 大鼠 (幼年、成年、老年) 的抗氧化与促氧化标志物，并影响其必需金属水平[5]。
MiADMSA (50 mg/kg；经灌胃口服；每日一次；连续 3 天) 可减轻砷和铅诱导的 Wistar 大鼠 (暴露于偏亚砷酸钠和/或醋酸铅的孕鼠所产雄性幼崽) 的氧化应激和凋亡标志物[6]。

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.
分子量

252.34

Formula

C9H16O4S2
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

MiADMSA 相关分类

  • 摩尔计算器

  • 稀释计算器

The molarity calculator equation

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量   浓度   体积   分子量 *
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The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start) × 体积 (start) = 浓度 (final) × 体积 (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    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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