2. Metabolic Enzyme/Protease Stem Cell/Wnt MAPK/ERK Pathway PI3K/Akt/mTOR Apoptosis Cell Cycle/DNA Damage Cytoskeleton
  3. Herbicide ERK p38 MAPK JNK PI3K Akt Apoptosis Microtubule/Tubulin
  4. Dinitramine

Dinitramine 是一种除草剂 (herbicide)。Dinitramine 可激活睾丸细胞中的 Erk/P38/JNK/MAPK 通路，并使其中的 PI3k/Akt 通路失活。Dinitramine 可诱导睾丸细胞发生内质网应激、胞质及线粒体内钙稳态失调、细胞凋亡 (apoptosis)，以及细胞周期基因表达下调。Dinitramine 会降低睾丸细胞的活力与增殖能力，并通过抑制微管蛋白 (tubulin) 合成来阻碍细胞分裂。Dinitramine 可诱导斑马鱼胚胎出现心脏发育异常、血管生成受抑、炎症反应、细胞凋亡及胚胎生长受损。

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Dinitramine

Dinitramine Chemical Structure

CAS No. : 29091-05-2

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Dinitramine 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Dinitramine is a herbicide. Dinitramine activates the Erk/P38/JNK/MAPK pathway and inactivates the PI3k/Akt pathway in testicular cells. Dinitramine induces endoplasmic reticulum stress, dysregulation of calcium homeostasis in the cytoplasm and mitochondria, apoptosis, and downregulated expression of cell cycle genes in testicular cells. Dinitramine reduces the viability and proliferation capacity of testicular cells, and inhibits cell division by suppressing the synthesis of tubulin. Dinitramine induces abnormal heart development, inhibited angiogenesis, inflammatory responses, apoptosis, and impaired embryonic growth in zebrafish embryos[1][2].

体外研究
(In Vitro)

Dinitramine (2-20 μM; 24 h) 降低 TM3 和 TM4 细胞的活力与增殖潜能，其中 20 μM 处理可使 TM3 细胞活力降至 78.7%、TM4 细胞活力降至 84.7%，并使两种细胞系的增殖潜能均降至 50%以下[1]。
Dinitramine (10-20 μM; 6 days) 可降低 3D 培养体系中 TM3 和 TM4 细胞的球状体密度与面积；其中 20 μM 处理可使 TM3 细胞球状体密度降低 22%、面积降低 12%，而 10 μM 和 20 μM 处理均可显著降低 TM4 细胞球状体的密度与面积[1]。
Dinitramine (0-20 μM; 24 h) 可诱导 TM3 和 TM4 细胞发生细胞周期阻滞与细胞死亡，抑制细胞中细胞周期进展基因 Ccnd1、Cdk4 和 Ccne1 的 mRNA 表达，激活细胞中的内质网应激[1]。
Dinitramine (0-20 μM) 升高 TM3 和 TM4 细胞的胞浆及线粒体基质钙水平；20 μM 处理可使 TM3 细胞的胞浆钙水平升高至 230%、TM4 细胞升高至 300%，同时使两种细胞系的线粒体基质钙水平均升高至 230%[1]。
Dinitramine (5-20 μM; 30 min) 可激活 Mapk 信号通路，并使 TM3 和 TM4 细胞中的 Pi3k/Akt 信号通路失活；在两种细胞系中，20 μM 处理 30 min 均可上调磷酸化 Erk1/2、P38 和 Jnk 的水平，同时下调磷酸化 Akt 和 Rps6kb1 的水平[1]。
Dinitramine (20 μM; 24 h) 与钙调节剂联合处理可恢复经 dinitramine 处理的 TM4 细胞的增殖潜能，但无法恢复 TM3 细胞的增殖潜能[1]。

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

Dinitramine 相关抗体:

Cell Viability Assay[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 2, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Reduced relative viability of TM3 cells to 78.7% and TM4 cells to 84.7% at 20 μM.
Reduced relative proliferative potential of TM3 and TM4 cells in a concentration-dependent manner to below 50% at 20 μM.

Cell Cycle Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 2, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Increased the number of TM3 and TM4 cells in the sub-G1 phase by approximately 2-fold compared to vehicle controls.
Reduced the number of TM4 cells in the G0/G1 phase by approximately 10%, with no remarkable changes in TM3 cell cycle phase distribution.

Real Time qPCR[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Significantly reduced the expression of cell cycle progression-related genes Ccnd1, Cdk4, and Ccne1 in both TM3 and TM4 cells.

Western Blot Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 0, 5, 10, and 20 μM
Incubation Time: 24 h
Result: Increased Grp78/Bip protein expression in TM3 and TM4 cells in a concentration-dependent manner.
Increased Ire1α protein levels by 1.5-fold in TM3 and 2.4-fold in TM4 cells at 20 μM.
Increased phosphorylated Eif2α levels by 2.3-fold in TM3 and 1.4-fold in TM4 cells at 20 μM.
Increased Chop protein levels by 2.3-fold in TM3 and 2-fold in TM4 cells at 20 μM.

Western Blot Analysis[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 5-20 μM
Incubation Time: 30 min
Result: Increased phosphorylated Erk1/2 levels to 1.7-fold in TM3 and 1.9-fold in TM4 cells at 20 μM.
Increased phosphorylated P38 and Jnk levels significantly in both cell lines at 20 μM.
Reduced phosphorylated Akt levels to approximately half in TM3 cells and to 0.75-fold in TM4 cells at 20 μM.
Reduced phosphorylated Rps6kb1 levels to approximately half in TM3 cells and 0.59-fold in TM4 cells at 20 μM.
Reduced phosphorylated Rps6 levels to approximately half in TM3 cells (no significant change in TM4 cells) at 20 μM.

Cell Proliferation Assay[1]

Cell Line: immature murine Leydig (TM3) cells, immature murine Sertoli (TM4) cells
Concentration: 20 μM
Incubation Time: 24 h
Result: Restored proliferative potential of TM4 cells by approximately 20% compared to dinitramine alone when co-treated with 1 μM 2-APB.
Restored proliferative potential of TM4 cells to 65% compared to dinitramine alone when co-treated with 2 μM BAPTA.
Did not alter proliferative potential of dinitramine-treated TM3 cells with co-treatment.
体内研究
(In Vivo)

Dinitramine (1.6-6.4 mg/L；水体浸泡；96 小时) 会在 Danio rerio (斑马鱼) 胚胎中诱导浓度依赖性的发育毒性、心脏毒性、血管损伤、炎症以及细胞凋亡[2]。

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

Animal Model: wild-type; fli1:eGFP transgenic[2]
Dosage: 1.6 mg/L; 3.2 mg/L; 6.4 mg/L
Administration: aqueous immersion; continuous exposure for 96 hours, medium refreshed every 24 hours
Result: Induced concentration-dependent malformations including shortened body length, reduced eye size, spinal curvature, swollen yolk sacs, and pericardial edema; increased pericardial edema to over 300% of control levels at 6.4 mg/L.
Reduced hatchability dose-dependently, reaching near 0% at 6.4 mg/L.
Decreased heart rate dose-dependently to 80 beats per minute at 6.4 mg/L (down from 184 bpm in controls); caused 3-fold enlargement of atrial long-axis diameter at 6.4 mg/L; significantly downregulated cardiac development genes (spaw, bmp4, bmp2b, erbb4b, myh6, itga5, lmna, actc1a, actc2) across all doses.
Reduced caudal vein plexus area to 80% of control and fluorescent intensity to 75% of control at 6.4 mg/L; caused abnormal formation of intersegmental vessels, dorsal longitudinal anastomotic vessel, dorsal aorta, and caudal vein; dysregulated expression of angiogenesis-related genes (kdr, vegfd, flt1, vegfaa).
Significantly upregulated inflammatory genes (il1b, nos2a, il6, tnfa, cox2a, cox2b) at 6.4 mg/L, with il1b expression increased 39-fold compared to controls.
Increased relative apoptotic cell numbers 4.8-fold (eye), 6.4-fold (brain), and 2.7-fold (tail) at 6.4 mg/L; upregulated pro-apoptotic genes (p53, casp8, casp9, casp3) and downregulated anti-apoptotic gene bcl2 across all doses.
分子量

322.24

Formula

C11H13F3N4O4
CAS 号
中文名称

敌乐胺
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

Dinitramine 相关分类

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Keywords:

Dinitramine29091-05-2敌乐胺HerbicideERKp38 MAPKJNKPI3KAktApoptosisMicrotubule/TubulinExtracellular signal regulated kinasesc-Jun N-terminal kinasePhosphoinositide 3-kinasePKBProtein kinase Bendoplasmic reticulum stresszebrafish embryosmicrotubulinErk/P38/Jnk Mapk pathwaycell cycleTM3 cellstesticular cellsPi3k/Akt pathwayTM4 cellsapoptosisherbicideInhibitorinhibitorinhibit

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