CAS NO: | 58-27-5 |
包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
500mg | 电议 |
1g | 电议 |
Physical Appearance | A solid |
Storage | Store at -20°C |
M.Wt | 172.18 |
Cas No. | 58-27-5 |
Formula | C11H8O2 |
Solubility | insoluble in H2O; ≥5.15 mg/mL in DMSO; ≥9.86 mg/mL in EtOH with ultrasonic |
Chemical Name | 2-methylnaphthalene-1,4-dione |
Canonical SMILES | CC1=CC(=O)C2=CC=CC=C2C1=O |
运输条件 | 蓝冰运输或根据您的需求运输。 |
一般建议 | 为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。 |
Menadione (vitamin K3), used as a nutritional supplement, is an inhibitor of mitochondrial DNA polymerase γ (pol γ), with an IC 50 value of 6 μM [1].
Pol γ is responsible for all aspects of mitochondrial DNA synthesis, including all replication, recombination of the mitochondrial genome, and repair of mitochondrial DNA damage [1].
In the extract of mitochondrion fraction from HCT116 (p53+/+ andp53–/–) cells, menadione at 30 μM inhibited pol γ by more than 80%. In HCT116 cells, 30 μM menadione also caused impairment of mitochondrial DNA replication and repair, and triggered a significant increase in reactive oxygen species (ROS), leading to apoptosis. At a lower concentration of 3 μM, menadione did not significantly increase the ROS level, but was able to effectively inhibit cancer cell proliferation, which could be reversed by supplementing glycolytic substrates [2].
In Emory mice, menadione at a low non-toxic dose of 0.12% (w/w), used as a dietary supplement for 10 to 12 weeks, caused early signs of cataract, such as prominent anterior suture, in 68% of the Emory mice [3].
References:
[1]. Mizushina Y, Yonezawa Y, Yoshida H. Selective inhibition of animal DNA polymerases by fat-soluble vitamins A, D, E and K and their related compounds. Current Enzyme Inhibition, 2007, 3(1): -.
[2]. Sasaki R, Suzuki Y, Yonezawa Y, et al. DNA polymerase gamma inhibition by vitamin K3 induces mitochondria-mediated cytotoxicity in human cancer cells. Cancer Science, 2008, 99(5): 1040-1048.
[3]. Bhuyan D K, Huang X, Kuriakose G, et al. Menadione-induced oxidative stress accelerates onset of Emory mouse cataract in vivo. Current eye research, 1997.
Cell experiment:[1] | |
Cell lines | HCT116p53+/+andp53–/–cells |
Reaction Conditions | 3 or 30 μM menadione for 24 h incubation |
Applications | Menadione at 30 μM inhibited DNA polymerase γ by more than 80%, caused impairment of mitochondrial DNA replication and repair, and induced a significant increase in reactive oxygen species (ROS), leading to apoptosis. At a lower concentration (3 μM), menadione did not cause a significant increase in ROS, but was able to effectively inhibit cell proliferation, which could be reversed by supplementing glycolytic substrates. |
Animal experiment:[2] | |
Animal models | Four-week-old Emory mice |
Dosage form | 0.04%, 0.12% and 0.4% (w/w) menadione mixed with freshly ground Purina Rodent Lab Chow 5001 By oral route for 10 to 12 weeks |
Applications | In Emory mice, menadione at a low non-toxic dose (0.12%, w/w), used as a dietary supplement for 10 to 12 weeks, caused early signs of cataract, such as prominent anterior suture, in 68% of the Emory mice. |
Note | The technical data provided above is for reference only. |
References: 1. Sasaki R, Suzuki Y, Yonezawa Y, et al. DNA polymerase gamma inhibition by vitamin K3 induces mitochondria-mediated cytotoxicity in human cancer cells. Cancer Science, 2008, 99(5): 1040-1048. 2. Bhuyan DK, Huang X, Kuriakose G, et al. Menadione-induced oxidative stress accelerates onset of Emory mouse cataract in vivo. Current eye research, 1997, 16(6): 519-526. |