InChI
1S/C12H10O4/c1-15-11-9(13)7-5-3-4-6-8(7)10(14)12(11)16-2/h3-6H,1-2H3
SMILES string
COC1=C(OC)C(=O)c2ccccc2C1=O
InChI key
ZEGDFCCYTFPECB-UHFFFAOYSA-N
assay
≥99%
form
solid
storage temp.
−20°C
Quality Level
Application
2,3-二甲氧基-1,4-萘醌已被用于研究乙醇对低氧和高氧条件下足细胞凋亡的影响。
用于研究ROS在细胞毒性、细胞凋亡和坏死中的作用。
Biochem/physiol Actions
2,3-二甲氧基-1,4-萘醌（DMNQ）具有通过氧化还原循环产生H2O2的能力，但无法与谷胱甘肽（GSH）结合。
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
dust mask type N95 (US), Eyeshields, Gloves
J M Dypbukt et al.
The Journal of biological chemistry, 269(48), 30553-30560 (1994-12-02)
Increasing concentrations (1-100 microM) of the redox cycling quinone, 2,3-dimethoxy-1,4-naphthoquinone (DMNQ), stimulated growth, triggered apoptosis, or caused necrosis of pancreatic RINm5F cells, depending on the dose and duration of the exposure. Following the exposure of RINm5F cells to 10 microM
Anda R Gliga et al.
Scientific reports, 7(1), 9284-9284 (2017-08-26)
Cerium oxide nanoparticles (nanoceria) display antioxidant properties and have shown cytoprotective effects both in vitro and in vivo. Here, we explored the effects of nanoceria on neural progenitor cells using the C17.2 murine cell line as a model. First, we
Yasuhiro Ishihara et al.
Toxicology and applied pharmacology, 214(2), 109-117 (2006-01-25)
Two mechanisms have been proposed to explain quinone cytotoxicity: oxidative stress via the redox cycle and the arylation of intracellular nucleophiles. As the redox cycle is catalyzed by NADPH cytochrome P450 reductase, cytochrome P450 systems are expected to be related
Extracellular glutathione and gamma-glutamyl transpeptidase prevent H2O2-induced injury by 2, 3-dimethoxy-1, 4-naphthoquinone
Shi M, et al.
Free radical biology & medicine, 15(1), 57-67 (1993)
R Bose et al.
Cell death & disease, 1, e92-e92 (2010-01-01)
Alterations in intrauterine programming occurring during critical periods of development have adverse consequences for whole-organ systems or individual tissue functions in later life. In this paper, we show that rat embryonic neural stem cells (NSCs) exposed to the synthetic glucocorticoid
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