Dihydrorotenone
(Synonyms: 二氢鱼藤酮) 目录号 : GC38620
Dihydrorotenone 是一种天然杀虫剂,是一种线粒体 (mitochondrial) 抑制剂。Dihydrorotenone 可能诱发帕金森综合症。Dihydrorotenone 通过触发内质网应激并激活 p38 信号通路来诱导人浆细胞凋亡 (apoptosis)
Cas No.:6659-45-6
Sample solution is provided at 25 µL, 10mM.
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Dihydrorotenone, a natural pesticide, is a potent mitochondrial inhibitor. Dihydrorotenone probably induces Parkinsonian syndrome. Dihydrorotenone induces human plasma cell apoptosis by triggering endoplasmic reticulum stress and activating p38 signaling pathway[1].
[1]. Zhang J, et al. The natural pesticide dihydrorotenone induces human plasma cell apoptosis by triggering endoplasmic reticulum stress and activating p38 signaling pathway. PLoS One. 2013 Jul 26;8(7):e69911.
Cas No. | 6659-45-6 | SDF | |
别名 | 二氢鱼藤酮 | ||
Canonical SMILES | O=C1[C@]2([H])[C@](COC3=CC(OC)=C(OC)C=C32)([H])OC4=C5C(O[C@@H](C(C)C)C5)=CC=C14 | ||
分子式 | C23H24O6 | 分子量 | 396.43 |
溶解度 | DMSO : 25 mg/mL (63.06 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
1 mM | 2.5225 mL | 12.6126 mL | 25.2251 mL |
5 mM | 0.5045 mL | 2.5225 mL | 5.045 mL |
10 mM | 0.2523 mL | 1.2613 mL | 2.5225 mL |
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Correction: The Natural Pesticide Dihydrorotenone Induces Human Plasma Cell Apoptosis by Triggering Endoplasmic Reticulum Stress and Activating p38 Signaling Pathway
PLoS One 2020 Jun 2;15(6):e0234162.PMID:32484839DOI:10.1371/journal.pone.0234162.
[This corrects the article DOI: 10.1371/journal.pone.0069911.].
[3H]Dihydrorotenone binding to NADH: ubiquinone reductase (complex I) of the electron transport chain: an autoradiographic study
J Neurosci 1996 Jun 15;16(12):3807-16.PMID:8656275DOI:10.1523/JNEUROSCI.16-12-03807.1996.
Abnormalities of mitochondrial energy metabolism may play a role in normal aging and certain neurodegenerative disorders. In this regard, complex I of the electron transport chain has received substantial attention, especially in Parkinson's disease. The conventional method for studying complex I has been quantitation of enzyme activity in homogenized tissue samples. To enhance the anatomic precision with which complex I can be examined, we developed an autoradiographic assay for the rotenone site of this enzyme. [3H]Dihydrorotenone ([3H]DHR) binding is saturable (KD = 15-55 nM) and specific, and Hill slopes of 1 suggest a single population of binding sites. Nicotinamide adenine dinucleotide (NADH) enhances binding 4- to 80-fold in different brain regions (EC50 = 20-40 microM) by increasing the density of recognition sites (Bmax). Nicotinamide adenine dinucleotide phosphate also increases binding, but NAD+ does not. In skeletal muscle, heart, and kidney, binding was less affected by NADH. [3H]DHR binding is inhibited by rotenone (IC50 = 8-20 nM), meperidine (IC50 = 34-57 microM), amobarbitol (IC50 = 375-425 microM), and MPP+ (IC50 = 4-5 mM), consistent with the potencies of these compounds in inhibiting complex I activity. Binding is heterogeneously distributed in brain with the density in gray matter structures varying more than 10-fold. Lesion studies suggest that a substantial portion of binding is associated with nerve terminals. [3H]DHR autoradiography is the first quantitative method to examine complex I with a high degree of anatomic precision. This technique may help to clarify the potential role of complex I dysfunction in normal aging and disease.
Biotransformations of 1',2'-dihydrorotenone by Streptomyces griseus
Appl Environ Microbiol 1985 Feb;49(2):451-2.PMID:3920966DOI:10.1128/aem.49.2.451-452.1985.
Dihydrorotenone yields three major products when incubated with growing cultures of Streptomyces griseus. These were isolated by solvent extraction and characterized by spectral methods as 1',2'-dihydro-6abeta-hydroxyrotenone, 1',2'-dihydro-2',6abeta-dihydroxyrotenone, and 1',2'-dihydro-1',6abeta-dihydroxyrotenone.
New screening system using Twist1 promoter activity identifies Dihydrorotenone as a potent drug targeting cancer-associated fibroblasts
Sci Rep 2020 Apr 27;10(1):7058.PMID:32341496DOI:10.1038/s41598-020-63996-4.
Cancer-associated fibroblasts (CAFs) are the most abundant stromal cells in tumor microenvironments. These cells strongly support tumor progression and are considered to be potent therapeutic targets. Therefore, drugs targeting CAFs have been developed, but most of them have failed in clinical trials. The discovery of additional drugs to inactivate or eliminate CAFs is thus essential. In this study, we developed a high-throughput screening system to find anti-CAF drugs using reporter cells that express Twist1 promoter-GFP. This screening system uses the activity of the Twist1 promoter as an indicator of CAF activation because Twist1 is known to be a central player in CAF activation. Using this screening system, we found that Dihydrorotenone (DHR), an inhibitor of electron transfer chain complex 1 in mitochondria, can effectively deactivate CAFs. DHR-treated CAFs exhibited reduced expression of CAF-enriched markers, decreased capability of collagen gel contraction, and impaired ability to engage in tumor-promoting activities, such as facilitating the proliferation and colonization of cancer cells. Furthermore, conditioned media from DHR-treated CAFs attenuated tumor progression in mice grafted with MNK28 cells. In conclusion, DHR can be considered as a candidate drug targeting CAFs.
Natural pesticide Dihydrorotenone arrests human plasma cancer cells at the G0/G1 phase of the cell cycle
J Biochem Mol Toxicol 2014 May;28(5):232-8.PMID:24615755DOI:10.1002/jbt.21558.
Dihydrorotenone (DHR) is a natural pesticide used for farming including organic produces. We recently found that DHR induces human plasma cell apoptosis by provoking endoplasmic reticulum stress. In the present study, we found that DHR arrested human plasma cancer cells at the G0/G1 phase of the cell cycle. Mechanistical studies demonstrated that cell cycle arrest was associated with downregulated cell cycle promotors including cyclin D2, cyclin D3, cyclin-dependent kinases (CDK4, CKD6), and phosphorylated-Rb. DHR inhibited cyclin D2 transactivation, thus inhibiting its mRNA expression. In addition, DHR upregulated the cell cycle repressors p21 and p53. DHR also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53. Moreover, DHR downregulated AKT and ERK phosphorylation, an incentive of cell cycle progression. Therefore, these results collectively demonstrated that DHR disrupts the cell cycle progress, which suggests that DHR is toxic to human plasma cells. Caution is thus suggested when handling with this agent.