Mequindox
(Synonyms: 乙酰甲喹) 目录号 : GC64409
Mequindox 是一种抗菌剂。Mequindox 是 DNA 合成的抑制剂。Mequindox 对小鼠具有遗传毒性和致癌性。
Cas No.:13297-17-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Mequindox is an antimicrobial agent[1]. Mequindox acts as an inhibitor of DNA synthesis. Mequindox induces genotoxicity and carcinogenicity in mice[2].
[1]. Qianying Liu, et al. Mequindox-Induced Kidney Toxicity Is Associated With Oxidative Stress and Apoptosis in the Mouse. Front Pharmacol. 2018 May 1;9:436.
[2]. Qianying Liu, et al. Mequindox Induced Genotoxicity and Carcinogenicity in Mice. Front Pharmacol. 2018 Apr 10;9:361.
| Cas No. | 13297-17-1 | SDF | Download SDF |
| 别名 | 乙酰甲喹 | ||
| 分子式 | C11H10N2O3 | 分子量 | 218.21 |
| 溶解度 | DMSO : 100 mg/mL (458.27 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.5827 mL | 22.9137 mL | 45.8274 mL |
| 5 mM | 0.9165 mL | 4.5827 mL | 9.1655 mL |
| 10 mM | 0.4583 mL | 2.2914 mL | 4.5827 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Mequindox resistance and in vitro efficacy in animal-derived Escherichia coli strains
Vet Microbiol 2015 Jun 12;177(3-4):341-6.PMID:25912025DOI:10.1016/j.vetmic.2015.04.007.
This study investigated the in vitro efficacy of Mequindox against enteropathogenic Escherichia coli (EPEC), and characterized the oqxAB genes as the main Mequindox resistance determinant in E. coli strains of animal origin. A total of 1123 E. coli isolates were collected from domestic animals in China from the 1970s to 2013, and Mequindox susceptibility was tested by broth microdilution. The percentage of E. coli isolates with increased Mequindox MICs of ≥ 64 μg/ml showed a rising trend each year throughout the study period. Mequindox showed good bactericidal activity in vitro towards 20 EPEC strains, although it had a wide mutant selection window. All 1123 E. coli isolates were tested for the presence of the oqxAB genes, and the operon was detected in 322 isolates, which accounted for 94.4% (322/341) of isolates with increased MICs to Mequindox (MIC ≥ 64 μg/ml). Of the isolates with Mequindox MIC ≤ 32 μg/ml, 98.8% (773/782) were oqxAB negative. Polymerase chain reaction-based stability testing revealed that the IS26-oqxAB circular intermediate was present in 93.4% (309/331) of the oqxAB-positive strains, indicating that this IS26-flanked Tn6010 element was unstable and prone to excision via IS26-mediated recombination. Functional analysis of the oqxAB genes confirmed that this operon alone is sufficient to confer resistance or increased MICs to multiple antimicrobials, including Mequindox. This is the first study to investigate the relationship between Mequindox susceptibility and oqxAB genotype, and may provide the basis for establishing the resistance breakpoint for Mequindox against E. coli.
Metabolism Profile of Mequindox in Sea Cucumbers In Vivo Using LC-HRMS
Antibiotics (Basel) 2022 Nov 11;11(11):1599.PMID:36421242DOI:10.3390/antibiotics11111599.
In this work, the metabolism behavior of Mequindox (MEQ) in sea cucumber in vivo was investigated using LC-HRMS. In total, nine metabolites were detected and identified as well as the precursor in sea cucumber tissues. The metabolic pathways of MEQ in sea cucumber mainly include hydrogenation reduction, deoxidation, carboxylation, deacetylation, and combinations thereof. The most predominant metabolites of MEQ in sea cucumber are 2-iso-BDMEQ and 2-iso-1-DMEQ, with deoxidation and carbonyl reduction as major metabolic pathways. In particular, this work first reported 3-methyl-2-quinoxalinecarboxylic acid (MQCA) as a metabolite of MEQ, and carboxylation is a major metabolic pathway of MEQ in sea cucumber. This work revealed that the metabolism of MEQ in marine animals is different from that in land animals. The metabolism results in this work could facilitate the accurate risk assessment of MEQ in sea cucumber and related marine foods.
Mequindox induced cellular DNA damage via generation of reactive oxygen species
Mutat Res 2012 Jan 24;741(1-2):70-5.PMID:22094289DOI:10.1016/j.mrgentox.2011.10.012.
Mequindox, a quinoxaline-N-dioxide derivative that possesses antibacterial properties, has been widely used as a feed additive in the stockbreeding industry in China. While recent pharmacological studies have uncovered potential hazardous effects of Mequindox, exactly how Mequindox induces pathological changes and the cellular responses associated with its consumption remain largely unexplored. In this study, we investigated the cellular responses associated with Mequindox treatment. We report here that Mequindox inhibits cell proliferation by arresting cells at the G2/M phase of the cell cycle. Interestingly, this mequindox-associated deleterious effect on cell proliferation was observed in human, pig as well as chicken cells, suggesting that Mequindox acts on evolutionarily conserved target(s). To further understand the mequindox-host interaction and the mechanism underlying mequindox-induced cell cycle arrest, we measured the cellular content of DNA damage, which is known to perturb cell proliferation and compromise cell survival. Accordingly, using γ-H2AX as a surrogate marker for DNA damage, we found that Mequindox treatment induced cellular DNA damage, which paralleled the chemical-induced elevation of reactive oxygen species (ROS) levels. Importantly, expression of the antioxidant enzyme catalase partially alleviated these mequindox-associated effects. Taken together, our results suggest that Mequindox cytotoxicity is attributable, in part, to its role as a potent inducer of DNA damage via ROS.
Mequindox Induced Genotoxicity and Carcinogenicity in Mice
Front Pharmacol 2018 Apr 10;9:361.PMID:29692735DOI:10.3389/fphar.2018.00361.
Mequindox (MEQ), acting as an inhibitor of deoxyribonucleic acid (DNA) synthesis, is a synthetic heterocyclic N-oxides. To investigate the potential carcinogenicity of MEQ, four groups of Kun-Ming (KM) mice (50 mice/sex/group) were fed with diets containing MEQ (0, 25, 55, and 110 mg/kg) for one and a half years. The result showed adverse effects on body weights, feed consumption, hematology, serum chemistry, organ weights, relative organ weights, and incidence of tumors during most of the study period. Treatment-related changes in hematology, serum chemistry, relative weights and histopathological examinations revealed that the hematological system, liver, kidneys, and adrenal glands, as well as the developmental and reproductive system, were the main targets after MEQ administration. Additionally, MEQ significantly increased the frequency of micronucleated normochromatic erythrocytes in bone marrow cells of mice. Furthermore, MEQ increased the incidence of tumors, including mammary fibroadenoma, breast cancer, corticosuprarenaloma, haemangiomas, hepatocarcinoma, and pulmonary adenoma. Interestingly, the higher incidence of tumors was noted in M25 mg/kg group, the lowest dietary concentration tested, which was equivalent to approximately 2.25 and 1.72 mg/kg b.w./day in females and males, respectively. It was assumed that the lower toxicity might be a reason for its higher tumor incidence in M25 mg/kg group. This finding suggests a potential relationships among the dose, general toxicity and carcinogenicity in vivo, and further study is required to reveal this relationship. In conclusion, the present study demonstrates that MEQ is a genotoxic carcinogen in KM mice.
Mequindox induces apoptosis, DNA damage, and carcinogenicity in Wistar rats
Food Chem Toxicol 2019 May;127:270-279.PMID:30922968DOI:10.1016/j.fct.2019.03.025.
Mequindox (MEQ) is a synthetic antibacterial agent. Recent studies showed that MEQ and its primary metabolites exhibit strong genotoxicity to mammalian cells, and MEQ induced carcinogenicity in mice. These findings suggest that chronic exposure to MEQ could lead to an increased risk of cancer later in life. In the present study, four groups of Wistar rats (55 rats/sex/group) were fed with diets containing MEQ (0, 25, 55, and 110 mg/kg) for 2 years. The results showed that the hematological system, liver, kidneys, and adrenal glands, as well as the developmental and reproductive systems, were the main targets for MEQ. Liver toxicity mediated by MEQ was associated with apoptosis and the nuclear factor κB (NF-κB) signaling pathway. In addition, MEQ increased the incidence of tumors in rats. Phosphorylated histone H2AX (γ-H2AX) is identified as a biomarker of cellular response to DNA double-strand breaks (DSB). Our data demonstrated that γ-H2AX expression was significantly increased in tumors. Thus, high levels of DSB might be responsible for carcinogenesis in rats, and further investigation is absolutely required to clarify the exact molecular mechanisms for carcinogenicity caused by MEQ in vivo.