Cereulide
Based on 1 Customer Validation
Cereulide is an orally active, blood-brain barrier-permeable emetic toxin. Cereulide acts as a potassium ionophore that inserts into membranes, forms complexes with K+, and transports K+ from the cytoplasm into the mitochondrial matrix. Cereulide disrupts the electrochemical gradient of the inner mitochondrial membrane, leading to mitochondrial swelling and dysfunction, uncoupling of oxidative phosphorylation, inhibition of ATP synthesis, ROS accumulation, and ultimately triggering apoptosis and autophagy. Cereulide exhibits multi-organ toxicity and can be used for research on emetic food poisoning.
For research use only. We do not sell to patients.
- Purity: 95.05%
- CAS No.: 157232-64-9
- Formula: C57H96N6O18
- Molecular Weight:1153.40
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Storage:
Sealed storage, away from moisture.
Powder -80°C, 2 years , -20°C, 1 year* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Cereulide (<1 ng/mL, chronic; 0.05-0.5 nM, 10 days; 0.2-500 nM, 24 h) induces mitochondrial dysfunction, impairs intestinal barrier function, inhibits cell proliferation, and triggers inflammation in Caco-2 cells, with maximal respiration reduced to 2% of baseline and ATP production to 6% of baseline at 0.5 nM after 10 days of exposure[1].
Cereulide (0.05-0.5 ng/mL, 24 h; 1 ng/mL, 2 days; 10 ng/mL, 8-24 h) dose-dependently impairs glucose-stimulated insulin secretion and induces apoptosis and necrosis in MIN6 cells and pancreatic islets, with complete loss of insulin secretion at 0.25 ng/mL in MIN6 cells after 24 h of exposure[1].
Cereulide (0.05-0.5 nM, 10 days) induces severe mitochondrial dysfunction in HepG2 cells, with maximal respiration reduced to 2% of baseline and ATP production to 6% of baseline at 0.5 nM after 10 days of exposure[1].
Cereulide (20 ng/mL, 1 min; 100-1000 ng/mL, 3 h; unspecified, 1 day) rapidly impairs cytotoxic function, induces mitochondrial damage, and triggers apoptosis in NK cells, with loss of cytotoxic capacity observed within 1 min of exposure to 20 ng/mL[1].
Cereulide (2.74-2.98 ng/mL; 24 h) reduces viability of HepaRG cells with an IC50 of 2.98 ng/mL and HEK293T cells with an IC50 of 2.74 ng/mL after 24 h of treatment[2].
Cereulide (0.3-1 ng/mL; 24 h) induces dose-dependent apoptosis in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 24 h) induces structural damage including mitochondrial dysfunction and apoptotic morphological changes in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 24 h) induces ER swelling in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.3-1 ng/mL; 3-24 h) activates the IRE1α/XBP1 and PERK/eIF2α ER stress pathways and upregulates pro-apoptotic CHOP in a time- and dose-dependent manner in HepaRG and HEK293T cells after treatment with 0.3 or 1 ng/mL for 3, 6, or 24 h[2].
Cereulide (0.3-1 ng/mL; 24 h) induces dose-dependent ROS accumulation in HepaRG and HEK293T cells after 24 h of treatment with 0.3 or 1 ng/mL[2].
Cereulide (0.5-1 ng/mL; 4 h) induces ER stress (increased p-eIF2α and CHOP) in HepaRG and HEK293T cells treated with 1 ng/mL or 0.5 ng/mL for 4 h that is mediated by ROS accumulation[2].
Cereulide (1 ng/mL; 48 h) reduces insulin content and increases cell death in fetal porcine islets of Langerhans[3].
Cereulide (10 ng/mL; 8-24 h) induces loss of mitochondrial membrane potential and necrotic/pyknotic cell death in murine insulinoma MIN6 cells[3].
Cereulide (5 ng/mL; 24 h) induces high rates of apoptosis in rat INS-1E cells, murine insulinoma MIN6 cells, and freshly isolated murine pancreatic islets[3].
Cereulide (0.5 ng/mL; 24 h) impairs mitochondrial structure and function, increases reactive oxygen species, and induces apoptosis in murine insulinoma MIN6 cells[3].
Cereulide (0.15-0.5 ng/mL; 24 h) significantly reduces or completely inhibits glucose-stimulated insulin secretion in murine insulinoma MIN6 cells and freshly isolated murine pancreatic islets[3].
Cereulide (2 nM) inhibits RNA synthesis in human hepatocellular carcinoma HepG2 cells[3].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) reduces cell viability of HepG2 liver cells in a concentration- and time-dependent manner, with cytotoxicity observed at lower concentrations after 24 h compared to 5 h[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) alters mitochondrial quantity and morphology in HepG2 liver cells, with an initial increase in mitochondrial number at 0.1 ng/mL followed by concentration-dependent decreases at higher concentrations, and mitochondrial aberrations detected at 2.5 ng/mL after 24 h[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) increases lysosomal number and/or size in HepG2 liver cells at concentrations 0.1-5 ng/mL after 5 and 24 h, with a maximum increase to 136% of solvent control at 2.5 ng/mL after 24 h, while higher concentrations reduce lysosomal signal[4].
Cereulide (0.1-50 ng/mL; 5 h, 24 h) increases lysosomal acidification in HepG2 liver cells at concentrations 2.5-50 ng/mL after 24 h, with no significant effects detected after 5 h[4].
Cereulide (0.1-1 ng/mL; 5 h, 24 h) upregulates transcription of autophagy-related genes MAP1LC3B and SQSTM1 in HepG2 liver cells at 1 ng/mL after 5 and 24 h, while marginally reducing transcription of lysosomal and other autophagy-related genes[4].
Cereulide (0.1-1 ng/mL; 24 h) increases LC3 protein expression in HepG2 liver cells at 0.1 and 1 ng/mL after 24 h, indicating induction of autophagy via the LC3 pathway[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:HepaRG cells, HEK293T cells
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Concentration:0.3 and 1 ng/mL
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Incubation Time:24 h
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Result:Caused a dose-dependent significant increase in the number of apoptotic cells in both HepaRG and HEK293T cells.
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Cell Line:HepaRG cells, HEK293T cells
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Concentration:0.3 and 1 ng/mL
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Incubation Time:3, 6 and 24 h
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Result:Caused time- and dose-dependent increases in phosphorylation of IRE1α and PERK, phosphorylation of eIF2α, levels of XBP1(s), and levels of CHOP in both cell lines.
Did not increase BiP levels at 3 h or 6 h, but significantly increased BiP levels at 24 h.
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Cell Line:HepaRG cells, HEK293T cells
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Concentration:0.5 ng/mL (HEK293T cells); 1 ng/mL (HepaRG cells)
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Incubation Time:4 h
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Result:Induced increases in p-eIF2α and CHOP levels that were reversed by NAC pretreatment in both cell lines.
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Cell Line:Murine insulinoma MIN6 cells
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Concentration:0.5 ng/mL
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Incubation Time:24 h
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Result:Caused swollen, disintegrated mitochondria in murine insulinoma MIN6 cells.
Increased reactive oxygen species by more than twofold in murine insulinoma MIN6 cells.
Reduced basal respiration rate to half in murine insulinoma MIN6 cells.
Increased caspase 3/7 activation in murine insulinoma MIN6 cells.
Elevated cytochrome C release into the cytoplasm in murine insulinoma MIN6 cells.
Upregulated pro-apoptotic mRNA markers including CHOP in murine insulinoma MIN6 cells.
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Cell Line:HepG2 liver cells
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Concentration:0.1, 1, 2.5, 5, 10 and 50 ng/mL
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Incubation Time:5 h; 24 h
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Result:Reduced cell viability to approximately 65-70% starting from 2.5 ng/mL after 5 h incubation.
Reduced cell viability to 46% at the highest tested concentration after 24 h incubation.
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Cell Line:HepG2 liver cells
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Concentration:0.1, 1, 2.5, 5, 10 and 50 ng/mL
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Incubation Time:5 h; 24 h
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Result:Increased MAP1LC3B and SQSTM1 transcript levels at 1 ng/mL after 5 h incubation.
Marginally reduced LAMP2, CTSD, and ATG16 transcript levels at 0.1 and 1 ng/mL after 5 h incubation.
Increased MAP1LC3B transcript levels to ~2.7-fold of solvent control at 1 ng/mL after 24 h incubation.
Increased SQSTM1 transcript levels to ~2.5-fold of solvent control at 1 ng/mL after 24 h incubation.
Reduced CTSD transcript levels to below 0.5-fold of solvent control at 1 ng/mL after 24 h incubation.
Marginally reduced LAMP2 and ATG16 transcript levels at 0.1 and 1 ng/mL after 24 h incubation.
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Cell Line:HepG2 liver cells
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Concentration:0.1 and 1 ng/mL
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Incubation Time:24 h
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Result:Increased LC3 fluorescence intensity to ~130% of solvent control at 0.1 ng/mL after 24 h incubation.
Increased LC3 fluorescence intensity to ~150% of solvent control at 1 ng/mL after 24 h incubation, similar to the positive control rapamycin.
Cereulide (10-20 μg per mouse; i.p.; single administration) induces dose-dependent hepatotoxicity in male BALB/c mice, with 20 μg being a lethal dose, 10 μg causing reversible toxicity, and 15 μg leading to significant liver injury[3].
Cereulide-containing *Bacillus cereus* cultures induce microvesicular steatosis and midzonal necrosis in rat livers, replicating fatal human hepatotoxicity[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (6-week-old, male, SPF, acclimated for 1 week post-purchase)[2]
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Dosage:10 μg/kg; 50 μg/kg; 200 μg/kg
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Administration:p.o.; daily; 28 days
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Result:Significantly decreased body weight; increased kidney and spleen indices; induced hepatocyte and glomerular swelling, inflammatory cell infiltration; increased mRNA levels of IL-6 and TNF-α in liver and kidney; significantly decreased SOD activity in liver and kidney; significantly increased MDA level in liver; increased mRNA levels of XBP1(s) and ATF4, and increased protein/phosphorylation levels of IRE1α/XBP1(s) and PERK/eIF2α/CHOP in liver and kidney; reached ~20% TUNEL-positive apoptotic cells in liver and ~22% in kidney (50 μg/kg).
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Animal Model:BALB/c (male)[3]
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Dosage:20 μg; 15 μg; 10 μg
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Administration:i.p.; single dose
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Result:Caused lethality at 20 μg
Induced marked hepatocyte swelling (due to mitochondrial swelling) and elevation of serum transaminases at 15 μg.
Allowed full recovery 4 weeks after 10 μg.
Chemical Information
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CAS No. 157232-64-9
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Appearance Solid
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Molecular Weight 1153.40
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Formula C57H96N6O18
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Color White to off-white
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Initial Source
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Sealed storage, away from moisture
Powder -80°C 2 years -20°C 1 year * In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
DMSO : 100 mg/mL (86.70 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
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Data Sheet (296 KB)
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SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
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Handling Instructions (2659 KB)
References
[1].
Yang S, et al. Cereulide and Emetic Bacillus cereus: Characterizations, Impacts and Public Precautions. Foods. 2023 Feb 15;12(4):833.
[Content Brief]
[2]. Li D, et al. Cereulide Exposure Caused Cytopathogenic Damages of Liver and Kidney in Mice. Int J Mol Sci. 2021;22(17):9148. Published 2021 Aug 24. [Content Brief]
[3]. Vangoitsenhoven R, et al. Cereulide food toxin, beta cell function and diabetes: Facts and hypotheses. Diabetes Res Clin Pract. 2015;109(1):1-5. [Content Brief]
[4]. Beisl J, et al. Cereulide and Deoxynivalenol Increase LC3 Protein Levels in HepG2 Liver Cells. Toxins (Basel). 2022;14(2):151. Published 2022 Feb 18. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 0.8670 mL | 4.3350 mL | 8.6700 mL | 21.6750 mL |
| 5 mM | 0.1734 mL | 0.8670 mL | 1.7340 mL | 4.3350 mL | |
| 10 mM | 0.0867 mL | 0.4335 mL | 0.8670 mL | 2.1675 mL | |
| 15 mM | 0.0578 mL | 0.2890 mL | 0.5780 mL | 1.4450 mL | |
| 20 mM | 0.0434 mL | 0.2168 mL | 0.4335 mL | 1.0838 mL | |
| 25 mM | 0.0347 mL | 0.1734 mL | 0.3468 mL | 0.8670 mL | |
| 30 mM | 0.0289 mL | 0.1445 mL | 0.2890 mL | 0.7225 mL | |
| 40 mM | 0.0217 mL | 0.1084 mL | 0.2168 mL | 0.5419 mL | |
| 50 mM | 0.0173 mL | 0.0867 mL | 0.1734 mL | 0.4335 mL | |
| 60 mM | 0.0145 mL | 0.0723 mL | 0.1445 mL | 0.3613 mL | |
| 80 mM | 0.0108 mL | 0.0542 mL | 0.1084 mL | 0.2709 mL |
Cereulide Related Classifications
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