2. Anti-infection Apoptosis Metabolic Enzyme/Protease Immunology/Inflammation NF-κB Cell Cycle/DNA Damage MAPK/ERK Pathway
  3. Fungal Apoptosis Caspase Reactive Oxygen Species (ROS) MDM-2/p53 SOD Bcl-2 Family PERK JNK p38 MAPK
  4. Bromuconazole

Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction.

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Bromuconazole

Bromuconazole Chemical Structure

CAS No. : 116255-48-2

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Bromuconazole Related Antibodies

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Description

Bromuconazole is a triazole fungicide with oral efficacy and blood-brain barrier permeability. Bromuconazole protects crops from various fungal contaminations. Bromuconazole exhibits cytotoxicity against a variety of cancer cells, induces G0/G1 cell cycle arrest and inhibits DNA synthesis in cancer cells, and triggers cytoskeletal structural disorder, genotoxic damage, apoptotic (apoptosis) cell death, and mitochondrial membrane depolarization. Bromuconazole activates caspase-3, induces excessive production of ROS, p53 and Bax, lipid peroxidation, increased activities of SOD and CAT, and downregulates Bcl-2. By upregulating p-ERK1/2 and p-JNK, Bromuconazole disrupts the MAPK signaling pathway, impairs the cellular stress response of human trophoblast cells and endometrial cells, and damages the implantation process. Bromuconazole is applicable to research related to glioma, colon cancer, reproductive injury (implantation dysfunction), and cardiac dysfunction[1][2][3][4][5][6][7].

In Vitro

Bromuconazole (0-500 μM; 24 h) induces concentration-dependent cytotoxicity in F98 and HCT116 cells, with IC50 values of 60 μM and 180 μM, respectively[1][2].
Bromuconazole (0-180 μM; 6-24 h) induces G0/G1 cell cycle arrest, inhibits DNA synthesis, triggers cytoskeletal structural disorder, genotoxic damage (DNA fragmentation and nuclear pyknosis), apoptotic cell death, and mitochondrial membrane depolarization in F98 and HCT116 cells[1].
Bromuconazole (15-60 μM; 24 h) induces concentration-dependent upregulation of p53 and Bax mRNA, downregulation of Bcl-2 mRNA, an increase in the Bax/Bcl-2 ratio, and concentration-dependent activation of caspase-3 in rat glioma F98 cells[1].
Bromuconazole (45-180 μM; 24 h) induces concentration-dependent activation of caspase-3, excessive ROS production, lipid peroxidation, and increased activities of SOD and CAT in HCT116 cells[2].
Bromuconazole (0-50 mg/L; 48 h) impairs the cell viability of HTR-8/SVneo and THESCs, with LC50 values of 28.05 mg/L and 33.41 mg/L respectively after 48 h of exposure[4].
Bromuconazole (30 mg/L; 24-48 h) impairs 3D sphere formation and self-assembly of HTR-8/SVneo and THESCs. It induces cell apoptosis by dysregulating the expression of apoptosis-related genes and increasing the BAX/BCL-XL protein ratio, induces G2/M cell cycle arrest by downregulating the expression of cell cycle-related genes, and impairs mitochondrial function by reducing mitochondrial membrane potential and downregulating the expression of mitochondrial function-related genes[4].
Bromuconazole (30 mg/L; 30 min to 24 h) induces reactive oxygen species (ROS) accumulation and endoplasmic reticulum (ER) stress in HTR-8/SVneo and THESCs cells by downregulating SOD1 and upregulating ER stress-related factors[4].
Bromuconazole (30 mg/L; 15 min) disrupts the MAPK signaling pathway by upregulating p-ERK1/2 and p-JNK in HTR-8/SVneo and THESCs cells[4].
Bromuconazole (30 mg/L; 24 h) induces inflammatory responses in HTR-8/SVneo and THESCs cells by dysregulating the mRNA expression of pro-inflammatory and anti-inflammatory cytokines[4].
Bromuconazole (30 mg/L; 24-48 h) inhibits the migration of HTR-8/SVneo and THESCs[4].
Bromuconazole (10-250 μM; 24 h) induces cytotoxicity, impairs energy metabolism, disrupts ion homeostasis, dysregulates the expression of genes related to myosin synthesis, and upregulates LEF1 protein expression in rat H9C2 cardiomyocytes[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Bromuconazole Related Antibodies

Cell Viability Assay[1]

Cell Line: rat glioma F98 cells
Concentration: 0, 10, 20, 40, 60, 80, 100, 120, 140, 150 μM
Incubation Time: 24 h
Result: Caused concentration-dependent F98 cell death, with an IC50 of 60 μM after 24 h of treatment.

Cell Cycle Analysis[1]

Cell Line: rat glioma F98 cells
Concentration: 15, 30, and
60 μM
Incubation Time: 24 h
Result: Caused dose-dependent accumulation of F98 cells in the G0/G1 phase: at 60 μM, G0/G1 phase cell distribution increased from 64.78% (untreated) to 89%.
Corresponding dose-dependent reduction in S phase cell distribution was observed: at 60 μM, S phase cell distribution decreased from 17.52% (untreated) to 1.5%.

Apoptosis Analysis[1]

Cell Line: rat glioma F98 cells
Concentration: 15, 30, and
60 μM
Incubation Time: 24 h
Result: Induced concentration-dependent apoptosis: apoptosis levels were 23.61% at 15 μM, 33.86% at 30 μM, and 55.94% at 60 μM, compared to 1.55% in untreated cells.

Real Time qPCR[1]

Cell Line: rat glioma F98 cells
Concentration: 15, 30, and
60 μM
Incubation Time: 24 h
Result: Caused concentration-dependent increases in p53 and Bax mRNA expression, and concentration-dependent decreases in Bcl-2 mRNA expression.
At 60 μM, p53 mRNA levels increased to 2.49-fold, Bax mRNA levels increased to 2.3-fold, Bcl-2 mRNA levels decreased to 0.3-fold, and the Bax/Bcl-2 ratio increased to 7.67-fold.

Cell Cytotoxicity Assay[2]

Cell Line: human colon carcinoma HCT116 cells
Concentration: 0, 50, 100, 150, 200, 250, 300, 350, 400 μM
Incubation Time: 24 h
Result: Caused a concentration-dependent increase in HCT116 cell mortality, with an IC50 of 180 μM.

Cell Cycle Analysis[2]

Cell Line: human colon carcinoma HCT116 cells
Concentration: 45, 90 and 180 μM
Incubation Time: 24 h
Result: Caused a concentration-dependent accumulation of cells in the G0/G1 phase (from 59.89% in untreated cells to 67.84%, 71.02%, and 84% at 45, 90, and 180 μM, respectively).
Caused a concentration-dependent reduction in cells in the S phase (from 18.9% in untreated cells to 11.03%, 9.26%, and 5.65% at 45, 90, and 180 μM, respectively).

Apoptosis Analysis[2]

Cell Line: human colon carcinoma HCT116 cells
Concentration: 45, 90 and 180 μM
Incubation Time: 24 h
Result: Caused a concentration-dependent increase in apoptosis ratio (from 11.15% in untreated cells to 22.45%, 30.92%, and 39.75% at 45, 90, and 180 μM, respectively).
Induced light green staining and crescent-shaped nuclei in treated cells, consistent with apoptotic morphology.\nCaused a concentration-dependent increase in total apoptosis (early + late apoptosis) from 12.29% in untreated cells to 24.5%, 34.02%, and 43.85% at 45, 90, and 180 μM, respectively.

Cell Viability Assay[4]

Cell Line: HTR-8/SVneo, T HESCs
Concentration: 0, 5, 10, 15, 20, 30, 40, and 50 mg/L
Incubation Time: 48 h
Result: Reduced cell viability in both cell lines.
Reached an LC50 value of 28.05 mg/L for HTR-8/SVneo cells.
Reached an LC50 value of 33.41 mg/L for T HESCs.

Apoptosis Analysis[4]

Cell Line: HTR-8/SVneo, T HESCs
Concentration: 0, 10, 20,
30 mg/L (annexin V/PI staining); 30 mg/L (mRNA and protein analysis)
Incubation Time: 48 h (annexin V/PI staining); 24 h (mRNA and protein analysis)
Result: Increased HTR-8/SVneo early apoptotic cells by 171.58% and late apoptotic cells by 146.96%.
Upregulated HTR-8/SVneo mRNA expression of BAK and CASP1.
Downregulated HTR-8/SVneo mRNA expression of BCL2 and BCL2L1.
Increased the HTR-8/SVneo BAX/BCL-XL protein ratio by 208.17%.
Increased T HESCs early apoptotic cells by 171.58% and late apoptotic cells by 176.12%.
Upregulated T HESCs mRNA expression of BAX and CASP1.
Downregulated T HESCs mRNA expression of BCL2.
Increased the T HESCs BAX/BCL-XL protein ratio by 152.46%.

Cell Cycle Analysis[4]

Cell Line: HTR-8/SVneo, T HESCs
Concentration: 0, 10, 20, and
30 mg/L (cell cycle analysis); 30 mg/L (mRNA analysis)
Incubation Time: 48 h (cell cycle analysis); 24 h (mRNA analysis)
Result: Reduced HTR-8/SVneo G0/G1 phase cells to 66.01%.
Increased HTR-8/SVneo S phase cells to 139.83%.
Increased HTR-8/SVneo G2/M phase cells to 118.42%.
Increased HTR-8/SVneo sub G1 phase cells to 234.14%.
Downregulated HTR-8/SVneo mRNA expression of CCNA2, CCNB1, CCND1, CCNE2, CDK1, and CDK4.
Reduced T HESCs G0/G1 phase cells to 85.95%.
Increased T HESCs G2/M phase cells to 138.99%.
Increased T HESCs sub G1 phase cells to 269.69%.
Downregulated T HESCs mRNA expression of CCNA2, CCNB1, CCND1, CCNE2, and CDK1 (no significant change in CDK4).

Real Time qPCR[4]

Cell Line: HTR-8/SVneo, T HESCs
Concentration: 30 mg/L
Incubation Time: 24 h
Result: Upregulated HTR-8/SVneo mRNA expression of proinflammatory cytokines IL21, IL21R, and CXCR2.
Downregulated HTR-8/SVneo mRNA expression of anti-inflammatory cytokines IL4R and CCL2.
Upregulated T HESCs mRNA expression of proinflammatory cytokines IL1β, IL18R1, and CXCR2.
Downregulated T HESCs mRNA expression of anti-inflammatory cytokines IL4R and CCL2.

Cell Migration Assay[4]

Cell Line: HTR-8/SVneo, T HESCs
Concentration: 30 mg/L
Incubation Time: 3-48 h (wound healing assay); 24 h (transwell assay)
Result: Delayed HTR-8/SVneo wound healing, with 15.78% of initial wound area remaining at 48 h (vs.
1.43% in control).
Reduced HTR-8/SVneo transwell-migrated cells to 52.50%.
Delayed T HESCs wound healing, with 7.61% of initial wound area remaining at 48 h (vs.
1.84% in control).
In Vivo

Bromuconazole (13.8-32.8 mg/kg/day; oral administration; daily; 90 days; 84-200 mg/kg/day; topical administration; daily; 90 days) induces dose-dependent hepatotoxicity in male albino rats, with greater toxicity observed via the oral route than the topical route; its characteristics include increased levels of hepatic enzymes, hepatic oxidative stress, increased liver weight, histopathological necrotic lesions, upregulated hepatic PXR and CYP3A1 expression as well as CYP3A1 activity, and downregulated hepatic CAR and CYP2B1 expression[3].
Exposure to Bromuconazole (50 ng/L-7.5 mg/L; i.g.; once daily for 7 consecutive days) induces cardiotoxicity in adult male AB strain zebrafish by disrupting cardiac energy metabolism, altering ion homeostasis and gene expression related to myosin synthesis, and abnormally activating LEF1[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: albino rats (male, adult, 160-200 g)[3]
Dosage: 13.8 mg/kg/day (oral); 32.8 mg/kg/day (oral); 84 mg/kg/day (topical); 200 mg/kg/day (topical)
Administration: p.o.; daily; 90 days; topical; daily; 90 days
Result: Increased serum ALT, AST , ALP , ACP, total bilirubin, direct bilirubin, indirect bilirubin, and liver MDA.
Decreased serum total protein, albumin, and liver SOD.
Increased liver weigh.
Induced 5.3-fold increase in hepatic CYP3A1 mRNA expression, 3.4-fold increase in PXR mRNA expression, 4.3-fold decrease in CYP2B1 mRNA expression, 2.7-fold decrease in CAR mRNA expression, and ~7-fold increase in hepatic CYP3A1 enzyme activity.
Animal Model: AB-strain (adult male, 4-6 months old, weight 450 mg, body length 38 mm)[5]
Dosage: 50 ng/L; 7.5 mg/L
Administration: i.g.; daily; 7 days
Result: Increased fatness index significantly.
Reduced body length.
Caused looser heart structure, increased ventricular and arteriole volume, thinner heart walls, more vacuoles in the ventricular cavity, and increased numbers of hypertrophic cardiomyocytes with reduced cardiomyocyte density in both dose groups.
Identified 684 differentially expressed genes, with significant enrichment in cardiac energy metabolism pathways.
Increased heart tissue triglycerides; reduced ATP content in a concentration-dependent manner.
Slightly increased TG, reduced TC and low-density lipoprotein (LDL), and increased high-density lipoprotein (HDL).
Reduced mRNA expression of glycolysis genes GK and HK1, lipid transport gene abca1b, and UCP2.
Downregulated ion balance-related genes ryr2b, atp2a2a, and Pln in a concentration-dependent manner.
Upregulated myosin synthesis-related gene myl4, while downregulated myh7l, tpm4b, and tnnt2a.
Activated LEF1 gene expression abnormally in heart tissue compared to controls.
Increased cardiac ejection fraction significantly compared to controls.
Molecular Weight

377.06

Formula

C13H12BrCl2N3O
CAS No.
SMILES

ClC1=CC=C(C(Cl)=C1)C2(OCC(Br)C2)CN3N=CN=C3
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Room temperature in continental US; may vary elsewhere.
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Keywords:

Bromuconazole116255-48-2FungalApoptosisCaspaseReactive Oxygen Species (ROS)MDM-2/p53SODBcl-2 FamilyPERKJNKp38 MAPKSuperoxide DismutaseProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinasec-Jun N-terminal kinasefungicideHTR-8/SVneo cellsTHESCs cellsF98 cellsHCT116 cellsgliomacolon cancerreproductive injurycardiac dysfunctionH9C2 cardiomyocytesalbino ratsZebrafishInhibitorinhibitorinhibit

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