Tebuconazole is an azole fungicide used primarily in agriculture, and it is orally active. It inhibits the CYP51 enzyme with IC50 values of 0.9 μM for Candida albicans CYP51 (CaCYP51) and 1.3 μM for the truncated version of Homo sapiens CYP51 (Δ60HsCYP51). Additionally, tebuconazole has been shown to induce lipid accumulation and oxidative stress in HepG2 cells. It also adversely affects MAC-T cells by reducing their viability and proliferation, inducing ER-stress-mediated apoptosis, and increasing oxidative stress levels[1].[2].[3].[4].[5].[6].
体内研究
Oral administration of tebuconazole (10-50 mg/kg, once daily for 28 days) induces various cytochrome P450s (CYPs) and oxidative stress in the liver, inhibits testicular P450 and glutathione S-transferase activities, and exhibits anti-androgenic effects in male rats[5].
Tebuconazole given at doses of 25 to 100 mg/kg, orally each day for 10 days, stimulates the proliferation of fetal Leydig cells and increases fetal serum testosterone and progesterone levels in pregnant rats[6].
体外研究
In experiments conducted with HepG2 cells, tebuconazole treatment ranging from 20 to 80 μM for 24 hours resulted in noticeable lipid accumulation[2].
Tebuconazole, in concentrations ranging from 20 to 80 μM over 12 hours, promotes the nuclear translocation of peroxisome proliferator-activated receptors (PPARs) and boosts the expression of genes related to lipid uptake and oxidation in HepG2 cells[2].
When administered to HepG2 cells at 20 to 80 μM for 24 hours, tebuconazole elevates oxidative stress, disrupts mitochondrial membrane potential, and reduces the levels of microsomal triglyceride transfer protein[2].
Tebuconazole exposure (0-750 μM, over 24 hours) reduces the viability and proliferation of MAC-T cells and triggers mitochondria-mediated apoptosis through the activation of endoplasmic reticulum (ER) stress[3].
At a range of 0 to 100 μM for 24 hours, tebuconazole causes dose-dependent cell death in H9c2 cardiomyoblasts and adult rat ventricular myocytes (ARVM)[4].
Tebuconazole, administered at 30 to 60 μM for 24 hours, leads to DNA damage, reactive oxygen species (ROS) generation, and lipid peroxidation in H9c2 cells[4].
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