Tebuconazole

Tebuconazole is an orally active agricultural azole fungicide which can also inhibit CYP51 with IC₅₀s of 0.9 and 1.3 μM for Candida albicans CYP51 (CaCYP51) and truncated Homo sapiens CYP51 (Δ60HsCYP51), respectively. Tebuconazole induces lipid accumulation and oxidative stress in HepG2 Cells. Tebuconazole decreases MAC-T cells viability and proliferation, induces ER-stress-mediated apoptosis and increases oxidative stress levels in MAC-T cells^{[1][2][3][4][5][6]}. IC50 & Target:IC50: 0.9 μM (CaCYP51), 1.3 μM (Δ60HsCYP51)^[1] In Vitro:Tebuconazole (TEB) (20–80 μM, 24 h) shows lipid accumulation in HepG2 cells^[2].
Tebuconazole (20–80 μM, 12 h) increases the nuclear translocation of peroxisome proliferator-activated receptors and the expression of lipid uptake and oxidation-related markers in HepG2 cells^[2].
Tebuconazole (20–80 μM, 24 h) increases oxidative stress levels, induces the loss of mitochondrial membrane potential and lower levels of microsomal triglyceride transfer protein in the HepG2 cells^[2].
Tebuconazole (0-750 μM, 24 hours) decreases MAC-T cells viability and proliferation and induced mitochondria-mediated apoptotic MAC-T cell death by activating ER stress^[3].
Tebuconazole (0-100 μM, 24 hours) induces dose-dependent cell death in H9c2 cardiomyoblasts and in adult rat ventricular myocytes (ARVM)^[4].
Tebuconazole (30-60 μM, 24 hours) induces DNA damage and ROS generation and lipid peroxidation in H9c2 cells^[4].
In Vivo:Tebuconazole (TEB) (10-50 mg/kg, p.o., once daily for 28 days) induces a multiplicity of CYPs and oxidative stress in liver; inhibits testicular P450 and glutathione S-transferase activities; and produces anti-androgenic effects in male rats^[5].
Tebuconazole (25-100 mg/kg, p.o., daily for 10 days) causes the proliferation of fetal Leydig cells and increases fetal serum testosterone and progesterone levels in gestational rat^[6].