Prochloraz is an imidazole antifungal that inhibits ergosterol biosynthesis via inhibition of the cytochrome P450-dependent 14α-demethylation of lanosterol, which results in disruption of the fungal cell membrane and cell death. Prochloraz inhibits human placenta microsomal aromatase in vitro (IC50 = 40 nM). Prochloraz also acts as an antagonist of the estrogen receptor (ER) and androgen receptor (AR) (IC50s = 25 μM and 4 μM, respectively) as well as activates the aryl hydrocarbon receptor (AhR; EC50 = 1 μM).
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Accessible (Haz class 3, 4, 5 or 8), International
Prochloraz is an imidazole antifungal that inhibits ergosterol biosynthesis via inhibition of the cytochrome P450-dependent 14α-demethylation of lanosterol, which results in disruption of the fungal cell membrane and cell death. Prochloraz at 0.005 and 0.01 mg/liter disrupted cell membrane integrity of conidia but reduced cell membrane permeability of mycelia. Prochloraz at 0.01 mg/liter reduced ergosterol content in mycelia by 41.8%[1]. Prochloraz antagonizes the androgen and the oestrogen receptor, agonizes the Ah receptor and inhibits aromatase activity. In vivo prochloraz acts as an antiandrogen in the Hershberger assay by reducing weights of reproductive organs, affecting androgen-regulated gene expressions in the prostate and increasing luteinizing hormone levels[2]. Prochloraz at 0.01 and 0.04 µg/ml significantly (P < 0.001) reduced rather than increased cell membrane permeability. Prochloraz significantly (P = 0.041) increased the mannan content in the cell wall of S. sclerotiorum. The observed mycelial growth inhibitions for the mixtures of prochloraz at 0.03 µg/ml and Congo red at a dose range from 0.05 to 0.4% (w/v) were lower than the expected inhibitions, indicating prochloraz might reduce the content of chitin in S. sclerotiorum[3]. Prochloraz administered alone is able to trigger oocyte maturation through the induction of specific genes, some of them being also triggered by LH(Luteinizing Hormone) [4].
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