Metabolism of a fungicide propiconazole by Cunninghamella elegans ATCC36112.

The metabolic breakdown of propiconazole by fungi was examined, and it was found that the microbial model (Cunninghamella elegans ATCC36112) efficiently degrades the triazole fungicide propiconazole through the action of cytochrome P450. This enzyme primarily facilitates the oxidation and hydrolysis processes involved in phase I metabolism. We observed major metabolites indicating hydroxylation/oxidation of propyl groups of propiconazole. Around 98% of propiconazole underwent degradation within a span of 3 days post-treatment, leading to the accumulation of five metabolites (M1-M5). The experiments started with a preliminary identification of propiconazole and its metabolites using GC-MS. The identified metabolites were then separated and identified by in-depth analysis using preparative UHPLC and MS/MS. The metabolites of propiconazole are M1 (CGA-118245), M2(CGA-118244), M3(CGA-136735), M4(GB-XLIII-42-1), and M5(SYN-542636). To further investigate the role of key enzymes in potential fungi, we treated the culture medium with piperonyl butoxide (PB) and methimazole (MZ), and then examined the kinetic responses of propiconazole and its metabolites. The results indicated a significant reduction in the metabolism rate of propiconazole in the medium treated with PB, while methimazole showed weaker inhibitory effects on the metabolism of propiconazole in the fungus C. elegans.

Metabolic pathway of tebuconazole by soil fungus Cunninghamella elegans ATCC36112.

Tebuconazole is the most widely used fungicide in agriculture. Due to its long half-life, tebuconazole residues can be found in the environment media such as in soil and water bodies. Here, the metabolic pathway of tebuconazole was studied in Cunninghamella elegans (C. elegans). Approximately 98% of tebuconazole was degraded within 7 days, accompanied by the accumulation of five metabolites. The structures of the metabolites were completely or tentatively identified by gas chromatography-mass spectrometry (GC-MS) and ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). To identify representative oxidative enzymes that may be involved in the metabolic process, treatment with piperonyl butoxide (PB) and methimazole (MZ) was performed. PB had a strong inhibitory effect on the metabolic reactions, while MZ had a weak inhibitory effect. The results suggest that cytochrome P450 (CYP) and flavin-dependent monooxygenase are involved in the metabolism of tebuconazole. Based on the results, we propose a metabolic pathway for the fungal metabolism of tebuconazole. Data are of interest to gain insight into the toxicological effects of tebuconazole and for tebuconazole bioremediation.

Metabolism of an insecticide fipronil by soil fungus Cunninghamella elegans ATCC36112.

In this study, the metabolic pathway of the phenylpyrazole insecticide fipronil in Cunninghamella elegans (C. elegans) was investigated. Approximately 92% of fipronil was removed within 5 days, and seven metabolites were accumulated simultaneously. The structures of the metabolites were completely or tentatively identified by GC-MS and 1H, 13C NMR. To determine the oxidative enzymes involved in metabolism, piperonyl butoxide (PB) and methimazole (MZ) were used, and the kinetic responses of fipronil and its metabolites were determined. PB strongly inhibited fipronil metabolism, while MZ weakly inhibited its metabolism. The results suggest that cytochrome P450 (CYP) and flavin-dependent monooxygenase (FMO) may participate in fipronil metabolism. Integrated metabolic pathways can be inferred from the control and inhibitor experiments. Several novel products from the fungal transformation of fipronil were identified, and similarities between C. elegans transformation and mammalian metabolism of fipronil were compared. Therefore, these results will help to gain insight into the fungal degradation of fipronil and potential applications in fipronil bioremediation. At present, microbial degradation of fipronil is the most promising approach and maintains environmental sustainability. In addition, the ability of C. elegans to mimic mammalian metabolism will assist in illustrating the metabolic fate of fipronil in mammalian hepatocytes and assess its toxicity and potential adverse effects.