摘要 :
In agricultural crops, honey bees may be exposed to multiple pesticides. However, in field realistic conditions mixtures of products classified as harmless to bees can lead to a synergistic increase of toxicity on honey bees, as k...
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In agricultural crops, honey bees may be exposed to multiple pesticides. However, in field realistic conditions mixtures of products classified as harmless to bees can lead to a synergistic increase of toxicity on honey bees, as known for ergosterol biosynthesis-inhibiting (EBI) fungicides combined with pyrethroids or neonicotinoids. For substances like fertilizers, usually no information on potential side effects on bees is available. Initially, effects from tank mixes containing insecticides, fungicides and fertilizers were investigated under laboratory conditions by use of a spray chamber contact test. For selected combinations, higher tier studies were carried out. Mixtures containing thiacloprid, boscalid and dimoxystrobin with boron fertilizers showed no increase of mortality. In contrast, tank mixes of thiacloprid formulations and EBI-fungicides resulted within 24 h in synergistic mortality increase in laboratory, semi-field and field. Actually, a short time interval of 24 h between individually applied potentially synergistic products like pyrethroid insecticides and EBI fungicides led to an increase of mortality up to 100% under laboratory conditions, indicating that the detoxification was still ongoing, resulting in an increased susceptibility for other stressors during the metabolization process. In conclusion, tank mixtures do not always lead to an increase of honey bee toxicity. However, former published findings about synergistic impacts between neonicotinoides and EBI-fungicides could be confirmed. The findings of our and other higher tier studies finally prompted the competent regulatory authority (BVL) to regulate these mixtures by restriction NB6613 since September 2018. Nevertheless, the investigation of potential interactions between mixing partners and their additive or synergistic effects are the basis for a better understanding and a logical risk assessment to ensure protection of honey bees.
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摘要 :
Fusarium head blight (FHB), caused by the Fusarium graminearum species complex, is a devastating fungal disease resulting in substantial yield and quality losses. Ergosterol biosynthesis inhibitors (EBIs) are the most popular chem...
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Fusarium head blight (FHB), caused by the Fusarium graminearum species complex, is a devastating fungal disease resulting in substantial yield and quality losses. Ergosterol biosynthesis inhibitors (EBIs) are the most popular chemicals for controlling FHB. Recently, the resistance of F. graminearum to EBIs has emerged in the field, and an amino acid substitution (G443S) of the sterol 14 alpha-demethylase FgCYP51A was detected in the field resistant strains. To further illustrate the resistance mechanism of F. graminearum to EBIs, site-directed mutants conferring the G443S substitution of FgCYP51A were generated from the progenitor strain PH-1 via genetic transformation with site-directed mutagenesis. We found that the FgCYP51A-G443S substitution significantly decreased the sensitivity of F. graminearum to EBIs with EC50 values ranging from 0.1190 to 0.2302 mu g mL(-1) and EC90 values ranging from 1.3420 to 9.1119 mu g mL(-1) for tebuconazole. Furthermore, the FgCYP51A-G443S substitution decreased sexual reproduction and virulence, which will reduce the initial infection source of pathogen populations in the field, while the increase of sporulation capability may enhance the frequencies of the disease cycle, thereby contributing to epidemics of FHB disease. Surprisingly, the FgCYP51A-G443S substitution accelerated DON biosynthesis by upregulating TRI5 expression and enhancing the fluorescence intensity of TRI1-GFP, the marker protein of Fusarium toxisomes. Thus, we concluded that the FgCYP51A-G443S substitution regulates EBI-fungicide resistance and DON biosynthesis, increasing the risk of fungicide resistance development in the field, thereby threatening the control efficacy of EBIs against FHB.
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