Chronic exposure of bumblebees to neonicotinoid imidacloprid suppresses the entire mevalonate pathway and fatty acid synthesis
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
30583045
DOI
10.1016/j.jprot.2018.12.022
PII: S1874-3919(18)30451-2
Knihovny.cz E-resources
- Keywords
- Bombus terrestris, Endocrine disruptor, Imidacloprid-olefin, Pesticide exposure, Proteomics, Terpenoid backbone biosynthesis pathway,
- MeSH
- Nitro Compounds pharmacology MeSH
- Insecticides pharmacology MeSH
- Mevalonic Acid metabolism MeSH
- Fatty Acids biosynthesis MeSH
- Neonicotinoids pharmacology MeSH
- Bees metabolism MeSH
- Animals MeSH
- Check Tag
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Nitro Compounds MeSH
- imidacloprid MeSH Browser
- Insecticides MeSH
- Mevalonic Acid MeSH
- Fatty Acids MeSH
- Neonicotinoids MeSH
Determining the side effects of pesticides on pollinators is an important topic due to the increasing loss of pollinators. We aimed to determine the effects of chronic sublethal exposure of the neonicotinoid pesticide imidacloprid on the bumblebee Bombus terrestris under laboratory conditions. The analytical standard of imidacloprid in sugar solution was used for the treatment. Verification of pesticides using UHPLC-QqQ-MS/MS in the experimental bumblebees showed the presence of only two compounds, imidacloprid and imidacloprid-olefin, which were found in quantities of 0.57 ± 0.22 and 1.95 ± 0.43 ng/g, respectively. Thus, the level of the dangerous metabolite imidacloprid-olefin was 3.4-fold higher than that of imidacloprid. Label-free nanoLC-MS/MS quantitative proteomics of bumblebee heads enabled quantitative comparison of 2883 proteins, and 206 proteins were significantly influenced by the imidacloprid treatment. The next analysis revealed that the highly downregulated markers are members of the terpenoid backbone biosynthesis pathway (KEGG: bter00900) and that imidacloprid treatment suppressed the entire mevalonate pathway, fatty acid synthesis and associated markers. The proteomics results indicate that the consequences of imidacloprid treatment are complex, and the marker changes are associated with metabolic and neurological diseases and olfaction disruption. This study provides important markers and can help to explain the widely held assumptions from biological observations. SIGNIFICANCE: The major finding is that all markers of the mevalonate pathway were substantially downregulated due to the chronic imidacloprid exposure. The disbalance of mevalonate pathway has many important consequences. We suggest the mechanism associated with the novel toxicogenic effect of imidacloprid. The results are helpful to explain that imidacloprid impairs the cognitive functions and possesses the delayed and time cumulative effect.
ALS Limited ALS Czech Republic Na Harfe 336 9 Prague CZ 190 00 Czechia
Crop Research Institute Drnovska 507 73 Prague CZ 161 06 Czechia
Proteomics Core Facility Faculty of Science Charles University Prague Czechia
R and D Department Biobest Group Ilse Velden 18 Westerlo B 2260 Belgium
References provided by Crossref.org
DIOXYGENASE FOR AUXIN OXIDATION 1 catalyzes the oxidation of IAA amino acid conjugates
