| The use of neonicotinoids has grown rapidly and they have been the most widely used insecticide in the world currently.They agonistically binding to the post-synaptic nicotinic acetylcholine receptor(nAChRs)in the insect nervous system blocks the nerve conduction,leads to paralysis and even death.There are more and more reports about the negative effects of neonicotinoids on non-target organisms,which has raised much conerns about their potential ecological risk.At present,the studies mainly focus on the toxicity toward pollinated insects,such as bees,but little is known about their toxic effects to other soil non-target oranisms.Caenorhabditis elegans(C.elegans),a free-living nematode in soil,is an excellent candidate for ecotoxicological evaluation,due to its short life cycle,easy to handling in the laboratory,sensitivity to external environment,and the whole genome known to human.To investigate the adverse effects of two neonicotinoids,imidacloprid and dinotefuran,to the soil model organism C.elegans following 24 h exposure at 1?g/L-10 mg/L,multiple endpoints at the physiological,biochemical and molecular level were examined.(1)At physiological level,nematode growth(body length),locomotion(body bend and head thrash frequency)and feeding behavior were all inhibited by a dose-dependent effect,which increased along with the increased neonicotinoid exposure concentration.The head thrash frequency of C.elegans is the most sensitive endpoints,10?g/L imidacloprid and 100?g/L dinotefuran exposure have significantly decreased the head thrash frequency compared to the control group(p<0.01),following is the body bend frequency>feeding behavior>body length(imidacloprid),and feeding behavior>body length>body bend frequency(dinotefuran).Two neonicotinoids induced different degree of inhibition,imidacloprid had greater influence on locomotion behavior,while dinotefuran had greater influence on growth and feeding behavior.Locomotion and feeding behavior can be used for quantitative evaluation of neurotoxic effects of C.elegans,and its inhibitory effects can reflect neurotoxic effects of neonicotinoids on C.elegans.(2)At the biochemical level,C.elegans lipofuscin accumulation,cell apoptosis and acetylcholine(AChE)activity are used to evaluate the toxicity of neonicotinoid.Significant influence were found above 1 mg/L imidacloprid and 100?g/L dinotefuran exposure on cell apoptpsis and AChE activity,while lipofuscin accumulation increase obviously only at the highest concentration.Of the three indicators,the effects of dinotefuran was higher than that of imidacloprid.The results showed toxicity of neonicotinoid to C.elegans at biochemical level,especially the negative effect on AChE activity showed the neurotoxicity.(3)At genes transcriptional level,after imidacloprid and dinotefuran exposure,hsp-16.48,ace-1,ace-3 and ace-4 were overexpressed,in construct,expression of hsp-16.2,ace-2 and ape-1 were decreased.In addition,mtl-1 and mtl-2 showed a different variation between imidacloprid and dinotefuran,imidacloprid exposure resulted in a decline,while dinotefuran led to the rise.The increase of hsp-16.48 expression indicated the stress and defense responses of C,elegans to external contaminants.The alteration of ace gene expression affected the acetylcholinesterase activity,which plays an important role in the fuction of neurotransimmers,resulting in changes in locomotion and feeding behavior.ape-1 gene relates to cell apoptosis,which indicated it.s suitable as a biomarkers indicator.In conclusion,neonicotinoids have exhibited a negative impact on C.elegans,not only at physiological and biochemical leve,but also at related genes transcription level.The inhibitory effects of locomotion,feeding behavior and AChE activity indicate neurotoxic of neonicotinoids to non-target organisms.Both imidacloprid and dinotefuranas showed neurotoxic effects on nematode,indicating that neonicotinoid insecticides have a toxicity effects to C.elegans. |
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