Abstract
Imidacloprid is a neonicotinoid insecticide that has been widely used to control insect pests in agricultural fields for decades. It shows insecticidal activity mainly by blocking the normal conduction of the central nervous system in insects. However, in recent years, imidacloprid has been reported to be an emerging contaminant in all parts of the world, and has different toxic effects on a variety of non-target organisms, including human beings, due to its large-scale use. Hence, the removal of imidacloprid from the ecosystem has received widespread attention. Different remediation approaches have been studied to eliminate imidacloprid residues from the environment, such as oxidation, hydrolysis, adsorption, ultrasound, illumination, and biodegradation. In nature, microbial degradation is one of the most important processes controlling the fate of and transformation from imidacloprid use, and from an environmental point of view, it is the most promising means, as it is the most effective, least hazardous, and most environmentally friendly. To date, several imidacloprid-degrading microbes, including Bacillus, Pseudoxanthomonas, Mycobacterium, Rhizobium, Rhodococcus, and Stenotrophomonas, have been characterized for biodegradation. In addition, previous studies have found that many insects and microorganisms have developed resistance genes to and degradation enzymes of imidacloprid. Furthermore, the metabolites and degradation pathways of imidacloprid have been reported. However, reviews of the toxicity and degradation mechanisms of imidacloprid are rare. In this review, the toxicity and degradation mechanisms of imidacloprid are summarized in order to provide a theoretical and practical basis for the remediation of imidacloprid-contaminated environments.
Highlights
Imidacloprid (1-((6-chloro-3-pyridinyl) methyl)-N-nitro-2-imidazolidnimine) is a colorless crystal neonicotinoid insecticide, which belongs to the chloronitroguanidine compounds, with a melting point of 143.8 ◦ C
Imidacloprid metabolites are the main cause of imidacloprid toxicity, and changes in liver energy metabolism are closely related to its hepatotoxicity, which occurs when animals and humans are exposed to high concentrations of imidacloprid
It is important to study the combined toxicity of pesticides at low concentrations; for instance, the combined toxic effect of triazophos and imidacloprid on zebrafish (Danio rerio) is more pronounced with the expression of the 26 genes related to oxidative stress, cell apoptosis, immune system, and hypothalamic–pituitary–thyroid and hypothalamic–pituitary–gonadal axes at the mRNA level, and the embryos of zebrafish are more affected by the subsequent synergistic effects [63]
Summary
Imidacloprid (1-((6-chloro-3-pyridinyl) methyl)-N-nitro-2-imidazolidnimine) is a colorless crystal neonicotinoid insecticide, which belongs to the chloronitroguanidine compounds, with a melting point of 143.8 ◦ C. Biological methods methods such as hydrolysis, oxidative decomposition, and light chemical degradation; and (3) Such as microbial degradation enzymes and engineering bacteria (Figure 2). These degradation-related biological methods such as microbial degradation enzymes and engineering bacteria (Figure 2) Imidacloprid in soil or water can be degraded by photolysis by sunlight (Figure 1). Approximately slower than of photolysis, but it is are not known as easy to to degrade produce imidacloprid secondary pollution via this process. Most of the Currently, approximately genes, enzymes, and bacteria are known to degrade imidacloprid resistance genes and enzymes come from insects, while most of the bacteria are Pseudomonas, Bacillus, efficiently.
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