Profenofos, an Acetylcholinesterase‐Inhibiting Organophosphorus Pesticide: A Short Review of Its Usage, Toxicity, and Biodegradation

Abstract

Pesticides play an important role in the protection of different crops. Among the diverse sets of pesticides used all over the world, the organophosphates are the most widely used group. Profenofos [O-(4-bromo-2-chlorophenyl) O-ethyl S-propyl phosphorothioate] is one of the most largely used organophosphate insecticides on field crops, vegetables, and fruit crops. The World Health Organization classifies this compound as moderately hazardous (Toxicity Class II), and its residues have been found in vegetables like okra [ (L.) Moench], gooseberries ( sp.), green chilies [ (L.)], curry leaves [ (L.) Spreng], mint leaves [ (L.)], and coriander leaves [ (L.)]. Dietary intake of profenofos (PFF) is the major exposure pathway for humans. When applied to agricultural fields, PFF residues spread into every part of the environment: ambient air, surface water, and soil. In this review, we discuss the worldwide usage of PFF pesticide, its toxic effects on humans and other living organisms in the environment, and biodegradation of this chemical by various microbial strains. To date, no complete biodegradation pathway has been established for PFF pesticide, calling for a study of this nature.

A dual-signal sensor for the analysis of parathion-methyl using silver nanoparticles modified with graphitic carbon nitride

“…Acetylcholinesterase (AChE) degrades acetylcholine and also can stop the excitatory effects of neurotransmitters on the postsynaptic membrane and ensure the normal transmission of neural signals in the body, so AChE plays a key role in the biological nerve conduction between cholinergic synapses [ 4 ]. OPs inhibit the activity of AChE in living organisms, leading to metabolic disorders of acetylcholine, delayed neurotoxicity, movement disorders, coma, paralysis of the respiratory center, and even death [ [5] , [6] , [7] ] (see Scheme 1 ).

Scheme 1 Mechanism of detecting organophosphorus pesticides based on g-C 3 N 4 /AgNPs.

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Covalent binding of the organophosphate insecticide profenofos to tyrosine on α- and β-tubulin proteins

“…Exposure to OP insecticides can lead to acute or chronic poisoning. The acute toxicity of OP insecticides is mainly due to inhibition of acetylcholinesterase (AChE) (Colovic et al, 2013; Kushwaha et al, 2016). However, AChE inhibition alone cannot explain a wide range of OP neurotoxicities, which includes deficits in cognition, learning and memory, depression, psychotic symptoms and other neurotoxicity when victims were exposed to OP insecticides at low doses and over a prolonged period (Casida and Quistad, 2004; Beseler and Stallones, 2008; Briceno et al, 2016; Campos et al, 2016; Voorhees et al, 2017).…”

“…Profenofos is an OP insecticide widely used on a variety of crops including cotton and vegetables, such as maize, potato, soybean, and sugar beet. In the United States, it is used exclusively on cotton and is primarily used against lepidopteran insects (US EPA, 2000; Kushwaha et al, 2016). Tubulin was selected for this study because covalent binding of OPs to tubulin is a potential mechanism of neurotoxicity (Jiang et al, 2010; Kushwaha et al, 2016).…”

“…In the United States, it is used exclusively on cotton and is primarily used against lepidopteran insects (US EPA, 2000; Kushwaha et al, 2016). Tubulin was selected for this study because covalent binding of OPs to tubulin is a potential mechanism of neurotoxicity (Jiang et al, 2010; Kushwaha et al, 2016). To render it possible to identify tubulin as a target protein of profenofos binding, an in vitro method was optimized to identify tubulin adducts with profenofos by matrix-assisted laser desorption ionization time-of-flight tandem mass spectrometry (MALDI-TOF/TOF) and liquid chromatograph-quadrupole time-of-flight mass spectrometry (LC-Q/TOF).…”

Composites based on conductive polymer with carbon nanotubes in DMMP gas sensors – an overview

“…Scheme A shows the mechanism of action acetylation and deacetylation of AChE. In general, enzymesubstrate complex is formed by the electrostatic attraction between an anionic site (the negative charge of the anionic site is due to the carboxylate anion of aspartic or glutamic acid) on the enzyme AChE and the positively charged nitrogen atom of the ACh on the human enzyme [9,10]. Acetylation of a serine hydroxyl (OH) in the esteric site of the enzyme AChE [Scheme A(i)] is catalyzed by the basic imidazole moiety of histidine, which interacts with the carboxyl group of glutamate (serine, histidine, and glutamate are part of a catalytic triad of esteric site of the enzyme AChE), leading to an acetylated enzyme.…”