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Frontiers in Microbiology 2020Acephate is an organophosphate pesticide that has been widely used to control insect pests in agricultural fields for decades. However, its use has been partially... (Review)
Review
Acephate is an organophosphate pesticide that has been widely used to control insect pests in agricultural fields for decades. However, its use has been partially restricted in many countries due to its toxic intermediate product methamidophos. Long term exposure to acephate and methamidophos in non-target organisms results in severe poisonous effects, which has raised public concern and demand for the removal of these pollutants from the environment. In this paper, the toxicological effects of acephate and/or methamidophos on aquatic and land animals, including humans are reviewed, as these effects promote the necessity of removing acephate from the environment. Physicochemical degradation mechanisms of acephate and/or methamidophos are explored and explained, such as photo-Fenton, ultraviolet/titanium dioxide (UV/TiO) photocatalysis, and ultrasonic ozonation. Compared with physicochemical methods, the microbial degradation of acephate and methamidophos is emerging as an eco-friendly method that can be used for large-scale treatment. In recent years, microorganisms capable of degrading methamidophos or acephate have been isolated, including sp., , , , and Enzymes related to acephate and/or methamidophos biodegradation include phosphotriesterase, paraoxonase 1, and carboxylesterase. Furthermore, several genes encoding organophosphorus degrading enzymes have been identified, such as , , and . However, few reviews have focused on the biochemical pathways and molecular mechanisms of acephate and methamidophos. In this review, the mechanisms and degradation pathways of acephate and methamidophos are summarized in order to provide a new way of thinking for the study of the degradation of acephate and methamidophos.
PubMed: 33013750
DOI: 10.3389/fmicb.2020.02045 -
Toxicology Reports Jun 2024Methamidophos is a highly hazardous organophosphate and is known to cause an acute cholinergic toxidrome. Methamidophos use is not allowed in South Africa and therefore...
Methamidophos is a highly hazardous organophosphate and is known to cause an acute cholinergic toxidrome. Methamidophos use is not allowed in South Africa and therefore local data pertaining to methamidophos poisoning is very limited, with no paediatric clinical cases described. Methamidophos is an active metabolite of acephate, a commonly used organophosphate, registered for agricultural use in South Africa. We present a paediatric case of methamidophos poisoning with prolonged clinical effects. The patient experienced a prolonged cholinergic toxidrome lasting 10 days, with a period of near-full recovery during this time. We discuss the biological plausibility of the detected methamidophos being a byproduct of acephate. In addition, we highlight the importance of closer monitoring of patients with organophosphate poisoning in areas where acephate is commonly used.
PubMed: 38173652
DOI: 10.1016/j.toxrep.2023.12.001 -
Journal of UOEH 2021We gave mice a 540 mg/kg dose of LD50 acephate, followed by an assessment of acephate, methamidophos (MP), and choline esterase (ChE) activity for up to 4 hours (hr) in...
We gave mice a 540 mg/kg dose of LD50 acephate, followed by an assessment of acephate, methamidophos (MP), and choline esterase (ChE) activity for up to 4 hours (hr) in order to investigate the time course of acephate intoxication. At 1 hr, the blood acephate and MP levels were 428 ± 90 µg/ml (mean ± SEM) and 4.2 ± 0.4 µg/ ml, respectively. The liver acephate levels were similar to those in the blood, but the liver MP levels were approximately 3.5 times that of the blood at 1 hr. The brain MP level tended to be higher than the blood MP at 1 hr. These levels decreased gradually over 4 hr, but the brain acephate and MP levels surpassed the blood levels significantly at 4 hr, and after 2 hr, respectively. Serum, liver, cerebrum, cerebellum, and brainstem cholinesterase activity (ChE) were inhibited at 1 hr, and remained inhibited in all but the cerebellum until the end of the experiment. The obtained data were applied to previously reported autopsy cases of acephate intake. Experimental data suggest that brain MP is involved in acute acephate-induced poisoning, even after a reduction in blood acephate. In autopsy cases with suspected acephate poisoning, the MP level in the brain should be considered in addition to the ChE activity to diagnose the cause of death.
Topics: Animals; Brain; Cholinesterase Inhibitors; Insecticides; Mice; Organothiophosphorus Compounds; Phosphoramides
PubMed: 34092764
DOI: 10.7888/juoeh.43.197 -
Neurotoxicity Research Oct 2017Although evidence indicates that exposure to organophosphorus (OP) pesticides induces neurobehavioral disorders, little is known about the effects of OP on aggressive...
Although evidence indicates that exposure to organophosphorus (OP) pesticides induces neurobehavioral disorders, little is known about the effects of OP on aggressive behaviour. Our study investigated the effects of repeated exposure to an OP pesticide, methamidophos, on the isolation-induced aggressive behaviour in mice. Forty seven male mice were individually housed for a month. Socially isolated animals were then confronted with a standard non-isolated opponent for 15 min (pre-treatment trial), and the latency and frequency of aggressive and general exploratory behaviours were recorded. Based on the presence of attack behaviour in the pre-treatment trial, mice were classified as isolation-induced aggressive and non-aggressive. All mice were then treated for 7 days with methamidophos (3.5 mg/kg/day, n = 22, intraperitoneal (i.p.)) or saline (1 mL/kg/day, control group, n = 25, i.p.), and a second trial was performed. Repeated exposure to methamidophos induced attack behaviour in non-aggressive mice. The treatment with methamidophos also decreased plasma butyrylcholinesterase and brain acetylcholinesterase activity. These results suggest that methamidophos has a pro-aggressive effect on socially isolated mice.
Topics: Acetylcholinesterase; Aggression; Animals; Brain; Butyrylcholinesterase; Injections, Intraperitoneal; Insecticides; Male; Mice; Motor Activity; Organothiophosphorus Compounds; Psychological Tests; Social Isolation
PubMed: 28540662
DOI: 10.1007/s12640-017-9750-9 -
Journal of Economic Entomology Feb 2019A piezoelectric quartz crystal impedance (PQCI) sensor was used to investigate influences of the insecticide methamidophos on proteinase activity in midguts of the wolf...
A piezoelectric quartz crystal impedance (PQCI) sensor was used to investigate influences of the insecticide methamidophos on proteinase activity in midguts of the wolf spider, Pardosa pseudoamulata (Araneae: Lycosidae). Results from PQCI indicated that low-concentration dose methamidophos (0.008%) can activate the proteinase but high-concentration dose methamidophos (0.016-0.032%) can inhibit the enzyme activity. The changes in subcellular structure of spider midgut cells were also observed. Electron micrographs of spider midgut epithelial cells showed that the low-dose methamidophos did not visibly impact the structure of these cells. Conversely, high-concentration dose methamidophos led to severe changes in the cell structure, including the karyotheca dissolved, the nucleolus, and the endoplasmic reticulum disappeared. These may contribute to changes in proteinase activity of spider. This work documents a feasible method for rapid and reliable detection of proteinase activity.
Topics: Animals; Female; Gastrointestinal Tract; Hydrolysis; Insect Proteins; Insecticides; Organothiophosphorus Compounds; Peptide Hydrolases; Spiders
PubMed: 30321348
DOI: 10.1093/jee/toy318 -
Journal of Toxicology. Clinical... 2001
Topics: Disease Outbreaks; Hong Kong; Humans; Insecticides; Organothiophosphorus Compounds; Vegetables
PubMed: 11527225
DOI: 10.1081/clt-100105151 -
International Journal of Environmental... Dec 2016Methamidophos is a representative organophosphate insecticide. The knowledge of its developmental neurotoxicity is limited, especially for zebrafish in the early stages...
Methamidophos is a representative organophosphate insecticide. The knowledge of its developmental neurotoxicity is limited, especially for zebrafish in the early stages of their life. Four hour post-fertilization (hpf) zebrafish embryos were exposed to several environmentally relevant concentrations of methamidophos (0, 25, and 500 μg/L) for up to 72 hpf. Locomotor behavior was then studied in the zebrafish larvae at this timepoint. Acridine orange (AO) staining was carried out in the zebrafish larvae, and the mRNA levels of genes associated with neural development ( and ) were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). The number of escape responders for mechanical stimulation was significantly decreased in exposed groups. AO staining showed noticeable signs of apoptosis mainly in the brain. In addition, the mRNA levels of and were both significantly down-regulated in exposed groups. Our study provides the first evidence that methamidophos exposure can cause developmental neurotoxicity in the early stages of zebrafish life, which may be caused by the effect of methamidophos on neurodevelopmental genes and the activation of cell apoptosis in the brain.
Topics: Animals; Apoptosis; Embryo, Nonmammalian; Gene Expression Regulation, Developmental; Insecticides; Larva; Neurotoxicity Syndromes; Organophosphorus Compounds; Organothiophosphorus Compounds; RNA, Messenger; Zebrafish
PubMed: 28036051
DOI: 10.3390/ijerph14010023 -
Methamidophos induces cytotoxicity and oxidative stress in human peripheral blood mononuclear cells.Environmental Toxicology Jan 2017Previous studies have shown that organophosphate pesticide (OP) exposure is associated with oxidative stress. Methamidophos (MET) is an OP widely used in agriculture,...
Previous studies have shown that organophosphate pesticide (OP) exposure is associated with oxidative stress. Methamidophos (MET) is an OP widely used in agriculture, which is regarded as a highly toxic pesticide and it is a potent inhibitor of acetylcholinesterase. The aim of this study was to evaluate whether MET can induce oxidative stress at low concentrations in primary cultures of human peripheral blood mononuclear cells (PBMCs). PBMCs from healthy individuals were exposed to MET (0-80 mg/L) for 0-72 h. We performed the MTT and neutral-red assays to assess the cytotoxicity. As indicators of oxidative stress, the levels of reactive oxygen species (ROS) were assessed using flow cytometry, and the malondialdehyde (MDA) and reduced glutathione (GSH) levels were determined. MET decreased the viability of PBMCs in a dose-dependent manner. At concentrations of 3, 10, or 20 mg/L for 24 h, MET increased the ROS production significantly compared with the vehicle control. Similarly, MET increased the levels of MDA at the same concentrations that increased ROS (10 and 20 mg/L); however, no changes in GSH levels were observed. These results suggest that MET increased the generation of oxidative stress in PBMCs. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 147-155, 2017.
Topics: Cell Survival; Dose-Response Relationship, Drug; Glutathione; Humans; Insecticides; Lipid Peroxidation; Male; Malondialdehyde; Monocytes; Organothiophosphorus Compounds; Oxidative Stress; Primary Cell Culture; Reactive Oxygen Species; Young Adult
PubMed: 26589457
DOI: 10.1002/tox.22220 -
Neurotoxicology 1997Methamidophos (O,S-dimethyl phosphoroamidothiolate, Tamaron), an organophosphate (OP) anticholinesterase of limited toxicity, is widely used as an insecticide and...
Methamidophos (O,S-dimethyl phosphoroamidothiolate, Tamaron), an organophosphate (OP) anticholinesterase of limited toxicity, is widely used as an insecticide and acaricide. To provide additional insight into the molecular basis of its action, we have used electrophysiological and biochemical techniques to study the effects of methamidophos on the neuromuscular junction of rat and frog and on the central nervous system of rat. Methamidophos has a relatively weak inhibitory action on cholinesterases in rat diaphragm muscle, brain and hippocampal homogenates, with IC50 values on the order of 20-20 microM. An even weaker anticholinesterase activity was found in frog muscle homogenates, with the IC50 being above 300 microM. As further evidence of anticholinesterase activity, methamidophos (1-100 microM) was able to reverse the blockade by d-tubocurarine (0.5-0.7 microM) of neuromuscular transmission in rat phrenic nerve-hemidiaphragm preparations. Inhibition of cholinesterase activity by methamidophos was long lasting, which is consistent with the formation by the agent of a covalent bond with the enzyme's active serine residue. The action was also slowly reversible, which suggests spontaneous reactivation of the enzyme. electrophysiological studies at the rat neuromuscular junction showed that, due to its anticholinesterase activity, methamidophos increased the amplitude and prolonged the decay phase of nerve-evoked and spontaneous miniature end-plate potentials. In contrast to other OP compounds, e.g., paraoxon (Rocha et al., 1996a), methamidophos did not affect neurotransmitter release, nor did it interact directly with the muscle nicotinic acetylcholine receptor. Moreover, it contrast to paraoxon, methamidophos did not affect the whole-cell currents induced by application of acetylcholine, glutamate or gamma-aminobutyric acid recorded to cultured hippocampal neurons. Based on these data, methamidophos appears to have a selective effect on cholinesterase.
Topics: Animals; Cholinesterase Inhibitors; Diaphragm; Evoked Potentials; In Vitro Techniques; Insecticides; Ion Channels; Male; Motor Endplate; Muscle Contraction; Neurotransmitter Agents; Organothiophosphorus Compounds; Patch-Clamp Techniques; Rats; Rats, Wistar; Synapses
PubMed: 9291508
DOI: No ID Found -
Toxicology and Applied Pharmacology Sep 2014Methamidophos (MET) is a highly toxic organophosphate (OP) pesticide that is widely used in developing countries. MET has male reproductive effects, including decreased...
Methamidophos (MET) is a highly toxic organophosphate (OP) pesticide that is widely used in developing countries. MET has male reproductive effects, including decreased fertility. We evaluated MET effects on sperm quality, fertilization and DNA integrity, exploring the sensitivity of different stages of spermatogenesis. Adult male mice received MET (3.75 or 5mg/kg-bw/ip/day/4 days) and were euthanized 1, 28 or 45 days post-treatment (dpt) to evaluate MET's effects on epididymal maturation, meiosis or mitosis, respectively. Spermatozoa were obtained from the cauda epididymis-vas deferens and were evaluated for sperm quality, acrosome reaction (AR; Coomassie staining), mitochondrial membrane potential (by JC-1), DNA damage (comet assay), oxidative damage (malondialdehyde (MDA) production), in vitro fertilization and protein phosphorylation (immunodetection), and erythrocyte acetylcholinesterase (AChE) activity. At 1-dpt, MET inhibited AChE (43-57%) and increased abnormal cells (6%). While at 28- and 45-dpt, sperm motility and viability were significantly reduced with an increasing MET dose, and abnormal morphology increased at 5mg/kg/day/4 days. MDA and mitochondrial activity were not affected at any dose or time. DNA damage (OTM and %DNA) was observed at 5mg/kg/day/4 days in a time-dependent manner, whereas both parameters were altered in cells from mice exposed to 3.75 mg/kg/day/4 days only at 28-dpt. Depending on the time of collection, initial-, spontaneous- and induced-AR were altered at 5mg/kg/day/4 days, and the fertilization capacity also decreased. Sperm phosphorylation (at serine and tyrosine residues) was observed at all time points. Data suggest that meiosis and mitosis are the more sensitive stages of spermatogenesis for MET reproductive toxicity compared to epididymal maturation.
Topics: Acetylcholinesterase; Acrosome Reaction; Animals; Body Weight; Comet Assay; DNA Replication; Female; Fertilization; In Vitro Techniques; Infertility, Male; Insecticides; Lipid Peroxidation; Male; Membrane Potential, Mitochondrial; Mice; Mice, Inbred ICR; Oocytes; Organ Size; Organothiophosphorus Compounds; Oxidative Stress; Phosphorylation; Reproduction; Spermatogenesis; Spermatozoa
PubMed: 24998973
DOI: 10.1016/j.taap.2014.06.017