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Applied Biochemistry and Biotechnology Sep 2022Monocrotophos (MCP) is systemic organophosphate insecticide used against crop pests. It is reported to cause mammalian toxicity through both acute and chronic exposure....
Monocrotophos (MCP) is systemic organophosphate insecticide used against crop pests. It is reported to cause mammalian toxicity through both acute and chronic exposure. In the present study, we have shown the protective role of N-acetylcysteine (NAC) against MCP-induced oxidative stress in frontal cortex, corpus striatum and hippocampus brain regions of rats. Male Albino Wistar rats were divided into control, NAC-treated, MCP and NAC + MCP-treated groups. An oral dose of MCP (0.9 mg/kg b.wt) and NAC (200 mg/kg b.wt) was administered for 28 days. Results showed an increase in lipid peroxidation (LPO) and protein oxidation followed by decreased antioxidant enzymes after 28 days of MCP exposure. Histopathological analysis showed that monocrotophos exposure caused neurodegenerative changes as evident by neurons with dystrophic changes in the form of shrunken hyperchromatic nuclei in all the regions of the rat brain. N-acetylcysteine supplementation to MCP-treated rats showed a reduction in oxidative stress and ameliorated cellular alterations in all of the three regions. The results of the study indicate that N-acetylcysteine offers neuroprotection by improving antioxidant response and decreasing oxidative stress in different regions of the rat brain.
Topics: Acetylcysteine; Animals; Antioxidants; Brain; Lipid Peroxidation; Male; Mammals; Monocrotophos; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Wistar
PubMed: 35587328
DOI: 10.1007/s12010-022-03967-9 -
PloS One Mar 2011Monocrotophos (MCP) is a widely used organophosphate (OP) pesticide. We studied apoptotic changes and their correlation with expression of selected cytochrome P450s...
Monocrotophos (MCP) is a widely used organophosphate (OP) pesticide. We studied apoptotic changes and their correlation with expression of selected cytochrome P450s (CYPs) in PC12 cells exposed to MCP. A significant induction in reactive oxygen species (ROS) and decrease in glutathione (GSH) levels were observed in cells exposed to MCP. Following the exposure of PC12 cells to MCP (10(-5) M), the levels of protein and mRNA expressions of caspase-3/9, Bax, Bcl(2), P(53), P(21), GSTP1-1 were significantly upregulated, whereas the levels of Bclw, Mcl1 were downregulated. A significant induction in the expression of CYP1A1/1A2, 2B1/2B2, 2E1 was also observed in PC12 cells exposed to MCP (10(-5) M), whereas induction of CYPs was insignificant in cells exposed to 10(-6) M concentration of MCP. We believe that this is the first report showing altered expressions of selected CYPs in MCP-induced apoptosis in PC12 cells. These apoptotic changes were mitochondria mediated and regulated by caspase cascade. Our data confirm the involvement of specific CYPs in MCP-induced apoptosis in PC12 cells and also identifies possible cellular and molecular mechanisms of organophosphate pesticide-induced apoptosis in neuronal cells.
Topics: Animals; Apoptosis; Blotting, Western; Glutathione; Immunohistochemistry; Insecticides; Monocrotophos; PC12 Cells; Rats; Reactive Oxygen Species; Transcription, Genetic; Xenobiotics
PubMed: 21445290
DOI: 10.1371/journal.pone.0017757 -
PloS One 2019
PubMed: 30875407
DOI: 10.1371/journal.pone.0214164 -
Arhiv Za Higijenu Rada I Toksikologiju Sep 2012Several episodes of mass poisoning by organophosphates (OPs) have been reported from the developing countries. The diagnosis of OP-poisoning is mainly based on the...
Several episodes of mass poisoning by organophosphates (OPs) have been reported from the developing countries. The diagnosis of OP-poisoning is mainly based on the characteristic clinical features and history of exposure to a known OP compound. Estimation of serum and red blood cell (RBC) cholinesterase activities are helpful in confirming the diagnosis. However, there is controversy regarding a definite relationship between serum cholinesterase activity and the severity of clinical manifestations and prognosis. This report describes an episode of mass monocrotophos poisoning that occurred due to accidental ingestion of monocrotophos-contaminated millet (so-called bavta) flour involving eight severely poisoned persons. Clinical presentation included severe abdominal pain, diarrhoea, vomiting, pupil narrowing, and difficulty breathing. On hospital admission, plasma cholinesterase (PChE) and especially RBC acetylcholinesterase (AChE) activities correlated well with clinical symptoms presented by the patients. This case study highlights the need for clinicians to be aware of OP-pesticide poisoning from food sources and the need to look for depressed PChE and AChE activities that may point to OP exposure, so that OP-poisoning can be identified immediately and patients can receive specific treatment, rather than general treatment for food poisoning.
Topics: Adolescent; Adult; Child; Diarrhea; Dyspnea; Female; Flour; Food Contamination; Foodborne Diseases; Humans; India; Insecticides; Male; Middle Aged; Monocrotophos; Organophosphate Poisoning; Pain; Respiratory Insufficiency; Sialorrhea; Vomiting
PubMed: 23152387
DOI: 10.2478/10004-1254-63-2012-2158 -
Neurotoxicology Mar 2012Neurotoxicity of organophosphate pesticide poisoning, a lead cause of death in South Asia, has not been clearly elucidated. Organophosphates inhibit acetylcholinesterase...
BACKGROUND
Neurotoxicity of organophosphate pesticide poisoning, a lead cause of death in South Asia, has not been clearly elucidated. Organophosphates inhibit acetylcholinesterase and neurotoxicity is primarily a result of acetylcholine induced hyperactivation in different regions of the brain. Neurotoxicity also results from oxidative stress induced by acetylcholinesterase inhibition in the brain. Determining the severity of acetylcholinesterase inhibition that induces oxidative damage may help in developing strategies that protect the brain from organophosphate induced toxicity.
AIM
To determine the level of acetylcholinesterase inhibition that induces oxidative stress in the brain following organophosphate pesticide poisoning.
METHODS
Brains of rats subject to acute monocrotophos poisoning (0.8 LD(50) by gavage) were assessed for acetylcholinesterase activity, antioxidant response and oxidative damage 2.5 and 8h after poisoning and on recovery from poisoning 24h later after poisoning. Assessments were made in the cortex, striatum and hippocampus, cholinergic rich regions and cerebellum, targets of organophosphate pesticide poisoning. Analysis was in comparison to non poisoned controls.
RESULTS
High acetylcholinesterase activities were noted in striatum followed by hippocampus, cerebellum and cortex. Acute severe monocrotophos poisoning inhibited acetylcholinesterase 87% in striatum, 67% in hippocampus, 58% in cerebellum, 53% in cortex and increased glutathione levels significantly in all brain regions 2.5h after poisoning. Significant lipid peroxidation and antioxidant enzymes were induced 8h after poisoning, directly correlated to high acetylcholinesterase inhibition (>67%). Recovery from monocrotophos poisoning was associated with absence of lipid peroxidation in the brain although acetylcholinesterase inhibition persisted.
CONCLUSIONS
Neurotoxicity of monocrotophos poisoning is characterized by oxidative damage in regions of the brain that exhibit high acetylcholinesterase activity and severe acetylcholinesterase inhibition. Recovery from poisoning is associated with prolonged induction of antioxidants that protect against oxidative damage.
Topics: Acetylcholinesterase; Analysis of Variance; Animals; Body Weight; Brain; Catalase; Cholinesterase Inhibitors; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Glutathione; Glutathione Peroxidase; Lacrimal Apparatus; Lipid Peroxidation; Monocrotophos; Muscle Strength; Neurotoxicity Syndromes; Oxidative Stress; Rats; Rats, Wistar; Salivation; Superoxide Dismutase; Time Factors
PubMed: 22285544
DOI: 10.1016/j.neuro.2012.01.008 -
Microbial Pathogenesis Feb 2020Soil contamination has enlarged over the decades due to intensive use of pesticides and chemical fertilizers in agronomy. Earthworms are significant organisms in the...
Soil contamination has enlarged over the decades due to intensive use of pesticides and chemical fertilizers in agronomy. Earthworms are significant organisms in the soil community. Earthworms are the major role in soil fertility in most ecological system and the production of biogenic structures. Moreover, earthworm gut mucus enhances the beneficial soil microorganism potential biological activities. They are used as model organisms for assessing the ecological risks of chemicals. Enrichment of essential nutrients in soil through earthworm is a cost-effective and eco-friendly approach. In India, the organophosphorus pesticide monocrotophos is commonly used to control agricultural pests. Hence, it is important to study the effect of monocrotophos on the gut microbiota in Lampito mauritii. A 15-day exposure to a low (1/10th of the LC after 96 h i.e., 0.093 ppm kg) and high sublethal concentration (1/3rd of the LC after 96 h i.e., 0.311 ppm kg) of monocrotophos led to reduced proliferation of the gut microbiota in L. mauritii. However, exposure for 30 days led to a recuperation of the microbial populations to near control values. Among the eight bacterial and five fungal species that inhabit the gut of L. mauritii, only six bacterial and three fungal species were able to survive after exposure to monocrotophos. In addition to the study, histopathological changes were observed in the intestine of L.mauritii after application of lower sublethal concentration of monocrotophos. Severe pathological changes such as vacuolization, degenerated nuclei, damaged villi and congestion of the blood sinuses were noticed in the intestine on 1st and, 5th day of the experiment. But in 30th day the damages were slowly recovered due to degradation of monocrotophos by the presence of some pesticides degrading bacterial and fungal species and regenerative capability of chloragogen cells in the intestine. The results suggested that reduced microbial populations and pathological damages in intestine were observed during the application of monocrotophos. So, the monocrotophos have several harmful impacts on earthworms.
Topics: Animals; Bacteria; Bacterial Load; Biopsy; Fungi; Gastrointestinal Microbiome; Intestinal Mucosa; Monocrotophos; Oligochaeta; Pesticides
PubMed: 31778757
DOI: 10.1016/j.micpath.2019.103893 -
Chemosphere Jan 2023Potassium (K) and phosphorus (P) are the important macronutrients needed for the plant development, but it is widely present in an insoluble form for the plant's uptake....
Potassium (K) and phosphorus (P) are the important macronutrients needed for the plant development, but it is widely present in an insoluble form for the plant's uptake. In order to increase the productivity, biofertilisers play crucial role in plant growth enhancement. Our present work focused to isolate potassium-phosphate solubilizing bacteria from the agricultural soil of tomato cultivated soil. Potassium and phosphate solubilization and degradation of monocrotophos was estimated spectrophotometrically. Out of thirteen isolates, two isolates proved to be the best P and K solubilizers. The bacterial isolates (SDKVG02 and SDKVG04) were optimized to obtain maximum P and K solubilization of 57.5 mg L-1 and 15.07 mg L-1 by the isolates. Pot experiments were conducted using SDKVG 02 and 04, immobilized on carrier materials, peat proving the best carrier with the total average green gram and chick pea length of 11.66 ± 0.0666 22.22 ± 0.0577. The MCP degradation percentage was achieved at 80 ppm of MCP with 75.8% and 64.10% by SDKVG 02 and SDKVG 04. Furthermore, production of organic acids such as malic acid, phthalic acid, ascorbic acid, nicotinic acid, and tartaric acid paves solubilization of P and K. The isolates were recognized based on 16S rRNA gene sequencing as Enterobacter hormaechei- SDKVG-02, Enterobacter cloacae SDKVG- 04. The KSB-PSB isolates also express N-fixing activity which is proved through In-silico analysis. It is worth to highlight SDKVG 02 and 04 would be potent biofertiliser exploited in increasing the soil fertility and crop productivity as well in degradation of monocrotophos present in the soil.
Topics: Monocrotophos; Phosphates; Potassium; RNA, Ribosomal, 16S; Soil
PubMed: 36410511
DOI: 10.1016/j.chemosphere.2022.137304 -
Molecular Neurobiology Jul 2017Expression of various cytochrome P450s (CYPs) in mammalian brain cells is well documented. However, such studies are hampered in neural/glial cells of human origin due...
Expression of various cytochrome P450s (CYPs) in mammalian brain cells is well documented. However, such studies are hampered in neural/glial cells of human origin due to nonavailability of human brain cells. To address this issue, we investigated the expression and inducibility of CYP2C8 and CYP3A4 and their responsiveness against cyclophosphamide (CPA) and organophosphorus pesticide monocrotophos (MCP), a known developmental neurotoxicant in human neural (SH-SY5Y) and glial (U373-MG) cell lines. CPA induced significant expression of CYP2C8 and CYP3A4 in both types of cells in a time-dependent manner. Neural cell line exhibited relatively higher constitutive and inducible expression of CYPs than the glial cell line. MCP exposure alone could not induce the significant expression of CYPs, whereas the cells preexposed to CPA showed a significant response to MCP. Similar to the case of CPA induced expressions, neural cells were found to be more vulnerable than glial cells. Our data indicate differential expressions of CYPs in cultured human neural and glial cell lines. The findings were synchronized with protein ligand docking studies, which showed a significant modulatory capacity of MCP by strong interaction with CYP regulators-CAR and PXR. Similarly, the known CYP inducer CPA has also shown significant high docking scores with the two studied CYP regulators. We also observed a significant induction in reactive oxygen species (ROS), lipid peroxides (LPO), micronucleus (MN), chromosomal aberration (CA), and reduction in reduced glutathione (GSH) and catalase following the exposure of MCP. Moreover, the expressions of apoptotic markers such as caspase-3, caspase-9, Bax, and p53 were significantly upregulated, whereas the levels of antiapoptotic marker, Bcl2, was downregulated after the exposure of MCP in both cell lines. These findings confirm the involvement of ROS-mediated oxidative stress, which subsequently triggers apoptosis pathways in both human neural (SH-SY5Y) and glial (U373-MG) cell lines following the exposure of MCP.
Topics: Apoptosis; Brain; Caspases; Catalase; Cell Death; Cell Line; Constitutive Androstane Receptor; Cyclophosphamide; Cytochrome P-450 CYP2C8; Cytochrome P-450 CYP3A; Cytochromes c; Enzyme Induction; Humans; Ligands; Lipid Peroxidation; Micronucleus Tests; Molecular Docking Simulation; Monocrotophos; Neurotoxins; Oxidative Stress; Pregnane X Receptor; Protein Biosynthesis; Reactive Oxygen Species; Receptors, Cytoplasmic and Nuclear; Receptors, Steroid; Transcription, Genetic; Xenobiotics; bcl-2-Associated X Protein
PubMed: 27206429
DOI: 10.1007/s12035-016-9938-7 -
Journal of Diabetes Jan 2015Our earlier studies had shown that monocrotophos (MCP), an organophosphorus insecticide (OPI), has the propensity to augment the secondary complications associated with...
BACKGROUND
Our earlier studies had shown that monocrotophos (MCP), an organophosphorus insecticide (OPI), has the propensity to augment the secondary complications associated with type-1 diabetes. The present study investigates whether rats exposed for prolonged periods to monocrotophos would develop insulin resistance mediated by alteration in glucose homeostasis.
METHODS
Male rats were administered sublethal doses of monocrotophos daily for 180 days. Interim blood samples were collected to measure alteration in blood glucose and lipid profile. Rats were also subjected to glucose and insulin tolerance test and fasting blood glucose and insulin levels were measured to calculate insulin resistance by HOMA-IR method. After 180 days, the rats were also evaluated for pancreatic histology and activities of hepatic gluconeogenetic enzymes.
RESULTS
Monocrotophos elicited a gradual and sustained increase in blood glucose and insulin resistance in rats with concomitant glucose intolerance and reduced insulin sensitivity. MCP exposure was also associated with increase in weights of key white adipose pads, activities of gluconeogenesis enzymes and increase in pancreatic islet diameter, all of which led to hyperglycemia, hyperinsulinemia and dyslipidaemia.
CONCLUSION
Long-term exposure of rats to MCP resulted in glucose intolerance with hyperinsulinemia, a hallmark of insulin resistance. Our data suggest that chronic exposure to low doses of monocrotophos, might lead to development of insulin resistance by altering lipid profile and glucose homeostasis.
Topics: Animals; Blood Glucose; Glucose Intolerance; Hyperglycemia; Hyperinsulinism; Insecticides; Insulin Resistance; Islets of Langerhans; Lipids; Male; Monocrotophos; Rats; Rats, Wistar
PubMed: 24698518
DOI: 10.1111/1753-0407.12158 -
Chemosphere Jan 2006The degradation of a widely used organophosphorus insecticide, monocrotophos (dimethyl (E)-1-methyl-2-methylcarbamoyl vinyl phosphate) in two Indian agricultural soils...
The degradation of a widely used organophosphorus insecticide, monocrotophos (dimethyl (E)-1-methyl-2-methylcarbamoyl vinyl phosphate) in two Indian agricultural soils at two concentration levels, 10 and 100 microg g(-1) soil under aerobic conditions at 60% water-holding capacity at 28+/-4 degrees C was studied in a laboratory. The degradation of monocrotophos at both concentrations in black vertisol and red alfinsol soils was rapid accounting for 96-98% of the applied quantity and followed the first-order kinetics with rate constants (k) of 0.0753 and 0.0606 day(-1) and half-lives (t1/2) of 9.2 and 11.4 days, respectively. Degradation of monocrotophos in soils proceeded by hydrolysis with formation of N-methylacetoacetamide. Even three additions of monocrotophos at 10 microg g(-1) soil did not result in its enhanced degradation. However, there was cumulative accumulation of N-methylacetoacetamide in soils pretreated with monocrotophos to the tune of 7-15 microg g(-1) soil. Both biotic and abiotic factors were involved in degradation of monocrotophos in soils.
Topics: Agriculture; Biodegradation, Environmental; Environmental Pollution; India; Kinetics; Monocrotophos; Soil; Soil Pollutants
PubMed: 15978655
DOI: 10.1016/j.chemosphere.2005.04.076