08-12-2021-0137 - insecticides, industrial chemicals and Methotrexate (indust ch; insecticide; etc.)

Pesticides
Herbicides: Glyphosate, Methotrexate, Triazine, Others
Insecticides: Pyrethroids and Abamectin, Others
Fungicides: Triazole, Azoxystrobin and Carbendazim, Others
Biopesticides
Rodenticides, Plant Growth Regulators, Adjuvants

Nature of Pesticides
Generic
Patented
https://www.businesswire.com/news/home/20190225005453/en/South-African-Crop-Protection-Market-by-Type-Nature-Form-of-Pesticide-Type-of-Crop-and-Market-Structure---Forecast-to-2022---ResearchAndMarkets.com

HPLC Analysis of Polyglutamate Metabolites of Methotrexate on TSKgel® NH2-100 and ODS-100V
Separation of Methotrexate (MTX)-PG; Methotrexate (MTX)-PG2; Methotrexate (MTX)-PG3 ; Methotrexate (MTX)-PG4; Methotrexate (MTX)-PG5; Methotrexate (MTX)-PG6; Methotrexate (MTX)-PG7
https://www.sigmaaldrich.com/US/en/search/90-15-3?focus=sitecontent&page=1&perPage=30&sort=relevance&term=90-15-3&type=site_content


Preparation of Cationic Liposomes & Transfection of Cells - Avanti® Polar Lipids
This procedure describes the Preparation of Cationic Liposomes & Transfection of Cells



Caffeinated fruit flies help identify potential genes affecting insecticide resistanceDate:March 27, 2014Source:Genetics Society of AmericaSummary:To understand genetic mechanisms underlying insecticide resistance, scientists employed fruit flies and caffeine, a stimulant surrogate for xenobiotics in lab studies on resistance. Crop pests are capable of outwitting the chemical compounds known as xenobiotics that are devised to kill them. This development of resistance to insecticides is a serious problem because it threatens crop production and thereby can influence the availability and costs of many foods as well as the economy.https://www.sciencedaily.com/releases/2014/03/140327101417.htm


Ethanol (including propranolol plus ethanol), haloperidol, pentamidine, quinine, salicylates, and sulfonamides ("sulfa drugs") have been associated with hypoglycemia. Other drugs that may be related to this condition include oral hypoglycemics, phenylbutazone, insulin, bishydroxycoumarin, p-aminobenzoic acid, propoxyphene, stanozolol, hypoglycin, carbamate insecticide, disopyramide, isoniazid, methanol, methotrexate, tricyclic antidepressants, cytotoxic agents, organophosphates, didanosine, chlorpromazine, fluoxetine, sertraline, fenfluramine, trimethoprim, 6-mercaptopurine, thiazide diuretics, thioglycolate, tremetol, ritodrine, disodium ethylenediaminetetraacetic acid (EDTA), clofibrate, angiotensin converting enzyme (ACE) inhibitors, and lithium.https://www.medscape.com/answers/122122-6305/which-drugs-increase-the-risk-of-hypoglycemia-low-blood-sugar
Automimmune Disease

Free Access
Insecticide use and risk of rheumatoid arthritis and systemic lupus erythematosus in the Women's Health Initiative Observational Study



Christine G. Parks, Brian T. Walitt, Mary Pettinger, Jiu-Chiuan Chen … See all authors
First published: 25 August 2010
https://doi.org/10.1002/acr.20335
https://onlinelibrary.wiley.com/doi/full/10.1002/acr.20335


A new study shows that women who are exposed to or use pesticides are more likely to develop lupus and rheumatoid arthritis - two very painful autoimmune diseases. Researchers found that women living on farms who personally handled pesticides were especially at risk of developing these diseases. In fact, they were almost three times more likely to become affected by lupus and rheumatoid arthritis, compared to women who never used pesticides.
https://www.rxwiki.com/news-article/pesticides-linked-increased-risk-lupus-and-rheumatoid-arthritis

Patents for A01N 43 - Biocides, pest repellants or attractants, or plant growth regulators containing heterocyclic compounds (92,096)
03/2013
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03/20/2013 EP2568812A1 Novel prolylcarboxypeptidase inhibitors
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03/20/2013 CN102972432A Long-lasting insecticide
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03/20/2013 CN102972418A Florasulam water dispersible granules and preparation method thereof
03/20/2013 CN102972417A Compounded herbicide for wheat fields
03/20/2013 CN102972416A Acaricidal composition containing fluacrypyrim and spirodiclofen
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03/20/2013 CN102972413A Pyridalyl and flutenzine-containing insecticidal compound
03/20/2013 CN102972412A Novel fruit tree weed composite herbicide and preparation method thereof
03/20/2013 CN102972411A Cornfield herbicide containing butachlor, atrazine and metolachlor
03/20/2013 CN102972410A Pesticide composition containing prothioconazole and methoxyl acrylic ester bactericides
03/20/2013 CN102972409A Seedling-protection micro-emulsion
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03/20/2013 CN102612935B Application method of wheat
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03/20/2013 CN102177898B Application of 2-arylmorpholine and salt thereof serving as insecticide
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03/20/2013 CN102119700B Synergetic antibacterial composition containing fluazinam and iprobenfos and use thereof
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03/20/2013 CN102119684B Bactericidal composition containing fluazinam and dimethachlon and application of same
03/20/2013 CN102113513B Pesticide composition containing chlorfenapyr and profenofos
03/20/2013 CN102113510B Insecticidal composition containing metaflumizone
03/20/2013 CN102067871B Pill for preventing and treating maize borer and corncob aphid insect damage and realizing corn height control
03/20/2013 CN102057917B Fungicidal combinations
03/20/2013 CN102057915B Chemical control preparation for enhancing stress resistance and seed yield of wheats and application thereof
03/20/2013 CN102007921B Composition containing fenoxaprop-p-ethyl and fluroxypyr-meptyl and application thereof
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03/20/2013 CN101961010B Absorbent disinfection dry powder and preparation method thereof
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03/20/2013 CN101703042B Plant bactericidal milk particles and preparation method thereof
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03/20/2013 CN101508692B Anthranilamides, process for the production thereof, and pest controllers containing the same
03/20/2013 CN101410013B Active ingredient combinations with insecticidal and acaricidal properties
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03/19/2013 US8399506 Combinations of 4 bromo-2-(4-chlorophenyl)-5-(trifluoromethyl)-1H-pyrrole-3-carbonitrile and oxidizing agents
03/19/2013 US8399498 Animal ectoparasite-controlling agent

https://www.google.com/patents/sitemap/en/Sitemap/A01/A01N/A01N_43_138.html


An enzyme inhibitor is a molecule that binds to an enzyme and decreases its activity. By binding to enzymes' active sites, inhibitors reduce the compatibility of substrate and enzyme and this leads to the inhibition of Enzyme-Substrate complexes' formation, preventing the catalysis of reactions and decreasing (at times to zero) the amount of product produced by a reaction. It can be said that as the concentration of enzyme inhibitors increases, the rate of enzyme activity decreases, and thus, the amount of product produced is inversely proportional to the concentration of inhibitor molecules. Since blocking an enzyme's activity can kill a pathogenor correct a metabolic imbalance, many drugs are enzyme inhibitors. They are also used in pesticides. Not all molecules that bind to enzymes are inhibitors; enzyme activators bind to enzymes and increase their enzymatic activity, while enzyme substrates bind and are converted to products in the normal catalytic cycle of the enzyme.

https://en.wikipedia.org/wiki/Enzyme_inhibitor

• DOI:10.1016/j.cbi.2013.12.015
Corpus ID: 40488687

Effects of avermectin on immune function and oxidative stress in the pigeon spleen.

• Ci Liu, M. Li, +4 authors Shu Li
• Published 2014
• Biology, Medicine
• Chemico-biological interactions

Avermectin (AVM) is a pesticide that can accumulate in the environment through spray-drift, runoff or field drainage. Residues of AVM or its metabolites in livestock feces have toxic effects on non-target aquatic and terrestrial organisms. In this study, changes in oxidative stress and immunity in pigeon spleen tissues were detected after subchronic exposure to AVM for 30, 60, and 90 days. In pigeon spleen, the activities of total anti-oxidation capability (T-AOC), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased significantly, whereas the levels of malondialdehyde (MDA), protein carbonyl (PCO), and DNA-protein crosslink (DPC) coefficients increased. Additionally, obvious ultrastructure alterations were observed. These results indicated that AVM induced oxidative stress and damaged the normal structure of spleen cells. The exposure to AVM could lead to increases in the mRNA levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and interleukin-4 (IL-4), as well as a decrease in the mRNA level of interferon-γ (IFN-γ), in a dose-time-dependent manner in pigeon spleen. The results imply that AVM induces immunosuppression in the spleen tissue of pigeons. The information presented in this study may be helpful for understanding the mechanism of AVM-induced immunotoxicity in birds. Collapse

https://www.semanticscholar.org/paper/Effects-of-avermectin-on-immune-function-and-stress-Liu-Li/c9b5b0609515293e147da8230e2439fc5332a304

Summary

Metronidazole is a nitroimidazole used to treat trichomoniasis, amebiasis, inflammatory lesions of rosacea, and bacterial infections, as well as prevent postoperative infections.

Brand Names

Flagyl, Flagystatin, Metrocream, Metrogel, Metrolotion, Nidagel, Noritate, Nuvessa, Pylera, Rosadan, Vandazole

Generic Name

Metronidazole

DrugBank Accession Number

DB00916

https://go.drugbank.com/drugs/DB00916

Organophosphate poisoning is an important cause of acute neurological dysfunction and respiratory distress.

Epidemiology

Organophosphate poisoning is common, often as a result of suicidal ingestion (acute high-level exposure) or occupational exposure to pesticides (chronic low-level exposure) 1. It is thought that worldwide, approximately 3 million people are exposed to toxic levels of organophosphates, including approximately 2 million hospitalizations for suicidal ingestion 1.

Clinical presentation

Acute organophosphate poisoning leads to three distinct sequential neurological syndromes.

1. acute cholinergic crisis and paralysis (type I paralysis)
   • it is characterized by an acute muscarinic syndrome that manifests within hours of initial toxic exposure, and is soon afterwards followed by an acute nicotinic syndrome 2,3
   • the features of the muscarinic syndrome are helpfully summarized by the popular mnemonic 'SLUDGEM-BBB': salivation, lacrimation, urination, diarrhea, gastric cramps, emesis, miosis, bronchorrhea, bronchospasm, bradycardia 2
   • the features of the nicotinic syndrome are not in the mnemonic (and thus are often forgotten) but include fasciculations and muscle weakness 2
   • seizures may also occur acutely 2
2. intermediate syndrome (type II paralysis)
   • this is a continuation or extension of the nicotinic syndrome that manifests days after initial toxic exposure 2,3
   • it is characterized by continued paralysis, with prominent involvement of neck flexors, ocular muscles, bulbar muscles, and respiratory muscles 2,3
   • some patients may also exhibit extrapyramidal symptoms (e.g. parkinsonism, choreoathetosis) 2,3
3. organophosphate-induced delayed polyneuropathy (type III paralysis)
   • this is an uncommon syndrome that occurs weeks after initial toxic exposure 2,3
   • it is characterized by a symmetric and predominantly motor axonal neuropathy leading to flaccid limb weakness 2

With chronic exposure to low-dose organophosphates, the chronic organophosphate-induced neuropsychiatric disorder may manifest 4. This is characterized by fatigue, memory impairment, extrapyramidal symptoms, autonomic dysfunction, and peripheral neuropathy 4. Interestingly, cholinergic symptoms of a muscarinic syndrome are not a feature of chronic low-dose exposure 4.

Pathology

Organophosphates are agents that bind to acetylcholinesterase and inhibit its action of normally hydrolyzing acetylcholine 2,5. Acetylcholine is a neurotransmitter that is found at neuronal synapses and neuromuscular junctions, and acts on acetylcholine receptors, namely the muscarinic (mAChR) and nicotinic acetylcholine receptors (nAChR) 2,5.

Muscarinic acetylcholine receptors are predominantly involved in the activation of the parasympathetic nervous system, but are also found in the central nervous system 2,5. Nicotinic acetylcholine receptors are located at the neuromuscular junction (muscle-type nicotinic acetylcholine receptors), but also upstream in the central and peripheral nervous systems (neuronal-type nicotinic acetylcholine receptors) 2,5.

In acute organophosphate poisoning, there is overactivation of both muscarinic and nicotinic receptors, resulting in the acute muscarinic and nicotinic syndromes, as described above 2. The intermediate syndrome is a sequelae of the acute nicotinic syndrome, and is due to a depletion in acetylcholine at the neuromuscular junction 2. Additionally, in the basal ganglia, this results in a neurotoxicity and relative dopamine excess, which accounts for the extrapyramidal symptoms that are sometimes also seen in the intermediate syndrome 6. Neurotoxicity disproportionally affects the basal ganglia due to their high metabolic demand and rich vasculature 6.

The mechanism underlying organophosphate-induced delayed polyneuropathy is not well understood, but is thought to be independent to the functioning of both muscarinic and nicotinic receptors, and may be due to inhibition of the enzyme neurotoxic esterase instead 2. Similarly, the mechanism behind the chronic organophosphate-induced neuropsychiatric disorder is also poorly understood 4.

Radiographic features

Imaging is generally only remarkable in the brain (the focus of this section), however some patients may also develop a chemical aspiration pneumonitis which may produce findings on chest imaging 7. Generally, brain imaging findings only become apparent during the intermediate syndrome, and are reversible within weeks.

CT

CT brain may show hypoattenuation bilaterally in the basal ganglia 8. Generally, and unlike other toxic encephalopathies, these areas do not show evidence of hyperattenuating macroscopic hemorrhage.

MRI

Similar to CT, symmetric and bilateral involvement of the basal ganglia may be appreciated on MRI brain during the intermediate syndrome 3,6. In particular, the putamen and caudate nucleiare predominantly affected 3,6. Signal characteristics include 3,6:

• T1: low signal
• T2/FLAIR: high signal
• T1 C+ (Gd): usually minimal or absent contrast enhancement
• DWI: increased diffusion signal

Two case reports have also described lesions, with the same signal characteristics, in the cerebellum 3,9. Additionally, one case study has described an eye of the tiger sign in a case of organophosphate poisoning, whereby there was central T2 high signal with a low signal rim in the globus pallidus bilaterally, suggestive of a hemorrhagic necrosis 10. It is likely that these are atypical radiographic manifestations of acute organophosphate poisoning.

Importantly, all signal changes completely resolve within weeks to months 6. Unlike other toxic encephalopathies, such as methanol poisoning, cystic sequelae usually do not eventuate 6.

Treatment and prognosis

Acute management is generally with resuscitation and pharmacotherapy such as atropine, an agent that competes with acetylcholine at muscarinic receptors, and pralidoxime, an agent that reactivates acetylcholinesterases at both the muscarinic and nicotinic receptors 2. This acute care often takes place in an intensive care unit 2.

There is currently no treatment for the intermediate syndrome or organophosphate-induced delayed polyneuropathy, and patients with those manifestations should be managed symptomatically 2,4.

Differential diagnosis

For involvement in and around the basal ganglia, consider:

• mitochondrial encephalopathies
  • Leigh disease
  • Kearns-Sayre syndrome
• other toxic encephalopathies
  • carbon monoxide neurotoxicity
  • cyanide neurotoxicity
  • methanol neurotoxicity
• metabolic disorders
  • Wilson disease
• prion encephalopathies
  • Creutzfeldt-Jakob disease

References

Related Radiopaedia articles

Toxic and metabolic encephalopathies

• toxic
  • overview by region[+]
  • by agent/substance
    • inhaled toxins[+]
    • oral toxins
      • cyanide poisoning
      • ethylene glycol poisoning
      • methanol poisoning
      • organophosphate poisoning
      • toluene poisoning
    • drugs (oral or IV) [+]
  • by systemic illness[+]
• deficiency[+]
• metabolic[+]
• mitochondrial[+]

Promoted articles (advertising)

1. Anatoxin-a interactions with cholinergic synaptic molecules.
   R S Aronstam et al., Proc Natl Acad Sci U S A,  1981
2. Expression of muscarinic acetylcholine and dopamine receptor mRNAs in rat basal ganglia.
   D M Weiner et al., Proc Natl Acad Sci U S A,  1990
3. THE EFFECT OF CHRONIC POISONING WITH DI-ISOPROPYL FLUOROPHOSPHATE ON NEUROMUSCULAR FUNCTION IN THE CAT
   CARLTON C. HUNT et al., J Pharmacol Exp Ther,  1947

1. Megacystis, mydriasis, and ion channel defect in mice lacking the alpha3 neuronal nicotinic acetylcholine receptor.
   W Xu et al., Proc Natl Acad Sci U S A,  1999
2. Chronic, episodic nicotine alters hypoglossal motor neuron function at a critical developmental time point in neonatal rats
   Lila Buls Wollman et al., eNeuro 
3. Newborn Sequencing Projects Demonstrate Successes, Challenges of Widespread Implementation
   Monica Heger, 360Dx,  2017
   
   
   https://radiopaedia.org/articles/organophosphate-poisoning?lang=us