Acute oral and percutaneous toxicity of phosalone in the rat, in comparison with azinphosmethyl and parathion

Pasquet, J; Mazuret, André; Fournel, J; Koenig, France H.

doi:10.1016/s0041-008x(76)80010-5

Cited by 22 publications

(16 citation statements)

References 2 publications

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“…Dermal toxicities to the female rat were approximately 1530 mg/kg (phosalone), 380 mg/ kg (phosalone oxon), 90 mg/kg (azinphosmethyl), and about 8 mg/kg (parathion). After oral dosing, all three compounds were clearly better inhibitors of plasma BChE compared to RBC AChE (Pasquet et al 1976). Reiter et al (1975) studied inhibition and recovery of blood ChEs in bonnet and rhesus monkeys.…”

Section: B Small Animalsmentioning

confidence: 92%

“…Visual discrimination performance deterioration coincided with peak enzyme inhibition (Reiter et al 1975). Pasquet et al (1976) studied the blood enzyme inhibition and toxicity of phosalone, azinphosmethyl, and parathion in rats. The oral LD 50 s were I 0 mg/kg (parathion), 25 mg/kg (azinphosmethyl), and 120 mg/kg (phosalone).…”

Section: B Small Animalsmentioning

confidence: 99%

“…Based on human death and poisoning cases, toxic doses range from 2 to 5 mg!kg and lethal doses from 3 to 6 mg!kg. By comparison, other oral LD 50 s for known poisons are strychnine (5 mglkg), arsenic (8 mglkg), parathion (10 mg!kg), azinphosmethyl (25 mg!kg), and phosalone (120 mglkg) (Morris and Lee 1984;Pasquet et al 1976). These alkaloids cross the gut wall, and the maximal uptake appears to occur in about 12 hr (Morris and Lee 1984).…”

Section: Possible Dietary Effects On Blood Esterase Activitymentioning

confidence: 99%

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Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Nigg

Knaak

2000

Reviews of Environmental Contamination and Toxicology

100

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Section: B Small Animalsmentioning

confidence: 92%

Section: B Small Animalsmentioning

confidence: 99%

Section: Possible Dietary Effects On Blood Esterase Activitymentioning

confidence: 99%

See 1 more Smart Citation

Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Nigg

Knaak

2000

Reviews of Environmental Contamination and Toxicology

100

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“…Activation of azinphos‐methyl occurs relatively fast: the conversion of the thion to the oxon form takes less than 10 minutes in an in vitro model using liver slices. In vivo signs and symptoms of cholinergic intoxication are observed 5–10 minutes after oral (Pasquet, Mazuret, Fournel, & Koenig, ) or intraperitoneal (Lorke, Nurulain, Hasan, Kuca, & Petroianu, ; Petroianu et al, ) administration.…”

Section: Organophosphates Evaluatedmentioning

confidence: 99%

Reversible cholinesterase inhibitors as pretreatment for exposure to organophosphates. A review

Lorke

Petroianu

2018

J of Applied Toxicology

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Organophosphorus compounds (OPCs), inhibitors of acetylcholinesterase (AChE), are useful agents as pesticides, but also represent a serious health hazard. Standard therapy with atropine and established oxime-type enzyme reactivators (pralidoxime, obidoxime) is unsatisfactory. Better therapeutic results are obtained, when reversible AChE inhibitors are administered before OPC exposure. This review summarizes the history of such a pretreatment approach and sums up a set of experiments undertaken in search of compounds that are efficacious when given before a broad range of OPCs. The prophylactic efficacy of 10 known AChE inhibitors, either already used clinically for different indications (physostigmine, pyridostigmine, ranitidine, tiapride, tacrine, amiloride, metoclopramide, methylene blue) or developed for possible therapeutic use in the future (7-methoxytacrine, K-27) was compared, when administered before exposure to six chemically diverse OPCs in the same experimental setting: ethyl-paraoxon, methyl-paraoxon, diisopropylfluorophosphate, terbufos sulfone, azinphos-methyl and dicrotophos. The experimental oxime K-27 was the most efficacious compound, affording best protection, when administered before terbufos sulfone, azinphos-methyl and dicrotophos, second best before ethyl- and methyl-paraoxon exposure and third best before diisopropylfluorophosphate administration. This ranking was similar to that of physostigmine, which was superior to the Food and Drug Administration-approved pretreatment for soman with pyridostigmine. Tiapride, amiloride, metoclopramide, methylene blue and 7-methoxytacrine did not achieve protection. No correlation was observed between the IC of the reversible AChE inhibitors and their protective efficacy. These studies indicate that K-27 can be considered a very promising broad-spectrum prophylactic agent in case of imminent organophosphate exposure, which may be related to its AChE reactivating activity rather than its AChE inhibition.

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“…Indeed, the high toxicity of OPs to humans had inspired their use as chemical warfare agents (e.g., the G‐ and V‐series nerve agents) . Mechanistically, these pesticides inhibit the activity of the enzyme acetyl cholinesterase, which causes toxic accumulation of the neurotransmitter acetylcholine and results in serious uncontrollable muscle contractions . These inhibitory and accumulation processes imperil human health by contraction of the pupils, profuse salivation, convulsions, involuntary urination and defecation, and even death by asphyxiation .…”

Section: Introductionmentioning

confidence: 99%

Catalytic Chemosensing Assay for Selective Detection of Methyl Parathion Organophosphate Pesticide

Zheng

Shen²,

Tang

et al. 2019

Chemistry A European J

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Herein, a catalytic chemosensing assay (CCA), based on a bimetallic complex, [RuII(bpy)2(CN)2]2(CuII)2 (bpy=2,2′‐bipyridine), is described. This complex integrates a task‐specific catalyst (CuI‐catalyst) and a signaling unit ([RuII(bpy)2(CN)2]) to specifically hydrolyze methyl parathion, a highly toxic organophosphate (OP) pesticide. The bimetallic complex catalyzed the hydrolysis of the phosphate ester to generate o,o‐dimethyl thiophosphate (DTP) anion and 4‐nitrophenolate. Intrinsically, 4‐nitrophenolate absorbed UV/Vis light at λmax=400 nm, creating the first level of the chemosensing signal. DTP interacted with the original complex to displace the chromophore, [RuII(bpy)2(CN)2], which was monitored by spectrofluorometry; this was classified as the second level of chemosensing signal. By integrating both spectroscopic and spectrofluorometric signals with a simple AND logic gate, only methyl parathion was able to provide a positive response. Other aromatic and aliphatic OP pesticides (diazinon, fenthion, meviphos, terbufos, and phosalone) and 4‐nitrophenyl acetate provided negative responses. Furthermore, owing to the metal‐catalyzed hydrolysis of methyl parathion, the CCA system led to the detoxification of the pesticide. The CCA system also demonstrated its catalytic chemosensing properties in the detection of methyl parathion in real samples, including tap water, river water, and underground water.

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Acute oral and percutaneous toxicity of phosalone in the rat, in comparison with azinphosmethyl and parathion

Cited by 22 publications

References 2 publications

Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Blood Cholinesterases as Human Biomarkers of Organophosphorus Pesticide Exposure

Reversible cholinesterase inhibitors as pretreatment for exposure to organophosphates. A review

Catalytic Chemosensing Assay for Selective Detection of Methyl Parathion Organophosphate Pesticide

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