Metabolism occurs principally by oxidation, hydrolysis by esterases, and by transfer of portions of the molecule to glutathione. Oxidation of organophosphorus insecticides may result in more or less toxic products. The glutathione transferase reactions produce products, that are, in most cases, of low toxicity. Hydrolytic and transferase reactions affect both thioates and their oxons. /Organophosphorus Pesticides/
来源:Hazardous Substances Data Bank (HSDB)
代谢
羟基磺酰是动物体内的主要代谢物，其次是磷硫代酸和磺酸。
Hydroxy sulfones were the major metabolites /in animals/, followed by phosphorothioic and sulfonic acids.
Male and female rats (Sprague-Dawley, 5/sex/dose) were administered an oral dose of (14)C-labelled cadusafos (at the butyl side chains) at rates of 1 and 21 mg/kg bw. Another group received multiple oral doses of 1 mg/kg bw (labelled and non-labelled material). Results from oral dosing were compared to those from iv dosing consisting of a single dose of about 0.8 mg/kg bw. The excretion pattern found in previous experiments was confirmed. Analyses of excretion profiles showed that the majority of (14)C activity was eliminated within the first 24 hours after dosing. In the fraction of non-conjugated neutral metabolites the majority of the radioactivity excreted in urine was contributed by methyl-1-methyl-2- hydroxypropane sulfone. Other metabolites detected were 0-ethyl-S-(2-butyl) phosphorothioic acid, S,S-di-(2-butyl) phosphorodithioic acid, methyl-2-butyl-sulfone and sulfoxide. 0-ethyl-S-(2-butyl)phosphorothioic acid, methylsulfonic acid, hydroxy sulfone and sec-butyl sulfonic acid were identified. As major polar metabolites in the remaining fractions such compounds as 4-hydroxy-2-butyl sulfonic acid, 3-hydroxy-2-butyl sulfonic acid, sec-butyl sulfonic acids, and S-(2-butyl) phosphorothioic acid were detected. In feces the parent compound was found at rates of 6-64% in the different oral dosing regimens with highest values after administration of a single oral high dose. In the iv dosed group parent compound was not detected in feces. Major fecal metabolites were sec-butyl sulfonic acid and monophosphorothioic acid-related acidic compounds. Cleavage of the thio-(sec-butyl) group is the initial step producing sec-butyl mercaptan and 0-ethyl-S-(2-butyl)phosphorothioic acid as major metabolites. Further cleavage and oxidation reactions may result in S-(2-butyl)phosphorothioic acid or 0-ethyl phosphorothioic acid, methyl sec-butyl sulfide, sulfoxide, sulfone and finally hydroxysulfones. Sec-butyl mercaptan can also be oxidized to butyl sulfonic acid, ethyl and methyl sulfonic acid. Formation of CO2 could be derived from either the sec-butyl mercaptan moiety or the corresponding sulfonic acid. CO2 may then be incorporated into urea or other endogenous substances.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
癌症分类：人类非致癌性证据E组
Cancer Classification: Group E Evidence of Non-carcinogenicity for Humans
来源:Hazardous Substances Data Bank (HSDB)
毒理性
副作用
其他毒物 - 有机磷酸酯
Other Poison - Organophosphate
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
毒理性
毒性数据
LC50 (大鼠) = 32毫克/立方米/4小时
LC50 (rat) = 32 mg/m3/4h
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
Airway protection. Insure that a clear airway exists. Intubate the patients and aspirate the secretions with a large-bore suction device if necessary. Administer oxygen by mechanically assisted pulmonary ventilation if respiration is depressed. Improve tissue oxygenation as much as possible before administering atropine, so as to minimize the risk of ventricular fibrillation. In severe poisonings, it may be necessary to support pulmonary ventilation mechanically for several days. /Organophosphate pesticides/
Atropine sulfate. Administer atropine sulfate intravenously, or intramuscularly if intravenous injection is not possible. Remember that atropine can be administered through an endotracheal tube if initial IV access if difficult to obtain. Depending on the severity of poisoning, doses of atropine ranging from very low to as high as 300 mg/day may be required, or even continuous infusion. The objective of atropine antidotal therapy is to antagonize the effects of excessive concentrations of acetylcholine at end-organs having muscarinic receptors. Atropine does not reactivate the cholinesterase enzyme or accelerate disposition of organophosphate. Recrudescence of poisoning may occur if tissue concentrations of organophosphate remain high when the effect of atropine wears off. Atropine is effective against muscarinic manifestations, but it is ineffective against nicotinic actions, specifically muscle weakness and twitching, and respiratory depression. Despite the limitations, atropine is often a life-saving agent in organophosphate poisonings. Favorable response to a test dose of atropine (1 mg in adults, 0.01 mg/kg in children under 12 years) can help differentiate poisoning by anticholinesterase agents from other conditions. However, lack of response, with no evidence of atropinization (atropine refractoriness) is typical of more severe poisonings. The adjunctive use of nebulized atropine has been reported to improve respiratory distress, decrease bronchial secretions, and increase oxygenation. ...Do not administer atropine or pralidoxime prophylactically to workers exposed to organophosphate pesticides. Prophylactic dosage with either atropine or pralidoxime may mask early signs and symptoms of organophosphate poisoning and thus allow the worker to continue exposure and possibly progress to more severe poisoning. Atropine itself may enhance the health hazards of the agricultural work setting: impaired heat loss due to reduced sweating and impaired ability to operate mechanical equipment due to blurred vision. This can be caused by mydriasis, one of the effects of atropine. /Organophosphate pesticides/
... Elimination of the phosphorus-containing residue may be via the urine or feces. Some bound residues remain in exposed animals. Binding seems to be to proteins, principally, and the turnover appears to be related to the half-life of these proteins. There are limited data showing that incorporation of residues into DNA occurs only in trace amounts and not by direct alkylation, such as might be believed to be associated with genetic damage. /Organophosphorus Pesticides/
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
容易被吸收、代谢并在尿液和粪便中排出。
Readily absorbed, metabolized and eliminated in urine and feces.
Adult rats (Sprague-Dawley, 5/sex) were dosed orally with single doses of 20 mg/kg bw (14)C-labelled cadusafos. Urine and feces were collected for 7 days. Animals were then sacrificed and carcass and tissues were analyzed for residual radioactivity. About 75% of the applied radioactivity was excreted in urine and about 15% in feces over the course of 7 days. Most radioactivity was eliminated within the first 24 hours after dosing. Highest residues were measured in liver and in adipose tissue with a mean value of 0.7 ppm. Another group of rats (5/sex) was monitored for (14)CO2. Expiration amounted to 13% of the applied radioactivity within three days. No sex difference in the elimination and distribution pattern was observed.
Rats (Crl:CD(SD)BR, 10/sex/group) received one of four dosing regimens with (14)C-labelled cadusafos. Dosing regimens were a single oral low dose of 1 mg/kg bw, a single iv dose of 0.8 mg/kg bw, multiple oral low doses of 1 mg/kg bw nonlabelled material over 14 days followed by an additional dose of labelled material and a control group. Urine and feces were collected for 7 days and tissues were then analyzed for remaining radioactivity. Animals for which 14CO2 was monitored were sacrificed 3 days after dosing. For all groups, more than 90% of the administered radioactivity was eliminated within 48 hours after dosing. Mean total urinary excretion was about 67%, 78% and 71% after oral single, iv and oral multiple dosing, respectively. Corresponding excretion values in feces were 10%, 5% and 7%. (14)CO2 expiration varied between 13% and 16% in the three dosing regimens. Residues in tissues were low. Highest levels were measured in liver and in fat showing mean concentrations of up to about 0.07 ppm in liver and 0.03 ppm in fat after oral dosing. In the iv study mean concentration in lung was highest with mean values of about 0.05 ppm, followed by a concentration of 0.03 ppm in liver and fat. No marked sex differences were observed.
Interrogation of the Substrate Profile and Catalytic Properties of the Phosphotriesterase from Sphingobium sp. Strain TCM1: An Enzyme Capable of Hydrolyzing Organophosphate Flame Retardants and Plasticizers
[EN] BICYCLYL-SUBSTITUTED ISOTHIAZOLINE COMPOUNDS<br/>[FR] COMPOSÉS ISOTHIAZOLINE SUBSTITUÉS PAR UN BICYCLYLE
申请人：BASF SE
公开号：WO2014206910A1
公开（公告）日：2014-12-31
The present invention relates to bicyclyl-substituted isothiazoline compounds of formula (I) wherein the variables are as defined in the claims and description. The compounds are useful for combating or controlling invertebrate pests, in particular arthropod pests and nematodes. The invention also relates to a method for controlling invertebrate pests by using these compounds and to plant propagation material and to an agricultural and a veterinary composition comprising said compounds.
The present invention relates to azoline compounds of formula (I) wherein A, B1, B2, B3, G1, G2, X1, R1, R3a, R3b, Rg1 and Rg2 are as defined in the claims and the description. The compounds are useful for combating or controlling invertebrate pests, in particular arthropod pests and nematodes. The invention also relates to a method for controlling invertebrate pests by using these compounds and to plant propagation material and to an agricultural and a veterinary composition comprising said compounds.
