Promecarb was rapidly metabolized and eliminated when administered orally to rats. By 96 hours after administration, over 90% had been recovered from the urine and feces, mainly the former. Promecarb equivalent radioactivity in the tissues did not exceed 0.02 ppm.
(5-(14)C)Promecarb was administered orally to male Sprague Dawley rats. Within 4 days, about 88% of the dose was eliminated in the urine. In addition to isothymol, there were unidentified metabolites. Hydrolysis with glucuronidase indicated the conjugation of isothymol with glucuronic acid. Other conjugates present were not identified.
Promecarb was applied to soil and then corn seedlings were planted. Analyses of stem and leaves of the plants indicated the presence of isothymol and four unidentified metabolites as early as 15 days after application.
Spontaneous hydrolysis of the carbamate-cholinesterase complex occurs in vivo, leading to the disappearance of clinical effects within 24 hr. /Carbamate pesticides/
Promecarb is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
No indication of carcinogenicity to humans (not listed by IARC).
Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).
As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)
... /CARBAMATE INSECTICIDES/ ARE RAPIDLY METABOLIZED, 80% OF DOSE BEING ELIMINATED IN URINE, MAINLY AS SULFATE OR GLUCURONIDE CONJUGATE, WITHIN 24 HR; 0.5 TO 1.5% IS FOUND IN FECES, 0.1 TO 1.0% IN THE MILK. /CARBAMATES/
In order to learn why cholinesterase remains inhibited longer in workers exposedto promecarb than in those exposed to propoxur, dogs were injected im or iv with approximately equitoxic doses of the compounds. It required 3 full days for cholinesterase activity to return to normal in a dog that received promecarb intramuscularly at a rate of 60 mg/kg, but recovery of cholinesterase activity was rapid after doses of propoxur sufficient to cause convulsions and marked ataxia. However, inhibition of cholinesterase activity was transient following intravenous administration of promecarb. It was concluded that prolonged inhibition of cholinesterase activity in days following im injection was the result of slow, continuing absorption and that, by extension, prolonged inhibition in workers has the same cause.
1.周国泰，化学危险品安全技术全书，化学工业出版社，1997 2.国家环保局有毒化学品管理办公室、北京化工研究院合编，化学品毒性法规环境数据手册，中国环境科学出版社.1992 3.Canadian Centre for Occupational Health and Safety,CHEMINFO Database.1998 4.Canadian Centre for Occupational Health and Safety, RTECS Database, 1989
Novel thienylpyridylcarboxamides of the formula (I)
The present application is also directed to a plurality of processes for preparing these compounds and their use for controlling unwanted microorganisms, and also novel intermediates and their preparation.
Compounds of formula I
wherein the substituents are as defined in claim 1, and the agrochemically acceptable salts and all stereoisomers and tautomeric forms of the compounds of formula I can be used as insecticides and can be prepared in a manner known per se.
