Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues. The metabolic processes were summarized as: 1) hydroxylation of the thiazolidine ring and subsequent glucuronidation (as shown by metabolite PIZ 1270), 2) hydroxylation of the cyanamide moiety (metabolite KNO 1891), 3) opening of the thiazolidine ring (e.g., metabolites KNO2672, PIZ1297F/WAK 6935), 4) formation of an oxazole ring (metabolite PIZ 1253), 5) oxidation and subsequent methylation of the thiazolidine ring (e.g., PIZ 1297E and PIZ 1269X), and 6) oxidative cleavage of the methylene bridge (PIZ 1243). Only minor gender-related quantitative differences in metabolite profiles were observed.
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
IDENTIFICATION AND USE: Thiacloprid is an insecticide of the neonicotinoid class. It is used to control aphids, codling moth, leafhoppers, leafminers, psylla, and whiteflies in potatoes, oilseed rape, pome fruit, vegetables, and ornamentals. HUMAN STUDIES: There is a case report of thiacloprid poisoning resulting from deliberate ingestion in a 23-year-old man, manifesting with status epilepticus, respiratory paralysis, rhabdomyolysis, metabolic acidosis, and acute kidney injury, and ultimately giving rise to refractory shock and death. In human peripheral blood lymphocytes in vitro thiacloprid increased the chromosome aberrations and sister chromatid exchange significantly at all concentrations (75, 150, and 300 ug/mL) both in the absence and presence of the metabolic activation and induced a significant increase in micronucleus and nucleoplasmic bridge formations at all concentrations for 24 hr and at 75 and 150 ug/mL for 48-hr treatment periods in the absence of the metabolic activation. Thiacloprid was also found to significantly induce nuclear bud formation at 300 ug/mL for 24 hr and at 150 ug/mL for 48-hr treatment times in the absence of the metabolic activation and at the two highest concentrations (150 and 300 ug/mL) in the presence of the metabolic activation. ANIMAL STUDIES: Evidence of carcinogenicity reported in rats based on increased incidence of thyroid follicular cell adenomas in males and possibly also in females and increased incidence of uterine tumors (adenocarcinomas). Evidence of carcinogenicity reported in mice based on increased incidence of ovarian luteomas. Thiacloprid impairs development and quality of both mouse and rabbit preimplantation embryos, and shows embryotoxicity even at acute reference dose. Developmental neurotoxicity described in rats based on decreased pre-weaning and post-weaning body weights in both sexes and delayed sexual maturation in the males, and altered performance in passive avoidance testing. In rats treated with thiacloprid, statistically significant increases in free triiodothyronine and free thyroxine serum hormone levels were observed. The potential genotoxic effect of thiacloprid formulation on bovine peripheral lymphocytes was evaluated using the comet assay and the cytogenetic endpoints. Whole blood cultures were treated with the insecticide at concentrations of 30, 60, 120, 240 and 480 ug/mL for 24, 48 hr and/or 2 hr of incubation. A statistically significant increase in the frequency of DNA damage, as well as in unstable chromosome aberrations (% breaks) were found after exposure to the insecticide at concentrations ranging from 120 to 480 ug/mL. ECOTOXICITY STUDIES: Caenorhabditis elegans is less susceptible to neonicotinoids than target species of pest insect. Chronic thiacloprid exposure of early-life stages of carp affected ontogeny and growth rate, and inhibited antioxidant capacity. Pheromone production was altered in moth Cydia pomonella, with a reduction of the major compound, codlemone, and one minor component. In worker bees, thiacloprid (24 hr oral exposure, 200 ug/L or 2000 ug/L) reduced hemocyte density, encapsulation response, and antimicrobial activity even at field realistic concentrations. Thiacloprid, as active substance and as formulation, poses a substantial risk to honey bees by disrupting learning and memory functions. Honey bees (Apis mellifera carnica) were exposed chronically to thiacloprid in the field for several weeks at a sublethal concentration. Foraging behavior, homing success, navigation performance, and social communication were impaired, and thiacloprid residue levels increased both in the foragers and the nest mates over time. Thiacloprid exposed free-flying bumblebee colonies were more likely to die prematurely, and those that survived reached a lower final weight and produced 46% fewer reproductives than colonies placed at control farms. Earthworms were exposed to thiacloprid (1 and 3 mg/kg) for 7, 14, and 28 days and then transferred to the clean soil for 35, 42, and 56 days. Results showed that activities of molecular indicators are inhibited following the exposure to thiacloprid at one or more sample times and then increased during the recovery course compared with the control. Significant DNA damage to E. fetida was also observed by olive tail moments in comet assay.
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
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).
Neurotoxin - Other CNS neurotoxin
Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.
ACGIH Carcinogen - Confirmed Animal.
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
毒理性
毒性数据
LC50（大鼠）= 1,223 毫克/立方米/4小时
LC50 (rat) = 1,223 mg/m3/4h
来源:Haz-Map, Information on Hazardous Chemicals and Occupational Diseases
吸收、分配和排泄
噻虫啉被迅速吸收并在经过以下代谢过程后迅速排出，体内残留很少。
Thiacloprid is rapidly absorbed and is rapidly excreted after the following metabolic processes, with little remaining in the tissues.
[EN] ACC INHIBITORS AND USES THEREOF<br/>[FR] INHIBITEURS DE L'ACC ET UTILISATIONS ASSOCIÉES
申请人：GILEAD APOLLO LLC
公开号：WO2017075056A1
公开（公告）日：2017-05-04
The present invention provides compounds I and II useful as inhibitors of Acetyl CoA Carboxylase (ACC), compositions thereof, and methods of using the same.
[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.
