1,2,3-trichloropropane is a colorless liquid with a strong acid odor. Denser than water and slightly soluble in water. Hence sinks in water. (USCG, 1999)
颜色/状态：
Colorless liquid
气味：
Odor described as being quite similar to that of trichloroethylene or chloroform
... Male F-344 rats were administered 30 mg/kg [(14)C]- 1,2,3-trichloropropane (TCP) (100 uCi/kg) ip and killed 4 hr later. The extent of covalent binding to hepatic protein, DNA, and RNA was 418, 244, and 432 pmol [(14)C]TCP equivalents/mg, respectively. An in vivo covalent binding time course showed no significant change in [(14)C]TCP equivalents bound to hepatic DNA (1-48 hr), while binding to protein was maximal by 4 hr and decreased significantly by 48 hr. The binding of TCP-associated radioactivity to hepatic protein and DNA was shown to be cumulative for two and three doses when given 24 hr apart. Pretreatment of animals with phenobarbital caused a decrease while pretreatment with SKF 525-A caused an increase in covalent binding of [(14)C]TCP equivalents to protein and DNA. Pretreatment of rats with beta-naphthoflavone did not alter the covalent binding of [(14)C]TCP equivalents to protein or DNA. However, glutathione depletion with L-buthionine-(R,S)-sulfoximine increased binding to protein by 342% while it decreased binding to DNA by 56%. Intraperitoneal administration of TCP also depleted hepatic GSH by 41 and 61% 2 hr after doses of 30 and 100 mg/kg. The in vivo binding data suggest a dual role for GSH in the bioactivation of TCP. It may, in part, be that GSH is involved in the bioactivation and covalent binding of TCP to hepatic DNA. However, it also appears to detoxify a reactive intermediate(s) that binds to protein.
Following acute oral exposure of male and female F344 rats (30 mg/kg) and male B6C3F1 mice (30 and 60 mg/kg), 1,2,3-trichloropropane (TCP) was rapidly absorbed, metabolized, and excreted ... Two urinary metabolites were isolated and identified by NMR, mass spectroscopy, and comparison with synthetic standards, as N-acetyl- and S-(3-chloro-2-hydroxypropyl)cysteine. Analyses of the early urine (0-6 hr) showed this mercapturic acid to be the major metabolite in rat urine and was only a minor component in mouse urine. 2-(S-Glutathionyl)malonic acid was identified by NMR and mass spectrometry and by chemical synthesis as the major biliary metabolite in rats.
In vitro studies using rat and human hepatic microsomes have shown that the halogenated hydrocarbon 1,2,3-trichloropropane (TCP) is bioactivated to the direct acting mutagen 1,3-dichloroacetone (DCA). The presence of DCA in microsomal incubations was confirmed by gas chromatography-mass spectrometry. DCA formation was totally dependent on the presence of NADPH. The rate of DCA formation using rat and human microsomes was 0.268 +/- 0.029 and 0.026 +/- 0.006 nmol/min/mg protein +/- SE, respectively. When hepatic microsomes were isolated from rats pretreated with the cytochrome P-450 inducers, phenobarbital, and dexamethasone, 24- and 2.5-fold increases, respectively, in the rate of DCA production, were observed. Pretreatment with beta-naphthoflavone resulted in a 50% inhibition in DCA formation. The inhibitors of cytochromes P-450, SKF 525-A and 1-aminobenzotriazol, produced 85 and 70% inhibitions of DCA formation, respectively. When alcohol dehydrogenase and NADH were added to microsomal incubations, two TCP-related alcohols, 1,3-dichloro-2-propanol and 2,3-dichloropropanol, were formed. These alcohols are products of the initial microsomal metabolites, DCA and 2,3-dichloropropanal. [14C]TCP equivalents bound covalently to rat hepatic microsomal protein. This binding was increased 8-fold when hepatic microsomes from phenobarbital pretreated rats were used. The addition of either glutathione or N-acetylcysteine to the incubations completely inhibited this binding. In the presence of N-acetylcysteine, 1,3-(2-propanone)-bis-S-(N-acetylcysteine) (PDM) was the only N-acetylcysteine conjugate detected. It represented 87% of TCP microsomal metabolism. The formation of PDM implicates DCA as the major microsomal protein-binding metabolite of TCP. The formation of DCA, a direct-acting mutagen, may be responsible for the mutagenicity of TCP in systems using rat hepatic microsomes ...
The endogenous formation of reactive intermediates from 1,2,3-trichloropropane plays a crucial role in the organotoxic, genotoxic, and carcinogenic action of 1,2,3-trichloropropane. The postulated formation of alkylating species is consistent with the presence of covalently bound radioactivity in liver and kidney and in target tissues of carcinogenic action after gavage administration of [(14)C]1,2,3-trichloropropane. Significant DNA adduct levels (as (14)C equivalents of 1,2,3-trichloropropane) were found in forestomach and liver in mice and in kidney, liver, pancreas, tongue, and forestomach in rats. A predominant role was assigned to episulfonium ions formed in situ during the metabolism of 1,2,3-trichloropropane in the liver and from processing of GSH conjugates of 1,2,3-trichloropropane in the kidney, leading to hepatotoxic and nephrotoxic lesions.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
毒性总结
识别和使用：1,2,3-三氯丙烷（TCP）是一种无色液体，具有刺鼻的、令人不快的气味。它被用作合成其他化学品（例如，杀虫剂）的中间体，并在生产聚合物（如多硫化物和六氟丙烯）中作为交联剂。以前的使用包括作为疏水性化合物和树脂的溶剂，用作油漆和清漆的去除剂，以及作为脱脂剂。
人类暴露和毒性：在100 ppm的浓度下，1,2,3-三氯丙烷的蒸气被实验对象认为由于眼睛和喉咙刺激以及令人不快的气味而无法接受。注意到在50 ppm时，1,2,3-TCP的蒸气是刺鼻的。1,2,3-TCP的急性/亚慢性神经毒性效应包括人类的中枢神经系统损伤。已有零星报道称人类因1,2,3-TCP导致的中毒性肝损伤。在体外微核试验中，与同期对照组相比，1,2,3-TCP未表现出致突变活性。在碱性单细胞凝胶电泳试验（彗星试验）中，评估了1,2,3-TCP在有无S9混合物的孤立人类淋巴ocytes中的DNA断裂能力和细胞毒性。1,2,3-TCP诱导了DNA断裂。1,2,3-TCP被怀疑是人类的致癌物。
动物研究：将0.5 mL的1,2,3-TCP应用于兔子的完整皮肤，半封闭条件下4小时，封闭条件下24小时，产生了轻微的可逆性刺激。与这些测试结果相比，另一项研究根据Draize测试中兔子完整和磨损皮肤上的刺激分数将1,2,3-TCP归类为严重刺激物。在兔子眼中滴入0.1 mL未稀释的1,2,3-TCP后，观察到轻微到中度的刺激，所有效果在2-7天内可逆。大鼠和小鼠的中毒症状包括虚脱、活动减少、共济失调、镇静、呼吸困难、抽搐、流泪、流涎、眼睛和鼻粘膜刺激以及肝脏和肾脏损伤。立即呼吸抑制是死亡的常见原因。延迟死亡（7-10天后）归因于肝脏损伤。三只狗经口给予1,2,3-TCP后，1-2小时内出现中枢神经系统抑制，并在1-2天内死亡。连续7天吸入0.4和0.8 mg/立方米的1,2,3-TCP在大鼠肺中引起出血，支气管、支气管和肺泡上皮脱落和破坏。给予113或149 mg/kg的1,2,3-TCP饮用水的 rats for 13 weeks developed renal pyknosis, glomerular adhesions, and accumulated protein in the tubular lumen. Intermittent 4-hour exposures for 11 days at 3 ppm of 1,2,3-TCP caused a decreased thickness of olfactory epithelium in rats. 在10 ppm或更高浓度下，在大鼠中发现了嗅上皮的变性，而在小鼠中在10到13 ppm浓度下发现了炎症和嗅上皮厚度的减少，在更高浓度下出现变性。在长期动物研究中测试的140种致癌化学物质中，1,2,3-TCP是导致小鼠子宫肿瘤的七种化学物质之一（自发肿瘤率为0.3%）。NTP对1,2,3-TCP进行了为期2年的毒理学和致癌性研究。1,2,3-TCP在大小鼠的多个部位诱导了良性或恶性肿瘤。怀孕大鼠在整个着床和器官形成期间通过腹腔注射给予15剂37 mg/kg的1,2,3-TCP，后代没有出现胎毒或致畸效应，但母体毒性明显。雄性大鼠口服五剂80 mg/kg/天，没有出现睾丸毒性的证据。在一项单代繁殖研究中，后代指数未受到1,2,3-TCP处理的影响。雄性大鼠经胃管给予1,2,3-TCP，剂量为125 mg/kg体重/天，持续120天，结果显示相对睾丸重量显著增加，相对附睾重量显著减少。然而，没有观察到对精子计数或精子形态的影响，也没有观察到睾丸或附睾的组织形态学变化。在处理过的雌性大鼠与未处理过的雄性大鼠交配的后代中，观察到生存率的损害。1,2,3-TCP在含有代谢活化的沙门氏菌鼠伤寒菌株TA 97、TA 100和TA 1535以及E. coli WP2 uvr A的细菌测试系统中具有致突变性。1,2,3-TCP未在原代大鼠肝细胞中诱导非计划性DNA合成。它在L5178Y小鼠淋巴瘤细胞的胸腺嘧啶激酶位点上诱导基因突变，在中国仓鼠V79和卵巢细胞中诱导姐妹染色单体
IDENTIFICATION AND USE: 1,2,3-Trichloropropane (TCP) is a colorless liquid with a acrid, unpleasant. It is used as an intermediate in the synthesis of other chemicals (e.g., pesticides) and as a crosslinking agent in the production of polymers, such as polysulfides and hexafluoropropylene. Former uses include a solvent for hydrophobic compounds and resins, as a paint and varnish remover, and as a degreasing agent. HUMAN EXPOSURE AND TOXICITY: Vapors of 1,2,3-trichloropropane were found to be objectionable to subjects at a concentration of 100 ppm because of eye and throat irritation and unpleasant odor. It was noted that vapors of 1,2,3-TCP were acrid at 50 ppm. Acute/subchronic neurotoxic effects of 1,2,3-TCP include CNS damage in humans. Sporadic cases of toxic hepatic injury from 1,2,3-TCP in humans have been reported. In an in vitro micronucleus assay, 1,2,3-TCP did not exhibit mutagenic activity compared to the concurrent control. The DNA breakage capacity and the cytotoxicity was assessed in the alkaline single cell gel electrophoresis test (comet assay) with and without S9-mix in isolated human lymphocytes. 1,2,3-TCP induced DNA breakage. 1,2,3-TCP is a suspected human carcinogen. ANIMAL STUDIES: A dose of 0.5 mL of 1,2,3-TCP applied to the intact skin of rabbits for 4 hr under semi-occlusive and for 24 hr under occlusive dressings produced mild reversible irritation. In contrast to these test results, another study classified 1,2,3-TCP as severely irritating, based on irritation scores from a Draize test on intact and abraded skin of rabbits. After instillation of 0.1 mL of undiluted 1,2,3-TCP, mild to moderate irritation of rabbit eyes was observed, with all effects being reversible within 2-7 days. Symptoms of intoxication in rats and mice included prostration, hypoactivity, ataxia, sedation, dyspnea, convulsions, lacrimation, salivation, irritation of the mucosa of eyes and nose, and liver and kidney damage. Immediate respiratory depression was a frequent cause of death. Delayed deaths (after 7-10 days) were ascribed to liver damage. Three dogs that received intragastic administration of 1,2,3-TCP had CNS depression, within 1-2 hours, and died within 1-2 days. Continuous inhalation of 0.4 and 0.8 mg/cu m of 1,2,3-TCP for 7 days caused hemorrhages in rat lungs with desquamation and destruction of bronchial, bronchiolar & alveolar epithelium. Rats given 113 or 149 mg/kg 1,2,3-TCP in drinking water for 13 weeks developed renal pyknosis, glomerular adhesions, and accumulated protein in the tubular lumen. Intermittent 4-hour exposures for 11 days at 3 ppm of 1,2,3-TCP caused a decreased thickness of olfactory epithelium in rats. A degeneration of the olfactory epithelium was found in rats at 10 ppm or higher concentrations, and inflammation and decreased thickness of the olfactory epithelium were found in mice at 10 to 13 ppm with degeneration at higher concentrations. Among 140 carcinogenic chemicals tested in long-term animal studies, 1,2,3-TCP was among the seven producing uterine neoplasms in mice (spontaneous tumor rate 0.3%). 1,2,3-TCP was evaluated in 2-year toxicology and carcinogenesis studies by the NTP. 1,2,3-TCP induced benign and/or malignant neoplasms at multiple sites in both rats and mice. 15 daily doses of 37 mg/kg 1,2,3-TCP were given by intraperitoneal injection to pregnant rats throughout implantation and organogenesis; there were no fetotoxic or teratogenic effects in the offspring, but maternal toxicity was evident. Male rats given five oral doses of 80 mg/kg/day showed no evidence of testicular toxicity. In a one-generation reproduction study, progeny indices were unaffected by treatment with 1,2,3-TCP. Male rats administered 1,2,3-TCP by gavage at a dosage of 125 mg/kg body weight per day for 120 days showed significant increases in relative testes weights and a significant decrease in relative epididymis weight. However, no effects on sperm count or sperm morphology and no histomorphological changes of testes or epididymis were observed. Impairment of survival rates was observed among pups of treated females that had been mated with untreated males. 1,2,3-TCP is mutagenic in bacterial test systems with Salmonella typhimurium strains TA 97, TA 100, and TA 1535 and E. coli WP2 uvr A in the presence of metabolic activation. 1,2,3-TCP did not induce unscheduled DNA synthesis in primary rat hepatocytes. It induced gene mutation at the thymidine kinase locus in L5178Y mouse lymphoma cells, sister chromatid exchange in Chinese hamster V79 and ovary cells and chromosomal aberrations in Chinese hamster ovary cells, only in the presence of metabolic activation. Additionally, 1,2,3-TCP enhanced the transformation of Syrian hamster embryo cells by simian adenovirus SA7.
Evaluation: There is inadequate evidence in humans for the carcinogenicity of 1,2,3-trichloropropane. There is sufficient evidence in experimental animals for the carcinogenicity of 1,2,3-trichloropropane. Overall evaluation: 1,2,3-Trichloropropane is probably carcinogenic to humans (Group 2A). In making the overall evaluation, the working group took into account the following evidence: (1) 1,2,3-Trichloropropane causes tumors at multiple sites and at high incidence in mice and rats. (2) The metabolism of 1,2,3-trichloropropane is qualitatively similar in human and rodent microsomes. (3) 1,2,3-Trichloropropane is mutagenic to bacteria and to cultured mammalian cells and binds to the DNA of animals treated in vivo.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
A2：疑似人类致癌物。
A2: Suspected human carcinogen.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌性证据
1,2,3-三氯丙烷根据实验动物研究的充分致癌性证据，合理预期为人类致癌物。
1,2,3-Trichloropropane is reasonably anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity from studies in experimental animals.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
致癌物分类
国际癌症研究机构致癌物：1,2,3-三氯丙烷
IARC Carcinogenic Agent:1,2,3-Trichloropropane
来源:International Agency for Research on Cancer (IARC)
To investigate the disposition of 1,2,3-trichloropropane (TCP), [(14)C]-TCP was administered iv to male Fischer 344 rats. Unchanged TCP and total radiolabel were determined in tissues and excreta at varying intervals after administration. The compound was distributed and eliminated rapidly ... Adipose tissue accumulated 37% of the dose within 15 min and retained more of the dose than any other tissue until 4 hr; most (69%) of the radiolabel in adipose tissue through 4 hr was unchanged TCP. After 4 hr, the liver contained the largest fraction of the dose, primarily as metabolites. Thus TCP disappeared from adipose tissue while metabolites appeared in liver and other tissues. Excretion was nearly complete (90% of the dose) in 24 hr and was predominantly via the urine (47% of the dose). Expiration was the only route by which unchanged TCP (5% of the dose) was excreted. In addition, 25% of the dose was expired as carbon dioxide. There were numerous other metabolites, none accounting for more than 10% of the dose. Nonvolatile metabolites were longer lived than the parent compound. On the basis of high water solubility, reaction with 2,4-dinitrofluorobenzene, and diminished radiolabel in bile of glycidol-treated rats, glutathione conjugation is suggested as an important metabolic route for TCP ...
... Following acute oral exposure of male and female F344 rats (30 mg/kg) and male B6C3F1 mice (30 and 60 mg/kg), 1,2,3-trichloropropane was rapidly absorbed, metabolized, and excreted. The major route of excretion of 1,2,3-trichloropropane was in the urine. By 60 hr postdosing, rats had excreted 50% and mice 65% of the administered dose by this route. Exhalation as (14)C02 and excretion in the feces each accounted for 20% of the total dose in 60 hr rats and 20 and 15%, respectively, in mice. No apparent sex-related differences were observed in the ability of the rats to excrete 1,2,3-trichloropropane derived radioactivity. At 60 hr, 1,2,3-trichloropropane derived radioactivity was most concentrated in the liver, kidney, and forestomach in both rats and male mice. Male mice eliminated 1,2,3-trichloropropane derived radioactivity more rapidly than rats and lower concentrations of radioactivity were found in tissues 60 hr after dosing in mice. ...
Six hours post-treatment the highest radioactivity was found in the forestomach, in the small intestine and in adipose tissue of male rats. After 24 hours the highest radioactivity was still found in the forestomach, but also in the large intestine. No increased radioactivity was observed in adipose tissue of male and female rats. After 60 hours radioactivity was detected in the forestomach (highest value), and in the liver and kidney. The injection of 30 or 60 mg [(14)C] 1,2,3-TCP to B6C3F1 mice resulted in high radioactivity in the forestomach, the liver and kidney 60 hours post-treatment. 1,2,3-TCP distribution in tissues was not dose dependent.
ORGANIC ELECTROLUMINESCENCE DEVICE AND ANTHRACENE DERIVATIVE
申请人：IKEDA Hidetsugu
公开号：US20110034744A1
公开（公告）日：2011-02-10
An anthracene derivative having a specific asymmetric structure is provided. The asymmetric anthracenes are useful in an organic electroluminescence device and exhibit efficient light emission and a long performance lifetime.
PHENANTHRENE DERIVATIVE, AND MATERIAL FOR ORGANIC EL ELEMENT
申请人：Kawamura Masahiro
公开号：US20100331585A1
公开（公告）日：2010-12-30
A phenanthrene derivative is represented by a formula (1) below. In the formula (1), Ar
1
and Ar
2
each represent an aromatic hydrocarbon ring group having 6 to 18 carbon atoms for forming the ring. The aromatic hydrocarbon ring group contains none of anthracene skeleton, pyrene skeleton, aceanthrylene skeleton and naphthacene skeleton. R
1
represents a substituent, the number of which may be 0, 1 or more. R
1
may be bonded in any position of the phenanthrene skeleton. n and m each represent an integer of 1 to 3. k represents an integer of 0 to 8.
AROMATIC AMINE DERIVATIVE AND ORGANIC ELECTROLUMINESCENT DEVICE USING SAME
申请人：Idemitsu Kosan Co., Ltd.
公开号：EP1997799A1
公开（公告）日：2008-12-03
Provided are a novel aromatic amine derivative represented by the following general formula (1) and an organic electroluminescent device including an organic thin film formed of one or a plurality of layers including at least a light emitting layer interposed between a cathode and an anode, in which at least one layer of the organic thin film contains the aromatic amine derivative alone or as a component of a mixture, which contributes to suppressing molecular crystallization and improving yield in the production of an organic electroluminescent device, whereby an organic electroluminescent device having a long lifetime can be obtained, and the aromatic amine derivative is capable of realizing the organic electroluminescent device:
where: R1 represents an aryl group or the like; a represents an integer of 0 to 4; b represents an integer of 1 to 3; and at least one of Ar1 to Ar4 represents a group represented by the following general formula (2):
where Ar5 represents a fused aromatic ring group and Ar6 represents an aryl group or an aromatic heterocyclic group,
where remaining groups of Ar1 to Ar4, none of which is represented by the general formula (2), each independently represent an aryl group or an aromatic heterocyclic group.
PROCESS FOR THE PREPARATION OF 2,3,3,3 TETRAFLUOROPROPENE
申请人：Wendlinger Laurent
公开号：US20130267740A1
公开（公告）日：2013-10-10
The present invention provides a process for preparing 2,3,3,3-tetrafluoropropene, comprising the following steps: (a) catalytic reaction of 1,1,1,2,3-pentachloropropane and/or 1,1,2,2,3-pentachloropropane with HF into product 2-chloro-3,3,3-trifluoropropene; (b) catalytic reaction of the thus-obtained 2-chloro-3,3,3-trifluoropropene into 2,3,3,3-tetrafluoropropene.
[EN] PROCESS FOR PREPARING 1,1,2,3-TETRACHLOROPROPENE<br/>[FR] PROCÉDÉ DE SYNTHÈSE DE 1,1,2,3-TÉTRACHLOROPROPÈNE
申请人：DAIKIN IND LTD
公开号：WO2011065574A1
公开（公告）日：2011-06-03
The present invention provides a process for preparing 1,1,2,3-tetrachloropropene, including heating 1,1,1,2,3-pentachloropropane in a gas phase in the absence of a catalyst to carry out a dehydrochlorination reaction. According to the process of the present invention, 1,1,2,3-tetrachloropropene (HCC-1230xa) can be efficiently produced by a simple and economically advantageous method that is suitable for industrial-scale production.
