四氯化碳 | 56-23-5

• 分子结构分类: 有机化合物 - 有机卤素化合物 - 卤代烷
• 中文名称: 四氯化碳
• 中文别名: 四氯甲；四氯甲烷
• 英文名称: tetrachloromethane
• 英文别名: Carbon tetrachloride；CCl4；perchloromethane
• CAS: 56-23-5
• 化学式: CCl₄
• 分子量: 153.823
• InChiKey: VZGDMQKNWNREIO-UHFFFAOYSA-N

物化性质

• 熔点：
  -23 °C
• 沸点：
  76-77 °C
• 密度：
  1.59
• 蒸气密度：
  5.31 (vs air)
• 物理描述：
  Carbon tetrachloride appears as a clear colorless liquid with a characteristic odor. Denser than water (13.2 lb / gal) and insoluble in water. Noncombustible. May cause illness by inhalation, skin absorption and/or ingestion. Used as a solvent, in the manufacture of other chemicals, as an agricultural fumigant, and for many other uses.
• 颜色/状态：
  Liquid
• 气味：
  Sweet
• 溶解度：
  In water, 793 mg/L at 25 °C
• 蒸汽密度：
  5.3 (NTP, 1992) (Relative to Air)
• 蒸汽压力：
  115 mm Hg at 25 °C
• 亨利常数：
  0.03 atm-m3/mole
• 大气OH速率常数：
  1.20e-16 cm3/molecule*sec
• 稳定性/保质期：

  1. 稳定性：稳定。

  2. 禁配物：活性金属粉末、强氧化剂。

  3. 应避免接触的条件：潮湿空气、光照。

  4. 聚合危害：不发生聚合。

• 自燃温度：
  Not flammable (USCG, 1999)
• 分解：
  Hazardous decomposition products formed under fire conditions - Carbon oxides, hydrogen chloride gas.
• 粘度：
  2.03X10-3 Pa.s at 250.00 K
• 腐蚀性：
  Liquid carbon tetrachloride attacks some forms of plastics, rubber, and coatings.
• 燃烧热：
  37.3 kg cal/g mol wt at 20 °C
• 汽化热：
  3.45X10+7 J/kmol at 250-33 K
• 表面张力：
  3.23X10-2 N/m at 25.33 K
• 电离电位：
  11.47 eV
• 气味阈值：
  Odor recognition in air: 2.14X10 ppm (chemically pure)
• 折光率：
  Index of refraction: 1.4601 at 20 °C/D
• 相对蒸发率：
  Evaporation rate: 12.8 (butyl acetate = 1)
• 保留指数：
  645.7;652;657;660;662;667;673;680;672;669;659;653.3;661;648.5;658;663;654.5;656.4;661;658;645;645;654;659;661;645;645;654.6;646;658;672;673;659;649

计算性质

• 辛醇/水分配系数(LogP)：
  2.8
• 重原子数：
  5
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  0
• 氢给体数：
  0
• 氢受体数：
  0

ADMET

代谢

禁食的雄性大鼠被给予了六种剂量的^14^ ，范围从非肝毒性的（0.1毫摩尔/千克）到严重肝毒性的（26毫摩尔/千克）。通过在8-12小时内以15分钟为间隔测量呼气中恢复的量，监测了CCl4、^14^ 和CHCl3通过呼出消除的时间过程和药代动力学。还确定了24小时内与肝脏大分子结合的^14^C标记代谢物恢复的量，以及24小时内通过尿液或粪便排出的量。用^14^ 和Na2^14^CO3进行了比较药代动力学研究。在所有剂量的^14^ 之后，主要的代谢物是CO2，与肝脏大分子结合的代谢物恢复量是 的二十到三十倍，而中等量的代谢物通过尿液和粪便排出。在低剂量的 时， 是最不丰富的代谢物，但在高剂量时，它是第二丰富的代谢物。在24小时时肝脏损伤的程度（以血清谷氨酸-丙酮酸转氨酶活性量化）与 通过产生 和 的代谢途径的量或速率之间的关联比通过产生肝脏结合的^14^C-代谢物或尿液排出的代谢途径的关联更强。时间过程和药代动力学数据表明，在给予肝毒性剂量的 后2小时内，导致 的主要 代谢途径受到损害。

Fasted male rats were given six doses of (14)CCl4 ranging from non-hepatotoxic (0.1 mmole/kg) to severely hepatotoxic (26 mmoles/kg). Time-course and pharmacokinetics of CCl4, (14)CO2 and CHCl3 elimination by exhalation were monitored by measuring amounts recovered in breath during discrete 15-min intervals for 8-12 hr. Amounts of (14)C-labeled metabolite recovered bound to liver macromolecules at 24 hr and excreted in urine or feces for 24 hr were also determined. Comparison pharmacokinetic studies were done with (14)CHCl3 and Na(2)14CO3. After all doses of (14)CCl4, the major metabolite was CO2, twenty to thirty times less metabolite was recovered bound to liver macromolecules, and intermediate amounts of metabolite were excreted in urine and feces. CHCl3 was the least abundant metabolite at low CCl4 doses, but the second most abundant at high doses. Stronger associations were found between the magnitude of liver injury at 24 hr (quantitated as serum glutamate-pyruvate transaminase activity) and the extent or rate of CCl4 metabolism by pathways leading to CO2 and CHCl3 than by pathways leading to (14)C-metabolites bound in liver or excreted in urine. Time-course and pharmacokinetic data indicated that a major pathway of CCl4 metabolism leading to CO2 became impaired within 2 hr after administration of hepatotoxic doses of CCl4.

来源:Hazardous Substances Data Bank (HSDB)

代谢

没有研究全面比较了四氯化碳（CCl4）在不同物种中的代谢速率。因此，使用在封闭、循环气体摄取系统中暴露于40-1800 ppm 的雄性动物组（F344大鼠、B6C3F1小鼠和叙利亚仓鼠）来评估 的体内代谢。对于每个物种，通过调整米氏-门登代谢常数Km（亲和力）和Vmax（容量）使用基于生理学的药代动力学（PBPK）模型，获得了摄取曲线族的优化拟合。结果显示，与大鼠相比，小鼠对 的代谢能力略高，亲和力较低，而仓鼠的代谢能力高于大鼠和小鼠，亲和力较低。将Vmax与Km的比值，按每毫克肝蛋白（L/hr/mg）进行物种间标准化，表明仓鼠比大鼠或小鼠代谢更多的 ，并且应该更易受到 诱导的肝毒性影响。这些物种比较针对通过鼻部吸入20 ppm (14)C标记的 4小时暴露的动物进行的毒代动力学研究进行了评估。毒代动力学研究结果与体内代谢速率一致，与大鼠相比，仓鼠和小鼠消除了更少的与代谢相关的放射性（(14)CO2和尿液/粪便），而与母体化合物相关的放射性（被困在活性炭上的放射性）更多。在这里确定的体内代谢常数，连同使用大鼠、小鼠、仓鼠和人肝微体测定的体外常数，用于估计人体的体内代谢速率分别为1.49 mg/hr/kg体重和0.25 mg/L用于Vmax和Km。按每毫克肝蛋白标准化代谢速率（Vmax/Km）， 的代谢速率在物种间有所不同，仓鼠>小鼠>大鼠>人类。

No study has comprehensively compared the rate of metabolism of carbon tetrachloride (CCl4) across species. Therefore, the in vivo metabolism of CCl4 was evaluated using groups of male animals (F344 rats, B6C3F1 mice, and Syrian hamsters) exposed to 40-1800 ppm CCl4 in a closed, recirculating gas-uptake system. For each species, an optimal fit of the family of uptake curves was obtained by adjusting Michaelis-Menten metabolic constants Km (affinity) and Vmax (capacity) using a physiologically based pharmacokinetic (PBPK) model. The results show that the mouse has a slightly higher capacity and lower affinity for metabolizing CCl4 compared to the rat, while the hamster has a higher capacity and lower affinity than either rat or mouse. A comparison of the Vmax to Km ratio, normalized for milligrams of liver protein (L/hr/mg) across species, indicates that hamsters metabolize more CCl4 than either rats or mice, and should be more susceptible to CCl4-induced hepatotoxicity. These species comparisons were evaluated against toxicokinetic studies conducted in animals exposed by nose-only inhalation to 20 ppm (14)C-labeled CCl4 for 4 hr. The toxicokinetic study results are consistent with the in vivo rates of metabolism, with rats eliminating less radioactivity associated with metabolism ((14)CO2 and urine/feces) and more radioactivity associated with the parent compound (radioactivity trapped on charcoal) compared to either hamsters or mice. The in vivo metabolic constants determined here, together with in vitro constants determined using rat, mouse, hamster, and human liver microsomes, were used to estimate human in vivo metabolic rates of 1.49 mg/hr/kg body weight and 0.25 mg/L for Vmax and Km, respectively. Normalizing the rate of metabolism (Vmax/Km) by milligrams liver protein, the rate of metabolism of CCl4 differs across species, with hamster > mouse > rat > human.

来源:Hazardous Substances Data Bank (HSDB)

代谢

为了使用基于动脉血：空气浓度比的吸入药物动力学方法估计活体内四氯化碳（CCl4）的代谢速率，我们测定了雄性、未经处理的大鼠在吸入空气中不同浓度四氯化碳（Cinh）暴露5小时后血液中四氯化碳浓度（Cart）的值，以及在暴露前24小时通过口服给药100或200微升/100克体重的四氯化碳预处理的大鼠。在暴露期间和暴露结束时，还测定了肝脏细胞色素P-450的含量。未经处理的大鼠的Cart-Cinh曲线呈现双相性质，在Cinh约为100 ppm时出现转变，表明在100 ppm以下时四氯化碳的代谢受到灌注限制，在100 ppm以上时则达到饱和。在100微升四氯化碳预处理的大鼠中，转变点的Cinh从100降低到50 ppm；这一百分比的降低与通过给药100微升四氯化碳引起的细胞色素P-450含量的降低一致。在200微升四氯化碳预处理的大鼠中，四氯化碳代谢酶活性被完全抑制，Cart-Cinh曲线呈现单一直线，斜率比未经处理的大鼠曲线的较陡部分更浅，反映了在暴露期间细胞色素P-450含量的丧失。计算得出的摄取速率曲线显示，在完全抑制的大鼠中继续摄取，这代表了仅脂肪负荷的贡献。代谢速率通过未经处理的大鼠的摄取速率减去200微升四氯化碳预处理的大鼠的摄取速率来近似，并随着Cinh的增加在可饱和代谢范围内逐渐降低。从这一速率曲线中，未经处理的大鼠的Vmax和Km分别为2.7 mg/kg/hr和大约0.3 mg/liter。代谢速率的逐渐降低可以用细胞色素P-450含量的迅速丧失来解释。100微升四氯化碳预处理的大鼠的Vmax下降了约57%，这与细胞色素P-450含量的下降非常一致。这些实验表明，这种方法对于研究挥发性化合物的代谢是有用和有效的。

To estimate the rate of CCl4 metabolism in vivo by using an inhalation pharmacokinetic approach based on arterial blood:air concentration ratios, the blood CCl4 concentrations (Cart) at the end of 5-hr exposure to varying concentrations of CCl4 in inhaled air (Cinh) were determined in male, naive rats and in rats pretreated with po administration of 100 or 200 microliters CCl4/100 g body weight 24 hr before exposure. Hepatic cytochrome P-450 content during and at the end of exposure was also determined. The biphasic nature of the Cart-Cinh curve for naive rats, with a transition at Cinh of about 100 ppm, indicated that CCl4 metabolism is perfusion-limited below 100 ppm and is saturated above 100 ppm. In 100 microliters CCl4-pretreated rats, Cinh at the transition point decreased from 100 to 50 ppm; this percentage decrease was consistent with the decreased cytochrome P-450 content induced by administration of 100 microliters CCl4. In 200 microliters CCl4-pretreated rats, where CCl4 metabolizing enzyme activity was completely inhibited, the Cart-Cinh curve gave a single line with a shallower slope than that of the steeper part of the curve for naive rats, reflecting a loss of cytochrome P-450 content during exposure. The curves of calculated uptake rate showed continued uptake in completely inhibited rats, representing the contribution of fat loading only. The rate of metabolism was approximated by the uptake rate for naive rats minus that for 200 microliters CCl4-pretreated rats, and decreased gradually with increasing Cinh over the range of saturable metabolism. From this rate curve, Vmax and Km for naive rats were 2.7 mg/kg/hr and of the order of 0.3 mg/liter, respectively. The gradual decrease in the rate of metabolism could be interpreted in terms of the rapid loss of cytochrome P-450 content. The Vmax for 100 microliters CCl4-pretreated rats decreased by about 57%, which was in good agreement with the decrease of cytochrome P-450 content. These experiments suggest the usefulness and validity of this approach for studying metabolism of a volatile compound.

来源:Hazardous Substances Data Bank (HSDB)

代谢

肝组织将四氯化碳还原为氯仿，并且有人提出碳-氯键的均裂会产生自由基，这些自由基随后能够烷基化酶的巯基团。

Liver tissue reduces carbon tetrachloride to chloroform, and it was suggested that homolytic cleavage of carbon-chlorine bond yields free radicals which can then alkylate the sulfhydryl groups of enzymes.

来源:Hazardous Substances Data Bank (HSDB)

代谢

四氯化碳能够轻易地从消化系统和呼吸系统中被吸收，通过皮肤吸收的速度较慢。它分布到所有主要器官，在脂肪、肝脏、骨髓、肾上腺、血液、大脑、脊髓和肾脏中浓度最高。一旦四氯化碳被吸收，它就会被细胞色素P-450酶代谢，产生三氯甲基自由基。在有氧条件下，三氯甲基自由基的代谢最终可以形成光气。在无氧条件下，该自由基可以发生反应形成氯仿、六氯乙烷或一氧化碳。四氯化碳主要通过呼出的空气和粪便排出，尿液中的相对含量较少。(L129)

Carbon tetrachloride is absorbed readily from the gastrointestinal and respiratory tracts, and more slowly through the skin. It is distributed to all major organs, with highest concentrations in the fat, liver, bone marrow, adrenals, blood, brain, spinal cord, and kidney. Once carbon tetrachloride is absorbed, it is metabolized by cytochrome P-450 enzymes, with the production of the trichloromethyl radical. Aerobically, metabolism of the trichloromethyl radical can eventually form phosgene. Anaerobically, the radical can undergo reactions to form chloroform, hexachloroethane, or carbon monoxide. Carbon tetrachloride is excreted primarily in exhaled air and in the feces, with relatively minimal amounts in the urine. (L129)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 毒性总结

四氯化碳是一种无色、重的液体。它被用作制冷剂、金属去油、氯化有机化合物、生产半导体以及作为溶剂（脂肪、油、橡胶等）。它曾经被用作驱虫剂。人体研究：过度暴露的潜在症状包括中枢神经系统抑制、嗜睡、眩晕、不协调、恶心和呕吐，以及肝脏和肾脏损伤。直接接触可能引起皮肤和眼睛刺激，并通过脱脂作用引起皮炎。肝脏损伤出现在24小时或更长时间后。肾脏损伤在中毒后往往仅在2到3周内明显。三份病例报告描述了患有肝硬化的患者出现肝肿瘤，这些患者曾经暴露于四氯化碳。四氯化碳通过其代谢中间产物与高分子和脂质过氧化发生共价结合。在利用人淋巴细胞的短期体外系统中，四氯化碳没有表现出DNA损伤活性。动物研究：肝脏和肾脏是四氯化碳毒性的靶器官。对肝脏的影响的严重程度取决于多种因素，如物种的易感性、暴露的途径和方式、饮食或共暴露于其他化合物，尤其是乙醇。此外，用各种化合物预处理，如苯巴比妥和维生素A，会增强肝脏毒性，而其他化合物，如维生素E，会减少四氯化碳的肝脏毒性。经皮应用后观察到中等刺激性，并且在兔眼应用后出现轻度反应。在孕晚期给予单剂量150毫克/动物的四氯化碳后，怀孕小鼠的胎儿死亡率增加。死亡原因是外周循环衰竭，主要是由于胎儿肝脏损伤。此外，在胎盘中发现了循环障碍和坏死，这也可能是导致胎儿死亡的原因。四氯化碳对经口、皮下或吸入暴露的大鼠没有致畸性。在肝脏损伤明显的剂量水平下，四氯化碳在大鼠中产生了睾丸毒性。在吸入200和400 ppm的25周后，雄性大鼠睾丸中的生殖细胞退化，伴有肝脏毒性和高死亡率。当四氯化碳以1.5毫克/千克的剂量水平ip给药时，在大鼠中也观察到了睾丸损伤。单次注射导致睾丸萎缩，睾丸和精囊重量减轻，以及异常精子发生的组织学证据。四氯化碳可能具有改变男性生育能力的雌激素性质。其雌激素活性表现为（a）抑制未成熟雌性大鼠肝脏微粒体对雌激素的羟基化，（b）增强雌激素的子宫肥大反应，（c）增加雌激素子宫摄取。四氯化碳在细菌中不具有诱变性。在几乎致死的剂量下，它在酵母中具有诱变性。它没有诱导培养的大鼠肝脏上皮细胞染色体损伤，也没有在大鼠体内暴露时诱导肝细胞的不定期DNA合成。四氯化碳在小鼠和大鼠中诱导了肝细胞瘤和肝细胞癌。诱导肝肿瘤的剂量高于诱导细胞毒性的剂量。生态毒理学研究：四氯化碳对几种鱼类和两栖类动物的胚胎-幼体阶段的毒性要比对成体大得多。

IDENTIFICATION AND USE: Carbon tetrachloride is a colorless, heavy liquid. It is used in refrigerants, metal degreasing, in chlorinating organic compounds, in the production of semiconductors, and as a solvent (fats, oils, rubber, etc). It was formerly used as anthelmintic. HUMAN STUDIES: Potential symptoms of overexposure are CNS depression, drowsiness, dizziness, incoordination, nausea, and vomiting as well as liver and kidney injury. Direct contact may cause skin and eye irritation, and dermatitis through defatting action. Liver damage appears after 24 hrs or more. Kidney damage is evident often only 2 to 3 weeks following the poisoning. Three case reports describe the occurrence of liver tumors associated with cirrhosis in people who had been exposed to carbon tetrachloride. Covalent binding to macromolecules and lipid peroxidation occur via metabolic intermediates of carbon tetrachloride. Carbon tetrachloride did not demonstrate the DNA damaging activity in a short-term in vitro system which utilized human lymphocytes. ANIMAL STUDIES: The liver and kidney are target organs for carbon tetrachloride toxicity. The severity of the effects on the liver depends on a number of factors such as species susceptibility, route and mode of exposure, diet or co-exposure to other compounds, in particular ethanol. Furthermore, pretreatment with various compounds, such as phenobarbital and vitamin A, enhances hepatotoxicity, while other compounds, such as vitamin E, reduce the hepatotoxic action of carbon tetrachloride. Moderate irritation after dermal application was seen and there was a mild reaction after application into the rabbit eye. Increased fetal mortality was observed in pregnant mice given single doses of 150 mg carbon tetrachloride per animal during the last part of pregnancy. Cause of death was failure of peripheral circulation, mainly due to fetal liver damage. Moreover, circulatory disturbances and necroses were found in the placentas, which probably also contributed to the death of the fetuses. Carbon tetrachloride was not teratogenic to rats exposed orally, subcutaneously, or via inhalation. Carbon tetrachloride produced testicular toxicity in the rat at dose levels where hepatic damage is evident. After 25 wk of inhalation exposure to 200 and 400 ppm, male rats show germ cell degeneration in the testes along with liver toxicity and a high mortality rate. Testicular damage was also observed in rats when carbon tetrachloride was administered ip at a dose level of 1.5 mg/kg. A single injection caused testicular atrophy, a decrease in testes and seminal vesicle weights, and histological evidence of abnormal spermatogenesis. Carbon tetrachloride may have estrogenic properties that can alter male fertility. Its estrogenicity is evidenced by (a) inhibition of hepatic microsomal hydroxylation of estrogens in immature female rats, (b) potentiation of the uterotrophic responses of estrogens, and (c) increased estrogen uterine uptake. Carbon tetrachloride was not mutagenic in bacteria. It was mutagenic in yeast at almost lethal doses. It did not induce chromosomal damage in cultured rat liver epithelial cells and did not induce unscheduled DNA synthesis in the hepatocytes of rats exposed in vivo. Carbon tetrachloride induced hepatomas and hepatocellular carcinomas in mice and rats. The doses inducing hepatic tumors were higher than those inducing cell toxicity. ECOTOXICITY STUDIES: Carbon tetrachloride is considerably more toxic to the embryo-larval stages of several species of fish and amphibians than it is to the adults.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 毒性总结

未代谢的四氯化碳会抑制中枢神经系统。四氯化碳的所有其他毒性作用都与它通过细胞色素P-450酶，特别是CYP2E1的生物转化有关。四氯化碳通过CYP2E1的代谢可能会导致在代谢过程中酶的破坏，要么是通过自由基直接攻击细胞色素，要么是高度局部的脂质过氧化导致P-450蛋白从微粒体膜上脱落。四氯化碳的反应性代谢物通过细胞大分子和脂质过氧化的卤代烷基化作用导致肝脏损伤。四氯化碳还会干扰细胞内钙稳态。细胞质中钙的增加可能是由于质膜损伤导致的细胞外钙流入和细胞内钙隔离减少。较高的钙水平激活了如蛋白酶等酶，这些酶水解邻近细胞中的蛋白质，导致病变的进展。四氯化碳的致癌性可能是由于某些反应性代谢物与核蛋白、脂质和DNA结合的结果。（T10，L129）

Unmetabolized carbon tetrachloride, depresses the central nervous system. All other toxic effects of carbon tetrachloride are related to its biotransformation via cytochrome P-450 enzymes, specifically CYP2E1. Metabolism of carbon tetrachloride by CYP2E1 may result in the destruction of the enzyme during the metabolic process, either by direct attack of radicals on the cytochrome(s) or highly localized lipid peroxidation resulting in detachment of P-450 proteins from the microsomal membranes. Reactive metabolites of carbon tetrachloride causes hepatic damage via haloalkylation of cellular macromolecules and lipid peroxidation. Carbon tetrachloride also perturbs the intracellular calcium homeostasis. Increased cytosolic levels of calcium may result from an influx of extracellular calcium caused by plasma membrane damage and decreased intracellular calcium sequestering. Higher levels of calcium activate enzymes such as proteases, which hydrolyze proteins in neighboring cells, leading to a progression of the lesion. Carbon tetrachloride's carcinogenicity is likely the result of certain reactive metabolites that bind to nuclear proteins, lipids, and DNA. (T10, L129)

来源:Toxin and Toxin Target Database (T3DB)

毒理性

• 致癌性证据

根据《致癌风险评估指南》(美国环保局, 2005a), 四氯化碳“可能对人类具有致癌性”, 基于以下两点:(1) 人类致癌性的证据不足, (2) 通过口服和吸入暴露在动物中具有充分的致癌性证据, 即多个物种(大鼠、小鼠和仓鼠)的肝脏肿瘤和鼠的嗜铬细胞瘤(肾上腺肿瘤)。

Under the Guidelines for Carcinogen Risk Assessment (U.S. EPA, 2005a), carbon tetrachloride is "likely to be carcinogenic to humans" based on: (1) inadequate evidence of carcinogenicity in humans and (2) sufficient evidence in animals by oral and inhalation exposure, i.e., hepatic tumors in multiple species (rat, mouse, and hamster) and pheochromocytomas (adrenal gland tumors) in mice.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 致癌性证据

评估：对于四氯化碳对人类致癌性的证据不足。对于四氯化碳对实验动物致癌性的证据是充分的。总体评估：四氯化碳可能对人类致癌（2B组）。

Evaluation: There is inadequate evidence in humans for the carcinogenicity of carbon tetrachloride. There is sufficient evidence in experimental animals for the carcinogenicity of carbon tetrachloride. Overall evaluation: Carbon tetrachloride is possibly carcinogenic to humans (Group 2B).

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 致癌性证据

A2; 可疑的人类致癌物

A2; Suspected human carcinogen

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

这篇论文报告了一位75岁的白人男性因摄入了未知量的四氯化碳（CCl4）——一种能诱导中枢神经系统抑制和严重的肾脏及肝脏损害的有毒物质——在两天重症监护后死亡的事件。采用气相色谱-火焰离子化检测（GC-FID）顶空法对 浓度进行了分析评估。尿液（328.5 mg/L）和胆汁（169.8 mg/L）中的 浓度很高，这证明了四氯化碳会通过尿液和胆汁广泛排泄。与肺部的高清除能力一致，全身静脉血（143.4 mg/L）中的 浓度几乎是动脉血（57.5 mg/L）的两倍半，这表明静脉血是将 血浓度与昏迷深度相关联的最佳样本。玻璃体液（170.5 mg/L）中的 浓度证明了这种化学物质能够进入眼睛，并且相对缓慢地释放到全身血液中。胰腺（657.9 mg/kg）、大脑（243 mg/kg）和睾丸（237.3 mg/kg）对 有很大的亲和力。大脑中 的浓度如下：皮层：243.2 mg/kg，基底神经节：216.1 mg/kg，延髓：243.3 mg/kg，小脑：175.3 mg/kg。由于昏迷深度与 浓度相关，大脑是毒理分析最合适的组织。肺部（127.3 mg/kg）、肾脏（150.5 mg/kg）、肌肉（71.1 mg/kg）、心肌（78.5 mg/kg）和脾脏（68.3 mg/kg）中的 浓度较低。肝脏（58.6 mg/kg），作为法医毒理学中经常分析的组织，显示出最低的浓度。

This paper reports a fatality involving a 75-year-old white male, who ingested an unknown quantity of carbon tetrachloride (CCl4) - a toxic agent able to induce central nervous system depression and severe renal and hepatic damage - and who died after two days of intensive care. The analytical assessment of CCl4 concentration was performed on several biological fluids and tissues employing gas chromatography-flame ionization detection (GC-FID) head space method. Both urine (328.5 mg/L) and bile (169.8 mg/L) had high concentrations of CCl4, proving that the chemical undergoes extensive urinary and biliary excretion. In accordance with the high clearance power of lungs, systemic venous blood, (143.4 mg/L) had a concentration of CCl4 almost two and half times greater than in arterial blood (57.5 mg/L), representing the best specimen to correlate CCl4 blood concentration with the deep of narcosis. Vitreous humor, (170.5 mg/L) concentration of CCl4 proves the capability of the chemical to enter eyes and its relatively slow release into the systemic blood. Pancreas (657.9 mg/kg), brain (243 mg/kg) and testis (237.3 mg/kg) have great affinity for CCl4. The concentrations of the chemical in brain are cortex: 243.2 mg/kg, basal ganglia: 216.1 mg/kg, medulla oblongata: 243.3 mg/kg and cerebellum: 175.3 mg/kg. As the depth of narcosis is correlated with CCl4 concentration, brain represents the most suitable tissue for toxicologic analysis. Lower concentrations of the chemical are found in lungs (127.3 mg/kg), kidneys (150.5 mg/kg), muscle (71.1 mg/kg), myocardium (78.5 mg/kg) and spleen (68.3 mg/kg). Liver (58.6 mg/Kg), a frequently analyzed tissue in forensic toxicology, shows the lowest concentration.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

四氯化碳（CCl4）的目标器官毒性、毒性机制和代谢过程已经被广泛研究。然而，关于其消除的信息却相对匮乏。先前的吸入研究表明，暴露于(14) 的大鼠和猴子粪便中出现了大量的(14)C。粪便中排泄的化合物(s)尚未得到很好的表征。对于许多抵抗代谢的亲脂性化合物来说，粪便排泄是消除的一个主要途径。这些化合物排泄的一种机制是从血液直接到肠腔的排泄。本研究的主要目的是确定粪便排泄是否对 的消除有显著贡献。次要目的是确定 及其代谢物(s)在Sprague-Dawley大鼠中的粪便排泄机制（胆汁和非胆汁，即直接排泄）。结果表明，在单次静脉注射（1 mmol/kg）后，胆汁和非胆汁机制都参与了 的粪便排泄，但这一途径只占给药剂量的不到1%。结果还表明，无论是在急性处理（静脉注射或腹腔注射）还是重复吸入暴露后， 都不会在粪便中以原形被消除。粪便排泄对 的整体消除没有显著贡献。

The target organ toxicity, mechanisms of toxicity, and metabolism of carbon tetrachloride (CCl4) have been studied extensively. However, there is a paucity of information concerning its elimination. Previous inhalation studies showed that a significant amount of (14)C appeared in the feces of rats and monkeys exposed to (14)CCl4. The nature of the compound(s) excreted in the feces has not been well characterized. Fecal excretion is a major route of elimination for many lipophilic compounds that are resistant to metabolism. A mechanism of excretion for these compounds is the direct exsorption from the blood to the lumen of the intestinal tract. The primary purpose of this study was to determine if fecal elimination contributes significantly to the elimination of CCl4. The secondary purpose was to determine the mechanism (biliary and/or nonbiliary, i.e., direct exsorption) of fecal elimination of CCl4 and/or its metabolite(s) in Sprague-Dawley rats. The results indicate that both biliary and nonbiliary mechanisms contribute to the fecal elimination of CCl4 following a single iv dose (1 mmol/kg), but this route accounts for less than 1% of the administered dose. The results also indicate that CCl4 is not eliminated unchanged in the feces following either acute treatment (iv or ip) or repeated inhalation exposures. Fecal elimination of CCl4 does not significantly contribute to the overall elimination of CCl4.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

四氯化碳（CCl4）对其肝毒性影响已进行了广泛研究。然而，关于其通过不同途径给药和暴露模式后组织沉积的信息却很少。本研究的主要目的是阐明四氯化碳在大鼠体内的摄取、分布和消除，这些大鼠接受了等效的口服和吸入暴露。体重325-375克的雄性Sprague-Dawley大鼠暴露于1000 ppm 2小时。其他组的大鼠通过单次口服给药或持续胃灌注2小时的方式给予总吸收剂量（179 mg /kg bw）。在暴露期间和暴露后选择时间点处死动物，并移除肝脏、肾脏、肺、脑、脂肪、骨骼肌、脾脏、心脏和胃肠道等组织，通过顶空气相色谱法测量其 含量。与口服给药和吸入组相比，胃灌注组的所有组织中 水平要低得多。吸入导致相对较高的组织 浓度，因为吸入的化学物质进入动脉循环并被输送到全身的器官。似乎合乎逻辑的是，肝脏在摄入后应该比吸入后积累更多的 。然而，当比较胃灌注组和吸入组的肝脏AUC值时，并未证明这一点。胃灌注组动物肝脏中显著较低的 浓度似乎是由于在2小时灌注期间进入肝脏的相对较小量的 非常迅速地被代谢清除。有人假设，如果 作为单一的大剂量口服给药，可能会超过肝脏和肺部的首次通过消除能力。确实，与胃灌注组相比，口服给药组所有组织的 沉积更多。 的摄取和消除的时间过程似乎主要受组织的血液灌注率和脂质含量的影响。例如，大脑和肝脏迅速摄取 。然后这些器官的 含量减少，因为 被代谢并重新分布到脂肪组织。 在脂肪中积累缓慢，但浓度非常高，并保持升高很长一段时间。因此，某些组织的 浓度可能并不反映血液水平。对于 急性肝毒性的最合适的内部剂量测量指标似乎是从0到30分钟的组织浓度与时间曲线下的面积。组织时间过程数据集对于完善和验证 和其他挥发性有机化学物的生理模型至关重要。

Carbon tetrachloride (CCl4) has been studied extensively for its hepatotoxic effects. There is a paucity of information, however, about its tissue deposition following administration by different routes and patterns of exposure. The specific objective of this study was to delineate the uptake, distribution, and elimination of CCl4 in tissues of rats subjected to equivalent oral and inhalation exposures. Male Sprague-Dawley rats (325-375 g) were exposed to 1000 ppm CCl4 for 2 hr. The total absorbed dose (179 mg CCl4/kg bw) was administered to other groups of rats as a single oral bolus or by constant gastric infusion over a period of 2 hr. Animals were terminated at selected time intervals during and post-exposure and tissues (liver, kidney, lung, brain, fat, skeletal muscle, spleen, heart, and GI tract) removed for measurement of their CCl4 content by headspace gas chromatography. CCl4 levels in all tissues were much lower in the gastric infusion group than in the oral bolus and inhalation groups. Inhalation resulted in relatively high tissue CCl4 concentrations, because inhaled chemicals enter the arterial circulation and are transported directly to organs throughout the body. It seems logical that the liver should accumulate more CCl4 following ingestion than following inhalation. This did not prove to be the case when comparing liver AUC values for the gastric infusion and inhalation groups. Substantially lower CCl4 concentrations in the liver of animals in the gastric infusion group appeared to be due to very rapid metabolic clearance of the relatively small amounts of CCl4 entering the liver over the 2-hr infusion period. It was hypothesized that the capacity of first-pass hepatic and pulmonary elimination could be exceeded, if CCl4 were given as a single, large oral bolus. Indeed, deposition of CCl4 in all tissues was greater in the oral bolus group than in the gastric infusion group. The time courses of uptake and elimination of CCl4 appeared to be governed largely by a tissue's rate of blood perfusion and lipid content. CCl4 was rapidly taken up, for example, by the brain and liver. These organs' CCl4 content then diminished, as CCl4 was metabolized and redistributed to adipose tissue. CCl4 accumulated slowly, but to very high concentrations, in fat and remained elevated for a prolonged period. Thus, concentrations of CCl4 in some tissues may not be reflective of blood levels. The most appropriate measure of internal dose for CCl4 acute hepatotoxicity appears to be the area under tissue concentrations versus time curve from 0 to 30 min. Tissue time-course data sets are essential for the refinement and validation of physiological models for CCl4 and other volatile organic chemicals.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

(14)C-四氯化碳（CCl4）在经口给予肝毒性剂量后3小时大量进入肝脏，少量进入大脑。尽管在给予 后12小时，肝脏匀浆中的硫代巴比妥酸（TBA）增加了，但大脑的TBA值几乎没有变化，这可能是因为大脑中细胞色素P-450和b5的水平非常低。这些结果表明， 对大脑没有直接的毒性作用。

[(14)C]-Carbon tetrachloride (CCl4) entered extensively into the liver and, to the small extent, into the brain 3 hr following the intragastric administration of the hepatotoxic dose. Although thiobarbituric acid (TBA) in the liver homogenates increased 12 hr after CCl4 administration, the brain showed little TBA values probably due to very low levels of chytochromes P-450 and b5 in the brain. These results suggest that CCl4 have no direct toxic effect upon the brain.

来源:Hazardous Substances Data Bank (HSDB)

安全信息

• 危险等级：
  6.1
• 危险品标志：
  T,N
• 安全说明：
  S23,S36/37,S45,S59,S61
• 危险类别码：
  R52/53,R40,R48/23,R59,R23/24/25
• WGK Germany：
  3
• 海关编码：
  2903140090
• 危险品运输编号：
  UN 1846 6.1/PG 2
• 危险类别：
  6.1(a)
• RTECS号：
  FG4900000
• 包装等级：
  II
• 储存条件：
  储存注意事项：应将物品储存在阴凉通风的库房中，远离火源和热源，确保库温不超过32℃，相对湿度不超过80%。保持容器密封，并与氧化剂、活性金属粉末及食用化学品分开存放，切忌混合存储。储存区域应配备泄漏应急处理设备和合适的收容材料。

SDS

Name:	Carbon Tetrachloride, 99+%, Spectrophotometric Grade Material Safety Data Sheet
Synonym:	Tetrachloromethane; Carbon tet; Carbona; Carbon chloride; Methane tetrachloride.
CAS:	56-23-5

Section 1 - Chemical Product MSDS Name: Carbon Tetrachloride, 99+%, Spectrophotometric Grade Material Safety Data Sheet
Synonym: Tetrachloromethane; Carbon tet; Carbona; Carbon chloride; Methane tetrachloride.

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SECTION 2 - COMPOSITION, INFORMATION ON INGREDIENTS

CAS#	Chemical Name	content	EINECS#
56-23-5	Carbon Tetrachloride	>99	200-262-8

Hazard Symbols: T N
Risk Phrases: 23/24/25 40 59 48/23 52/53

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SECTION 3 - HAZARDS IDENTIFICATION EMERGENCY OVERVIEW Toxic by inhalation, in contact with skin and if swallowed. Limited evidence of a carcinogenic effect. Dangerous for the ozone layer.
Toxic : danger of serious damage to health by prolonged exposure through inhalation. Harmful to aquatic organisms; may cause long-term adverse effects in the aquatic environment.Cancer suspect agent. Potential Health Effects
Eye:
Causes eye irritation. Vapors cause eye irritation.
Skin:
Causes skin irritation. May be absorbed through the skin in harmful amounts. Contact with the skin defats the skin.
Ingestion:
May cause liver and kidney damage. May cause central nervous system depression, characterized by excitement, followed by headache, dizziness, drowsiness, and nausea. Advanced stages may cause collapse, unconsciousness, coma and possible death due to respiratory failure. Substance is a hepatotoxin and is capable of producing a toxic effect on the liver.
Inhalation:
May cause liver and kidney damage. Exposure produces central nervous system depression. May be harmful if inhaled.
Chronic:
Prolonged or repeated skin contact may cause dermatitis. Chronic ingestion may cause effects similar to those of acute ingestion. May cause liver and kidney damage. May cause cancer according to animal studies. Chronic exposure may cause visual disturbances. Carbon tetrachloride is a CNS depressant.

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SECTION 4 - FIRST AID MEASURES
Eyes:
In case of contact, immediately flush eyes with plenty of water for at least 15 minutes. Get medical aid.
Skin:
In case of contact, immediately flush skin with plenty of water for at least 15 minutes while removing contaminated clothing and shoes. Get medical aid immediately. Wash clothing before reuse.
Ingestion:
Potential for aspiration if swallowed. Get medical aid immediately. Do not induce vomiting unless directed to do so by medical personnel. Never give anything by mouth to an unconscious person.
Inhalation:
Poison material. If inhaled, get medical aid immediately. Remove victim to fresh air. If not breathing, give artificial respiration. If breathing is difficult, give oxygen.
Notes to Physician:

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SECTION 5 - FIRE FIGHTING MEASURES
General Information:
As in any fire, wear a self-contained breathing apparatus in pressure-demand, MSHA/NIOSH (approved or equivalent), and full protective gear. Material will not burn. Use water spray to keep fire-exposed containers cool. Containers may explode in the heat of a fire. Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
Extinguishing Media:
Use extinguishing media most appropriate for the surrounding fire.

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SECTION 6 - ACCIDENTAL RELEASE MEASURES
General Information: Use proper personal protective equipment as indicated in Section 8.
Spills/Leaks:
Absorb spill with inert material (e.g. vermiculite, sand or earth), then place in suitable container. Avoid runoff into storm sewers and ditches which lead to waterways. Clean up spills immediately, observing precautions in the Protective Equipment section. Isolate area and deny entry. Provide ventilation.

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SECTION 7 - HANDLING and STORAGE
Handling:
Wash thoroughly after handling. Remove contaminated clothing and wash before reuse. Avoid contact with eyes, skin, and clothing. Keep container tightly closed. Do not breathe vapor. Use only with adequate ventilation.
Storage:
Store in a tightly closed container. Store in a cool, dry, well-ventilated area away from incompatible substances.

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SECTION 8 - EXPOSURE CONTROLS, PERSONAL PROTECTION
Engineering Controls:
Facilities storing or utilizing this material should be equipped with an eyewash facility and a safety shower. Use adequate general or local exhaust ventilation to keep airborne concentrations below the permissible exposure limits. Use only under a chemical fume hood. Personal Protective Equipment
Eyes:
Wear chemical goggles.
Skin:
Wear appropriate protective gloves to prevent skin exposure.
Clothing:
Wear appropriate protective clothing to prevent skin exposure.
Respirators:
Follow the OSHA respirator regulations found in 29 CFR 1910.134 or European Standard EN 149. Always use a NIOSH or European Standard EN 149 approved respirator when necessary.

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SECTION 9 - PHYSICAL AND CHEMICAL PROPERTIES
Physical State: Liquid
Color: clear, colorless
Odor: chloroform-like
pH: Not available.
Vapor Pressure: 91 mm Hg @ 20 deg C
Viscosity: 0.97 PAS 20 deg C
Boiling Point: 76 deg C @ 760 mm Hg
Freezing/Melting Point: -23 deg C
Autoignition Temperature: Not applicable.
Flash Point: Not applicable.
Explosion Limits, lower: Not available.
Explosion Limits, upper: Not available.
Decomposition Temperature: >100 deg C
Solubility in water: Insoluble.
Specific Gravity/Density: 1.5900 g/cm3
Molecular Formula: CCl4
Molecular Weight: 153.82

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SECTION 10 - STABILITY AND REACTIVITY
Chemical Stability:
Stable under normal temperatures and pressures.
Conditions to Avoid:
Light, excess heat.
Incompatibilities with Other Materials:
Alkali metals, powdered aluminum, powdered magnesium, zinc powder, ethylene, allyl alcohol, barium, fluorine, dimethylformamide, powered beryllium, decaborane, potassium tert-butoxide.
Hazardous Decomposition Products:
Hydrogen chloride, chlorine, phosgene, carbon monoxide, carbon dioxide, chlorine dioxide, which may be spontaneously explosive.
Hazardous Polymerization: Will not occur.

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SECTION 11 - TOXICOLOGICAL INFORMATION RTECS#: CAS# 56-23-5: FG4900000
LD50/LC50:
CAS# 56-23-5: Dermal, guinea pig: LD50 = >9400 uL/kg; Draize test,
rabbit, eye: 2200 ug/30S Mild; Draize test, rabbit, eye: 500 mg/24H Mild; Draize test, rabbit, skin: 4 mg Mild; Draize test, rabbit,
skin: 500 mg/24H Mild; Inhalation, mouse: LC50 = 9526 ppm/8H;
Inhalation, rat: LC50 = 8000 ppm/4H; Oral, mouse: LD50 = 8263 mg/kg;
Oral, rabbit: LD50 = 5760 mg/kg; Oral, rat: LD50 = 2350 mg/kg; Skin,
rabbit: LD50 = >20 gm/kg; Skin, rat: LD50 = 5070 mg/kg.
Carcinogenicity:
Carbon Tetrachloride - Not listed by ACGIH, IARC, NIOSH, NTP, or OSHA.
Other:
See actual entry in RTECS for complete information.

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SECTION 12 - ECOLOGICAL INFORMATION
Ecotoxicity:
Fish: Fathead Minnow: LC50 = 20.8-41.4 mg/L; 96 Hr.; Flow-through; 21.7 degrees CFish: Bluegill/Sunfish: LC50 = 27-125 mg/L; 96 Hr.; Static Conditions; 23 degrees CBacteria: Phytobacterium phosphoreum: EC50 = 6.0 mg/L; Not available; Microtox testBacteria: Phytobacterium
phosphoreum: EC50 = 33.0 mg/L; 30 minutes; Microtox test

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SECTION 13 - DISPOSAL CONSIDERATIONS Dispose of in a manner consistent with federal, state, and local regulations.

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SECTION 14 - TRANSPORT INFORMATION IATA
Shipping Name: CARBON TETRACHLORIDE
Hazard Class: 6.1
UN Number: 1846
Packing Group: II IMO
Shipping Name: CARBON TETRACHLORIDE
Hazard Class: 6.1
UN Number: 1846
Packing Group: II RID/ADR
Shipping Name: CARBON TETRACHLORIDE
Hazard Class: 6.1
UN Number: 1846
Packing group: II

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SECTION 15 - REGULATORY INFORMATION European/International Regulations European Labeling in Accordance with EC Directives
Hazard Symbols: T N
Risk Phrases:
R 23/24/25 Toxic by inhalation, in contact with skin and if swallowed. R 40 Limited evidence of a carcinogenic effect. R 59 Dangerous for the ozone layer.
R 48/23 Toxic : danger of serious damage to health by prolonged exposure through inhalation. R 52/53 Harmful to aquatic organisms; may cause long-term adverse effects in the aquatic environment.
Safety Phrases:
S 23 Do not inhale gas/fumes/vapour/spray. S 36/37 Wear suitable protective clothing and gloves. S 45 In case of accident or if you feel unwell, seek medical advice immediately (show the label where possible). S 59 Refer to manufacturer/supplier for information on recovery/recycling. S 61 Avoid release to the environment. Refer to special instructions/Safety data sheets. WGK (Water Danger/Protection) CAS# 56-23-5: 3 United Kingdom Occupational Exposure Limits United Kingdom Maximum Exposure Limits Canada None of the chemicals in this product are listed on the DSL/NDSL list. CAS# 56-23-5 is not listed on Canada's Ingredient Disclosure List. Exposure Limits CAS# 56-23-5: OEL-ARAB Republic of Egypt:TWA 5 ppm (30 mg/m3);Skin OEL-AUSTRALIA:TWA 5 ppm (30 mg/m3);Skin;Carcinoge OEL-BELGIUM:TWA 5 ppm (31 mg/m3);Skin;Carcinogen OEL-CZECHOSLOVAKIA:TWA 10 mg/m3;STEL 20 mg/m3 OEL-DENMARK:TWA 2 ppm (13 mg/m3);Skin OEL-FINLAND:TWA 5 ppm (31 mg/m3);STEL 10 ppm (63 mg/m3);Skin;CAR OEL-FRANCE:TWA 2 ppm (12 mg/m3);STEL 10 ppm (60 mg/m3) OEL-GERMANY:TWA 10 ppm (65 mg/m3);Skin;Carcinogen OEL-HUNGARY:STEL 10 mg/m3;Skin;Carcinogen OEL-INDIA:TWA 5 ppm (30 mg/m3);Skin;Carcinogen OEL-JAPAN:TWA 10 ppm (63 mg/m3);Skin;Carcinogen OEL-THE NETHERLANDS:TWA 2 ppm (12.6 mg/m3);Skin OEL-THE PHILIPPINES:TWA 10 ppm (65 mg/m3);Skin OEL-POLAND:TWA 20 mg/m3 OEL-RUSSIA:TWA 10 ppm;STEL 20 mg/m3 OEL-SWEDEN:TWA 2 ppm (13 mg/m3);STEL 3 ppm (19 mg/m3);Skin;CAR OEL-SWITZERLAND:TWA 5 ppm (30 mg/m3);STEL 10 ppm (60 mg/m3);Skin OEL-THAILAND:TWA 10 ppm;STEL 25 ppm OEL-UNITED KINGDOM:TWA 10 ppm (65 mg/m3);STEL 20 ppm;Skin OEL IN BULGARIA, COLOMBIA, JORDAN, KOREA check ACGIH TLV OEL IN NEW ZEALAND, SINGAPORE, VIETNAM check ACGI TLV US FEDERAL TSCA CAS# 56-23-5 is not listed on the TSCA inventory. It is for research and development use only.

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SECTION 16 - ADDITIONAL INFORMATION
MSDS Creation Date: 7/20/1999 Revision #4 Date: 11/06/2002 The information above is believed to be accurate and represents the best information currently available to us. However, we make no warranty of merchantability or any other warranty, express or implied, with respect to such information, and we assume no liability resulting from its use. Users should make their own investigations to determine the suitability of the information for their particular purposes. In no way shall the company be liable for any claims, losses, or damages of any third party or for lost profits or any special, indirect, incidental, consequential or exemplary damages, howsoever arising, even if the company has been advised of the possibility of such damages.

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SECTION 16 - ADDITIONAL INFORMATION
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制备方法与用途

制备方法

1. 甲烷热氯化法：将甲烷与氯气混合，在400～430℃下发生热氯化反应，制得粗品和副产盐酸。粗品经过中和、干燥、蒸馏提纯后得到成品。副产物包括三氯甲烷、四氯乙烯和六氯乙烷，均可回收销售。
2. 二硫化碳法：在90～100℃下，以铁为催化剂使氯气与二硫化碳反应，经分馏、中和、精馏得到成品。此方法投资少且产品易提纯，但成本较高，设备容易腐蚀。
3. 甲烷氧氯化法：氯利用率高，无氯化氢及废卤代烃污染。
4. 高压氯解法：避免生成四氯乙烯。
5. 甲醇氢氯化法：产品质量好，经济效益高。此外，二氯甲烷和三氯甲烷的生产均可联产四氯甲烷。

具体的制备过程如下：

• 将100L工业品四氯化碳、15L95%乙醇、1.5g42%氢氧化钠及乙酸铅混合，搅拌并加热沸腾至硫化物含量合格。然后加水洗涤三次以上，弃去水层后加入浓硫酸（每100kg四氯化碳加硫酸10kg），搅拌酸洗至试验合格，再用水洗涤三次，加5%氢氧化钠溶液，充分搅拌后静置并弃去水层，重复碱洗至酸度合格。在合格的四氯化碳中加入适量无水氯化钙和少量无水碳酸钠，充分静置，滤去干燥剂，在常压下蒸馏，收集76～77.5℃馏分即为成品。

合成制备方法

1. 甲烷热氯化法：将甲烷与氯气混合，在400～430℃下发生反应，生成粗品和副产盐酸。粗品经过中和、干燥、蒸馏提纯后得到成品。
2. 二硫化碳法：在90～100℃下以铁为催化剂使氯气与二硫化碳反应，产物经分馏、中和及精馏得到成品。此方法投资少且产品易提纯，但成本高，设备容易腐蚀。
3. 甲烷氧氯化法：提高氯利用率，避免生成四氯乙烯。
4. 高压氯解法：防止生成四氯乙烯。
5. 甲醇氢氯化法：产品质量好，经济效益高。此外，二氯甲烷和三氯甲烷的生产均可联产四氯甲烷。

具体的制备过程如下：

• 将100L工业品四氯化碳、15L95%乙醇、1.5g42%氢氧化钠及乙酸铅混合，搅拌并加热沸腾至硫化物含量合格。然后加水洗涤三次以上，弃去水层后加入浓硫酸（每100kg四氯化碳加硫酸10kg），搅拌酸洗至试验合格，再用水洗涤三次，加5%氢氧化钠溶液，充分搅拌后静置并弃去水层，重复碱洗至酸度合格。在合格的四氯化碳中加入适量无水氯化钙和少量无水碳酸钠，充分静置，滤去干燥剂，在常压下蒸馏，收集76～77.5℃馏分即为成品。

用途简介

用作灭火剂、有机溶剂、制冷剂以及生产氟里昂的原料，还可作为清洗剂、溶剂、萃取剂、杀虫剂和分析试剂等。

用途

1. 主要用作优良的溶剂、干洗剂、灭火剂、制冷剂、香料浸出剂以及农药。
2. 用于合成氟里昂、尼龙7及尼龙9的单体，还可制备三氯甲烷和药物；在金属切削中作为润滑剂。
3. 用作分析试剂，如标准氯测定溶剂和清洗剂、萃取溶剂、杀虫剂等。
4. 用于有机合成，作为溶剂、制冷剂、有机物的氯化剂、香料浸出剂及纤维脱脂剂等。 [17]

反应信息

• 作为反应物：
  描述：

  四氯化碳 在 异丙醇 作用下， 以 乙腈 为溶剂， 生成 二氯甲烷
  参考文献：
  名称：

  双金属Au / Ag系统用于有机氯化物脱氯的设计：簇效应作用的实验和理论证据

  摘要：

  Au / Ag双金属体系脱氯活性的实验研究表明，形成了多种氯化双金属Au / Ag簇，其定义明确的Au：Ag比为1：1至4：1。介导C–Cl键断裂的是Au / Ag簇物种的形成，因为单独的Au和Ag都没有表现出可比的活性。在M06 / 6-311G（d）和SDD理论水平上，通过ESI-MS，GC-MS，NMR和量子化学计算研究了产物的性质和脱氯机理。结果表明，由于热力学因素，双金属簇的形成促进了脱氯活性：金属簇的C–Cl键断裂在热力学上是有利的，并导致了氯化双金属物种的形成。合适的Au：在本工作中进行的联合实验和理论研究确定了有效加氢脱氯过程中的银比。在此机理发现之后，合成了分子双金属簇，该簇成功参与了CCl的加氢脱氯反应4作为低分子量环境污染物，在二氯二苯基三氯乙烷（DDT）的脱氯中作为生态毒性杀虫剂。设计的双金属系统的高活性使其可以在温和条件下于室温下进行脱氯过程。

  DOI：

  10.1021/om500620u
• 作为产物：
  描述：

  三氯乙酰氯 以 neat (no solvent) 为溶剂， 生成 四氯化碳
  参考文献：
  名称：

  anonymous, Beilsteins Handbuch der organischen Chemie, 4. Auflage. J. Springer, Berlin 1918, Bd. 1, S. 65

  摘要：

  DOI：
• 作为试剂：
  描述：

  在 sodium tetrahydroborate 、 四氯化碳 、 三苯基膦 作用下， 以 四氢呋喃 、 二氯甲烷 为溶剂， 以400 mg的产率得到
  参考文献：
  名称：

  FUSED CYCLIC COMPOUNDS AND USE THEREOF

  摘要：

  The invention relates to fused cyclic compounds, a composition containing the same and the use thereof.

  公开号：

  WO2024120433A1

文献信息

• Polyfluoroarylcarbonimidoyl dichlorides and chlorides. A new method of obtaining such compounds from polyfluoroaromatic amines and compounds of the CCl3R-type in the presence of AlCl3
  作者：T.I. Savchenko、I.V. Kolesnikova、T.D. Petrova、V.E. Platonov

  DOI：10.1016/s0022-1139(00)81166-5

  日期：1983.5

  polyfluorinated amines of the benzene, diphenyl, naphthalene and pyridine series with CCl4 in the presence of AlCl3 have been Investigated. A new method is proposed for producing polyfluoroarylcarbonimidoyl dichlorides ArfNCCl2. The reaction is shown to be sufficiently general and applicable in the series of polychlorinated anilines and low-base anilines of the hydrocarbon series as well. The possibility

  研究了在AlCl 3存在下苯，联苯，萘和吡啶系列的一些多氟胺与CCl 4的反应。提出了一种新的制备聚氟芳基碳亚氨基二氯化物Ar f N = CCl 2的方法。该反应显示出足够普遍，并且适用于烃系列的多氯苯胺和低碱苯胺系列。已经研究了反应中可能包含其他类型的CCl 3 R化合物和其他路易斯酸的可能性。讨论了影响反应过程的因素以及多氟芳基碳亚氨基二氯化物的形成机理。
• New route to fluorinated arylcarbonimidoyl chlorides: Interaction of polyfluoroaryl-amines with halomethanes in the presence of lewis acids
  作者：T.I. Savchenko、T.D. Petrova、I.V. Kolesnikova、V.E. Platonov

  DOI：10.1016/s0022-1139(00)84039-7

  日期：1980.12

  the preparation of polyfluoroarylcarbonimidoyl chlorides by high-temperature copyrolysis of polyfluoroaromatic amines with CCl4 or pentafluorobenzotrichloride. In presented paper we wish to report a new and convenient route to carbonimidoyl chlorides by interaction of polyfluoroaromatic amines with CCl4 or pentafluorobenzotrichloride in the presence of AlCl3 at ordinary temperature. This method gives

  近来，我们已经描述了通过用CCl 4或五氟苯并三氯化物对聚氟芳族胺进行高温共水解来制备聚氟芳基碳亚氨基氯化物。在提出的论文中，我们希望报告在常温下，在AlCl 3存在下，多氟芳族胺与CCl 4或五氟苯并三氯化物的相互作用，从而获得一种新的简便的方法来制备碳亚氨基酰氯。该方法以高收率得到碳亚氨基酰氯。
• [EN] 6H-THIENO`2, 3-B!PYRROLE DERIVATIVES AS ANTAGONISTS OF GONADOTROPIN RELEASING HORMONE (GNRH)<br/>[FR] DERIVES DE 6H-THIENO`2,3-B!PYRROLE EN TANT QU'ANTAGONISTES DE LA GONADOLIBERINE (GNRH)
  申请人：ASTRAZENECA AB

  公开号：WO2004018480A1

  公开（公告）日：2004-03-04

  The invention relates to a group of novel thieno-pyrrole compounds of Formula (I): wherein: R1, R2, R3, R4 and R5 are as defined in the specification, which are useful as gonadotrophin releasing hormone antagonists. The invention also relates to pharmaceutical formulations of said compounds, methods of treatment using said compounds and to processes for the preparation of said compounds.

  这项发明涉及一组新型噻吩-吡咯烷化合物的化学式（I）：其中：R1、R2、R3、R4和R5如规范中定义，这些化合物可用作促性腺激素释放激素拮抗剂。该发明还涉及所述化合物的药物配方、使用所述化合物的治疗方法以及所述化合物的制备方法。
• One-Pot Synthesis of Tertiary Amides from Organic Trichlorides through Oxygen Atom Incorporation from Air by Convergent Paired Electrolysis
  作者：Zhongli Luo、Kenji Imamura、Yoshihito Shiota、Kazunari Yoshizawa、Yoshio Hisaeda、Hisashi Shimakoshi

  DOI：10.1021/acs.joc.1c00161

  日期：2021.4.16

  A convergent paired electrolysis catalyzed by a B12 complex for the one-pot synthesis of a tertiary amide from organic trichlorides (R-CCl3) has been developed. Various readily available organic trichlorides, such as benzotrichloride and its derivatives, chloroform, dichlorodiphenyltrichloroethane (DDT), trichloro-2,2,2-trifluoroethane (CFC-113a), and trichloroacetonitrile (CNCCl3), were converted

  已经开发了一种由B 12络合物催化的聚合成对电解，用于一锅法从有机三氯化物（R-CCl 3）合成叔酰胺。各种易得的有机三氯化物，例如苯并三氯化物及其衍生物，氯仿，二氯二苯基三氯乙烷（DDT），三氯-2,2,2-三氟乙烷（CFC-113a）和三氯乙腈（CNCCl 3）在存在下通过在室温下从空气中引入氧气来合成叔胺。提出了由钴配合物介导的成对电解中酰胺的形成机理。
• Selective reduction of a C Cl bond in halomethanes with Et3GeH at nanoscopic Lewis acidic Aluminium fluoride
  作者：Gisa Meißner、Michael Feist、Thomas Braun、Erhard Kemnitz

  DOI：10.1016/j.jorganchem.2017.04.030

  日期：2017.10

  activation of CCl bonds of hydrochlorofluoromethanes and chloromethanes at moderate reaction conditions using ACF in a combination with Et3GeH is presented. The reactions of the chloromethanes (CH3Cl, CH2Cl2, CHCl3 and CCl4) in the presence of Et3GeH and ACF as catalyst led to the activation of only one CCl bond resulting in the hydrodechlorination. Friedel-Crafts reactions with benzene as solvent are suppressed

  提出了在中等反应条件下，使用ACF与Et 3 GeH的组合，选择性活化氢氯氟甲烷和氯甲烷的C Cl键。在作为催化剂的Et 3 GeH和ACF的存在下，氯甲烷（CH 3 Cl，CH 2 Cl 2，CHCl 3和CCl 4）的反应导致仅一个C Cl键的活化而导致加氢脱氯。Et 3 GeH抑制了以苯为溶剂的Friedel-Crafts反应。实现了氢氯氟甲烷的选择性加氢脱氯，因为C F键转变为C没有发生由ACF和Et 3 GeH结合的H键。支撑脉冲TA ®实验中示出的固体催化剂和Et之间的相互作用3 GeH的，溶剂苯或CH 2氯2。

表征谱图