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(1R,2R,3R,6S,7S)-1,8,9,10,11,11-hexachlorotetracyclo[6.2.1.13,6.02,7]dodeca-4,9-diene

中文名称
——
中文别名
——
英文名称
(1R,2R,3R,6S,7S)-1,8,9,10,11,11-hexachlorotetracyclo[6.2.1.13,6.02,7]dodeca-4,9-diene
英文别名
——
(1R,2R,3R,6S,7S)-1,8,9,10,11,11-hexachlorotetracyclo[6.2.1.13,6.02,7]dodeca-4,9-diene化学式
CAS
——
化学式
C12H8Cl6
mdl
——
分子量
364.9
InChiKey
QBYJBZPUGVGKQQ-FMNXKPGOSA-N
BEILSTEIN
——
EINECS
——
  • 物化性质
  • 计算性质
  • ADMET
  • 安全信息
  • SDS
  • 制备方法与用途
  • 上下游信息
  • 反应信息
  • 文献信息
  • 表征谱图
  • 同类化合物
  • 相关功能分类
  • 相关结构分类

计算性质

  • 辛醇/水分配系数(LogP):
    4.5
  • 重原子数:
    18
  • 可旋转键数:
    0
  • 环数:
    4.0
  • sp3杂化的碳原子比例:
    0.67
  • 拓扑面积:
    0
  • 氢给体数:
    0
  • 氢受体数:
    0

ADMET

代谢
阿德林的DOMINANT反应是在双键处进行环氧化以形成6,7-环氧B二氯。这种氧化反应可以是光化学的或生物学的(混合功能氧化酶)并且在土壤、植物组织和所有研究过的动物中发生。阿德林在植物和动物中也被降解为六氯-六氢-1,4-内亚甲基-茚-5,7-二羧酸和转化为阿德林-反式二醇。在动物中,5-羟基二氯、9-酮二氯和酮-光二氯被形成作为排泄代谢物。在排泄之前,羟基代谢物大部分被共轭。
DOMINANT REACTION OF ALDRIN IS EPOXIDATION AT DOUBLE BOND TO FORM 6,7-EPOXIDE B DIELDRIN. ... /SRP: THIS OXIDN CAN BE PHOTOCHEMICAL OR BIOLOGICAL (MIXED-FUNCTION OXIDASES) & OCCURS/ IN SOILS, PLANT TISSUES, & IN ALL ANIMALS STUDIED. ... ALDRIN IS ALSO DEGRADED IN PLANTS & ANIMALS TO HEXACHLORO-HEXAHYDRO-1,4-ENDO-METHYLENE-INDENE-5,7-DICARBOXYLIC ACID & TO ALDRIN-TRANS-DIOL. IN ANIMALS 5-HYDROXYDIELDRIN, 9-KETO-DIELDRIN & KETO-PHOTODIELDRIN ARE ... FORMED AS EXCRETORY METABOLITES. BEFORE EXCRETION THE HYDROXY METABOLITES ARE LARGELY CONJUGATED.
来源:Hazardous Substances Data Bank (HSDB)
代谢
最广泛降解的艾氏剂和狄氏剂排泄产物报道是一种六氯代二羧酸(4,5-开环艾氏剂-4,5-二羧酸),并且人们普遍认为这是一种终末哺乳动物代谢物。这种假设被两种五氯代二羧酸(占22%)的鉴定所驳斥,这些酸在大鼠静脉注射(3.5毫克/千克)... 4,5-开环艾氏剂-4,5-二羧酸后的尿液中被发现。
THE MOST EXTENSIVELY DEGRADED EXCRETION PRODUCT OF ALDRIN & DIELDRIN REPORTED ... IS A HEXACHLORINATED DICARBOXYLIC ACID /4,5-SECO-ALDRIN-4,5-DICARBOXYLIC ACID/, & IT HAS BEEN WIDELY ASSUMED THAT THIS IS A TERMINAL MAMMALIAN METABOLITE. THIS ASSUMPTION ... /IS/ DISCREDITED BY IDENTIFICATION OF TWO PENTACHLORINATED DICARBOXYLIC ACIDS (22%) IN URINE OF RATS DOSED IV (3.5 MG/KG) WITH ... /4,5-SECO-ALDRIN-4,5-DICARBOXYLIC ACID/.
来源:Hazardous Substances Data Bank (HSDB)
代谢
在添加到从菜豆(法国豆)根和茎以及马铃薯块茎的悬浮培养物中的时候,农药阿德林和狄艾德林(滴滴涕)的吸收和代谢过程(0-100天)是相似的,其中狄艾德林的产生迅速,而其他代谢产物的出现则有所延迟。当阿德林和狄艾德林在子培养后的10天或20天添加到菜豆培养物中时,阿德林通常转化为狄艾德林的过程发生了,但其他代谢产物的产生减少了。狄艾德林的产生在快速生长期达到最大,并且可能与其他转化过程无关。
TIME COURSES (0-100 DAYS) OF UPTAKE & METABOLISM OF ALDRIN & DIELDRIN ADDED AT SUBCULTURE TO SUSPENSION CULTURES FROM PHASEOLUS VULGARIS (FRENCH BEAN) ROOT & SHOOT & SOLANUM TUBEROSUM (POTATO) TUBER WERE COMPARABLE, WITH RAPID DIELDRIN PRODN & DELAYED APPEARANCE OF OTHER METABOLITES. WHEN ALDRIN & DIELDRIN WERE ADDED TO PHASEOLUS CULTURES AT 10 OR 20 DAYS AFTER SUBCULTURE, USUAL EXTENT OF CONVERSION OF ALDRIN TO DIELDRIN OCCURRED, BUT WITH REDUCED PRODN OF OTHER METABOLITES. DIELDRIN PRODN WAS MAXIMUM DURING RAPID GROWTH PHASE & PROBABLY INDEPENDENT OF OTHER CONVERSIONS.
来源:Hazardous Substances Data Bank (HSDB)
代谢
在大鼠肝脏的微粒体中,通过还原型烟酰胺腺嘌呤二核苷酸刺激了艾氏剂向狄氏剂的环氧化。在精囊和肉芽组织的微粒体中,还原型烟酰胺腺嘌呤二核苷酸对艾氏剂的环氧化没有影响。显然,在肝脏中,艾氏剂是通过单加氧酶途径环氧化,在肉芽组织和精囊中通过前列腺素合酶介导途径,而在肺中则是通过这两种途径。
In microsomes from rat liver, aldrin epoxidation into dieldrin was stimulated by reduced nicotinamide adenine dinucleotide . ... In microsomes from seminal vesicles and granulation tissue, reduced nicotinamide adenine dinucleotide had no effect on aldrin epoxidation. ... Apparently, in the liver, aldrin is epoxidized by monooxygenase pathway, in granulation tissue and seminal vesicles by prostaglandin synthase-mediated pathway, and in the lung by both pathways.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 毒性总结
识别:阿德林是一种氯化的环二烯类杀虫剂。纯阿德林是一种白色结晶固体。工业级阿德林呈棕色。阿德林已用于各种配制剂中,包括可乳化浓缩液、可湿性粉剂、颗粒剂、粉剂和碳氢液体中的溶液。阿德林有一种温和的化学气味,并且在大多数有机溶剂(如芳烃、酯、酮、石蜡和卤化溶剂)中非常易溶。阿德林的杂质包括八氯环戊烯、六氯丁二烯、甲苯以及由阿德林反应期间聚合形成的化合物混合物以及酮类化合物。阿德林是一种非常有效的土壤杀虫剂,已用于处理种子。它已用于控制白蚁、玉米根虫、种子玉米甲虫和蛆虫、线虫、水稻水象甲、蚱蜢和日本甲虫。 人体暴露:中枢神经系统似乎是主要作用部位,会导致癫痫发作。有毒暴露会产生震颤、眩晕、过度兴奋、癫痫和昏迷。中毒主要通过皮肤吸收发生。流行病学研究没有显示任何致癌风险。吸收可以通过吸入、皮肤和胃肠途径发生。阿德林在体内的临床毒性实际上是由于其迅速代谢为狄氏剂。症状反映了由于GABA神经传递抑制导致的CNS毒性。头痛、震颤、过度兴奋、癫痫和昏迷已被注意到。通过呼吸吸收发生,呼出的阿德林浓度低于吸入的浓度。阿德林在肝脏中迅速转化为狄氏剂。因此,在血液或组织中很少发现阿德林。尸检病例显示大脑、肝脏和脂肪组织中狄氏剂的水平。在慢性口服人体给药后,血液中狄氏剂的浓度按照一级动力学指数衰减,估计半衰期为369天。消除主要通过胆汁通过粪便发生。9-羟基狄氏剂似乎是被排泄的主要代谢物。狄氏剂也通过母乳排泄。在局部或静脉给药后,少量狄氏剂代谢物通过尿液排泄。在摄入后,尿液中也可能发现狄氏剂代谢物。在儿童中有少数阿德林中毒的案例,其CNS刺激的迹象与成人相似。急性摄入后可能导致死亡。胎儿集中狄氏剂,污染的母乳摄入增加了非常年轻人群中CNS效果的风险。在花卉种植者接触包括阿德林在内的多种杀虫剂后,注意到了姐妹染色单体交换和交换型染色体畸变增加。心血管并发症包括在过量服用后的血压波动和心动过速。在急性过量后的几天内注意到了血尿素氮水平、明显血尿和白蛋白尿的增加。在杀虫剂制造工人中没有看到皮炎。在至少四年的随访中,杀虫剂制造工人的正常血液学参数被注意到。 动物/细菌/病毒/细胞研究:几个物种的阿德林吸入暴露导致死亡。在二甲苯中单次皮肤应用阿德林导致测试动物死亡。给大鼠口服阿德林会引起惊厥。阿德林在SV-40转化的人成纤维细胞(VA-4)中诱导了非计划性DNA合成,无论在大鼠肝微粒体存在与否的情况下。在用阿德林或狄氏剂处理后,大肠杆菌质粒的DNA断裂速率与未处理的质粒DNA的断裂速率没有差异,这表明至少在这些研究中,这些化合物没有直接与DNA相互作用。在培养的大鼠胸腺细胞和人淋巴细胞中测试了阿德林和狄氏剂对三胸苷摄取的影响。在实验条件下,这两种化合物似乎对胸苷摄取有边缘效应,提示DNA合成受到抑制。阿德林和狄氏剂没有在Fischer 344大鼠肝细胞原代培养中诱导非计划性DNA合成。在使用高代谢能力的新鲜分离肝细胞进行肝细胞原代培养/DNA修复试验来监测DNA损伤的产生,通过测量DNA修复合成。阿德林和狄氏剂关于DNA修复的结果是模棱两可的,但没有对DNA造成损害。阿德林在大鼠肝细胞碱性洗脱分析中诱导了DNA链断裂。阿德林和狄氏剂抑制了6-硫鸟嘌呤敏感和6-硫鸟嘌呤抗性的人畸胎瘤细胞之间的缝隙连接细胞间通讯。在几个研究中没有发现恶性肿瘤发病率增加。在动物试验中,发现肝脏肿瘤包括肝细胞腺瘤的发病率增加。在动物研究中,阿德林确实导致胎儿死亡率增加,腭裂和蹼足的发病率增加,以及出生后存活率降低。
IDENTIFICATION: Aldrin is a chlorinated cyclodiene insecticide. Pure aldrin is a white crystalline solid. Technical grade aldrin is tan in color. Aldrin has been used in various formulations which include emulsifiable concentrates, wettable powders, granules, dusts and solutions in hydrocarbon liquids. Aldrin has a mild chemical odor, and is very soluble in most organic solvents (aromatics, esters, ketones, paraffins and halogenated solvents. Impurities of aldrin include octachlorocyclopentene, hexachlorobutadiene, toluene and a mixture of compounds formed by polymerization during the aldrin reaction along with carbonyl compounds. Aldrin is very effective soil insecticide and has been used to treat seeds. It has been used to control termites, corn root worms, seed corn beetle and maggot, wire worms, rice water weevil, grasshoppers and Japanese beetles. HUMAN EXPOSURE: The CNS seems to be the primary site with resultant seizures. Toxic exposures produce tremors, giddiness, hyperexcitability, seizures and comas. Poisoning occurs mainly through absorption through the skin. Epidemiological studies do not show any carcinogenic risk. Absorption can occur by inhalation, dermal and gastrointestinal routes. Clinical toxicity from aldrin actually is due to its rapid metabolism in the body to dieldrin. Symptoms reflect CNS toxicity due to GABA neurotransmission inhibition. Headache, tremors, hyperexcitability, seizures and comas have been noted. Respiratory absorption occurs, expiratory aldrin concentrations are decreased compared to inspired concentrations. Aldrin is rapidly converted to dieldrin primarily in the liver. Consequently little aldrin is found in the blood or tissues. Autopsy cases show dieldrin levels in the brain, liver and adipose tissue. After chronic oral human administration, blood dieldrin concentrations decreases exponentially following first order kinetics with an estimated half life of 369 days. Elimination occurs primarily through the feces via the bile. 9-Hydroxydieldrin seems to be the major metabolite excreted. Dieldrin is also excreted in the breast milk. Small amounts of dieldrin metabolites are excreted in the urine after either topical or iv administration. Dieldrin metabolites may also be found in the urine after ingestion. There have been a few cases of aldrin toxicity in children with resulting signs of CNS stimulation similar to adults. Death has resulted after acute ingestion. The fetus concentrates dieldrin, and the possibility of contaminated breast milk consumption increase the risk of CNS effects in the very young. Increased sister chromatid exchanges and exchange type chromosome aberrations were noted in floriculturists after exposure to several pesticides including aldrin. Cardiovascular complications include blood pressure fluctuations and tachycardia after overdose. Blood urea nitrogen levels, gross hematuria and albuminuria for several days after an acute overdose was noted. No dermatitis was seen in pesticide manufacturing workers. Normal hematological parameters were noted in pesticide manufacturing workers during at least a four years of follow up. ANIMAL/BACTERIAL/VIRAL/CELL STUDIES: Inhalation exposure to aldrin in several species resulted in death. Single dermal applications of aldrin in xylene produced death in test animals. Oral administration of aldrin to rats causes convulsions. Aldrin induced unscheduled DNA synthesis in SV-40 transformed human fibroblast cells (VA-4) both in the presence and absence of rat liver microsomes, The DNA breakage rates in Escherichia coli plasmid after treatment with aldrin or dieldrin did not differ from those in untreated plasma DNA suggesting that, at least in these studies, the compounds did not interact directly with DNA. The effects of aldrin and dieldrin on the uptake of tritiated thymidine by cultured rat thymocytes and human lymphocytes were tested under different experimental conditions. Both compounds appeared to have marginal effects on thymidine uptake, suggesting inhibition of DNA synthesis. Aldrin and dieldrin did not induce unscheduled DNA synthesis in primary cultures of Fischer 344 rat hepatocytes. In the hepatocyte primary culture/DNA repair test using freshly isolated hepatocytes of high metabolic capability to monitor the production of DNA damage by measuring DNA repair synthesis. Aldrin and dieldrin gave equivocal results concerning DNA repair, but there was no damage to DNA. Aldrin induced DNA strand breaks in an alkaline elution rat hepatocyte assay. Both aldrin and dieldrin inhibited gap junctional intercellular communication between 6-thioguanine sensitive and 6-thioguanine resistant human teratocarcinoma cells in culture. No increased incidence of malignant neoplasms have been found in several studies. In animal assays there was an increased incidence of hepatic tumors including hepatocellular adenomas. In animal studies, aldrin did cause an increase in fetal mortality, increased incidence of cleft palate and webbed foot and a decreased postnatal survival have been reported.[
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
人类致癌性证据不足。动物致癌性证据有限。总体评估:第3组:该物质对人类致癌性无法分类。
Inadequate evidence of carcinogenicity in humans. Limited evidence of carcinogenicity in animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its carcinogenicity to humans.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
癌症分类:B2组可能的人类致癌物
Cancer Classification: Group B2 Probable Human Carcinogen
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
分类:B2;可能的人类致癌物。分类依据:经口给予的艾氏剂在三种不同品系的小鼠中,无论雄性还是雌性,都显著增加了肿瘤反应。结构上相关的化学品,包括代谢物狄氏剂,已经观察到肿瘤诱导作用。人类致癌性数据:不足。动物致癌性数据:充分。
CLASSIFICATION: B2; probable human carcinogen. BASIS FOR CLASSIFICATION: Orally administered aldrin produced significant increases in tumor responses in three different strains of mice in both males and females. Tumor induction has been observed for structurally related chemicals, including dieldrin, a metabolite. HUMAN CARCINOGENICITY DATA: Inadequate. ANIMAL CARCINOGENICITY DATA: Sufficient.
来源:Hazardous Substances Data Bank (HSDB)
毒理性
  • 致癌性证据
在美国环保局(EPA)的《致癌物风险评估指南(拟议)框架》内,建议与小鼠肝脏肿瘤反应相关的艾氏剂/狄氏剂的最合适的癌症风险描述符是“不太可能是一种人类致癌物”,这个描述符与EPA引用的苯巴比妥的例子一致。
Within the framework of EPA's Proposed Guidelines for Carcinogen Risk Assessment, it is proposed that the most appropriate cancer risk descriptor for aldrin/dieldrin, relating to the mouse liver tumor response, is 'not likely a human carcinogen', a descriptor consistent with the example of phenobarbital cited by EPA.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
母血、胎盘和脐带血来自同一母亲/儿童对被分析,以确定在100名妇女研究中有机氯杀虫剂从母亲到胎儿的转移。在所有分析的样本中均检测到艾氏剂,表明存在胎盘转移。发现杀虫剂浓度与孕妇年龄、饮食习性及居住地区之间存在相关性。
MATERNAL BLOOD, PLACENTA, & UMBILICAL CORD BLOOD OF SAME MOTHER/CHILD PAIR WERE ANALYZED TO DETERMINE ORGANOCHLORINE PESTICIDE TRANSFER FROM MOTHER TO FETUS IN STUDY OF 100 WOMEN. ALDRIN WAS DETECTED IN ALL SAMPLES ANALYZED, INDICATING PLACENTAL TRANSFER. CORRELATION WAS FOUND BETWEEN PESTICIDE CONCN & AGE, DIETETIC HABITS & AREA OF RESIDENCE OF PREGNANT WOMEN.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
在血浆中,阿特拉津和狄尔津主要与α-和β-脂蛋白组分相关联。
IN PLASMA, BOTH ALDRIN & DIELDRIN ARE ASSOCIATED MAINLY WITH ALPHA- & BETA-LIPOPROTEIN FRACTIONS ... .
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
ALDRIN尚未在...普通人群中发现,也未曾发现于...从事其制造的男性的体脂中;只在这些男性的血液中发现了微量。急性中毒的人...会迅速转化为/狄尔特林/...。
ALDRIN HAS NOT BEEN FOUND IN ... GENERAL POPULATION OR ... IN BODY FAT OF MEN ENGAGED IN MANUFACTURING IT; ONLY TRACES ARE FOUND IN BLOOD OF SUCH MEN. PERSONS ACUTELY POISONED ... MAKE THE CONVERSION /TO DIELDRIN/ ... RAPIDLY.
来源:Hazardous Substances Data Bank (HSDB)
吸收、分配和排泄
(36)CL Aldrin...在给大鼠和断奶仔猪口服后迅速吸收,并集中在肝脏和脂肪储存处,从这些地方...它仅缓慢排出。(14)C Aldrin喂给大鼠后通过粪便排出(12周内剂量的90%)和尿液(10%),是一系列亲水性代谢产物和少量未改变的Aldrin和Dieldrin的混合物。
(36)CL ALDRIN ... IS RAPIDLY ABSORBED AFTER ORAL ADMIN TO RATS & WEANLING PIGS & BECOME LOCALIZED IN LIVER & FAT DEPOTS, FROM WHICH ... IT IS ONLY SLOWLY EXCRETED. (14)C ALDRIN FED TO RATS IS EXCRETED IN FECES (90% OF DOSE IN TWELVE WK) & URINE (10%), AS MIXT OF HYDROPHILIC METABOLITES TOGETHER WITH SMALL AMT OF UNCHANGED ALDRIN & DIELDRIN.
来源:Hazardous Substances Data Bank (HSDB)

表征谱图

  • 氢谱
    1HNMR
  • 质谱
    MS
  • 碳谱
    13CNMR
  • 红外
    IR
  • 拉曼
    Raman
hnmr
mass
cnmr
ir
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  • 峰位数据
  • 峰位匹配
  • 表征信息
Shift(ppm)
Intensity
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Assign
Shift(ppm)
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测试频率
样品用量
溶剂
溶剂用量
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