首页> 外文期刊>Archives of Environmental Contamination and Toxicology >Metabolic conversion of 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) to 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) in the male F344/NCr Rat.
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Metabolic conversion of 1,1-dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) to 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene (DDE) in the male F344/NCr Rat.

机译:在雄性F344 / NCr中将1,1-二氯-2,2-双(对氯苯基)乙烷(DDD)代谢转化为1,1-二氯-2,2-双(对氯苯基)乙烯(DDE)鼠。

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摘要

1,1-Dichloro-2,2-bis(p-chlorophenyl)ethane (DDD) and 1,1-dichloro-2, 2-bis(p-chlorophenyl)ethylene (DDE) levels were measured by capillary gas chromatography with electron capture detection in liver and blood serum of male F344/NCr rats exposed for 2 weeks to DDD at dietary concentrations ranging from 8.51 ppm to 2,000 ppm. DDD burdens in serum ranged from <0.006 microM (limit of detection) in control rats to 1.1 microM in the rats fed DDD at 2,000 ppm. The corresponding liver burdens in these animals ranged from <0.006 micromol/kg liver (controls) to 11 micromol/kg liver in rats fed DDD at 2,000 ppm. Levels of DDE in serum or liver were undetectable (<0. 006 microM in serum; <0.006 micromol/kg liver) in rats fed control diet or diet containing 8.51 or 25.5 ppm DDD. The liver and serum burdens of DDE increased with dietary DDD concentration, reaching a maximum of 0.53 microM in serum and 4.7 micromol/kg liver in rats fed 2,000 ppm DDD. As a percentage of total DDD equivalents detected in liver or serum, the DDE burdens increased to a maximum of 36% and 31% in the serum and liver, respectively, of rats fed 689 ppm DDD. The possibility that the DDE might have been generated artifactually in the diet prior to administration to the rats was ruled out by analysis with capillary gas chromatography of the diet containing 2, 000 ppm DDD. The identification of DDE as a metabolite in liver extracts of rats fed 2,000 ppm DDD was confirmed with GC-MS. The results confirmed the presence of DDE as a metabolite of DDD.
机译:用电子毛细管气相色谱法测定1,1-二氯-2,2-双(对氯苯基)乙烷(DDD)和1,1-二氯-2,2-双(对氯苯基)乙烯(DDE)水平在饮食浓度为8.51 ppm至2,000 ppm的DDD中暴露2周的雄性F344 / NCr大鼠的肝脏和血清中的捕获检测。血清中DDD的负担范围从对照组大鼠的<0.006 microM(检测极限)到以2,000 ppm饲喂DDD的大鼠的1.1 microM。这些动物中相应的肝脏负担在以2,000 ppm饲喂DDD的大鼠中,从<0.006微摩尔/千克肝脏(对照组)到11微摩尔/千克肝脏。在饲喂对照饮食或含8.51或25.5 ppm DDD的大鼠中,血清或肝脏中的DDE水平无法检测到(血清中<0.006 microM;肝脏<0.006 micromol / kg肝脏)。饮食中DDD的浓度会增加DDE的肝脏和血清负担,在喂食2,000 ppm DDD的大鼠中,血清中的DDE最高为0.53 microM,肝脏的最高含量为4.7 micromol / kg。以在肝脏或血清中检测到的总DDD当量的百分比表示,喂食689 ppm DDD的大鼠的血清和肝脏中DDE的负担分别增加至最大36%和31%。通过对包含2,000 ppm DDD的饮食进行毛细管气相色谱分析,排除了在向大鼠给药之前饮食中人为产生DDE的可能性。用GC-MS确认了DDE作为喂食2,000 ppm DDD的大鼠肝提取物中的代谢产物。结果证实了DDE作为DDD的代谢产物的存在。

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