Organohalogen Compounds in Pet Dog and Cat: Do Pets Biotransform Natural Brominated Products in Food to Harmful Hydroxlated Substances?
Organohalogen Compounds in Pet Dog and Cat: Do Pets Biotransform Natural Brominated Products in Food to Harmful Hydroxlated Substances?
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DOI：
10.1021/acs.est.5b04216
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发表时间：
2016-01-05
影响因子：
11.4
通讯作者：
Tanabe, Shinsuke
中科院分区：
文献类型：
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作者：
Mizukawa, Hazuki;Nomiyama, Kei;Tanabe, Shinsuke
由于暴露于有机卤素污染物及其羟基化代谢物，宠物猫甲状腺功能亢进症的增加越来越受到关注。本研究调查了宠物狗和猫血液中的多氯联苯（PCBs）和多溴联苯醚（PBDEs）及其羟基化和甲氧基化衍生物（OH-PCBs，OH-PBDEs和MeO-PBDEs）。我们还测量了市售宠物食品中这些化合物的残留水平。多氯联苯和羟基多氯联苯的化学分析表明，羟基多氯联苯的水平是1至2个数量级的猫和狗的食品比在他们的血液中低，这表明羟基多氯联苯在宠物狗和猫的来源是多氯联苯与他们的食物摄入。在宠物食品和血液中发现的OH-/MeO-PBDE的主要同系物是来自海洋生物的天然产物（60 H-/MeO-BDE 47和2 'OH-/MeO-BDE 68）。特别是，在猫血中观察到60 H-BDE 47的浓度高于2 'OH-BDE 68和两种MeO-PBDE同源物，尽管MeO-BDE在猫食中占主导地位，这表明猫体内60 H-BDE 47从6 MeO-BDE 47发生了有效的生物转化。我们进行了体外去甲基化实验，以确认使用肝微粒体的MeO-PBDEs到OH-PBDEs的生物转化。结果表明，在两只动物体内，6 MeO-BDE 47和2 'MeO-BDE 68均脱甲基为60 H-BDE 47和2' OH-BDE 68，但未检测到BDE 47的羟基化代谢物。目前的研究表明，宠物猫通过含有鱼味的猫粮产品接触到MeO-PBDE，猫血液中的OH-PBDE来自天然MeO-PBDE同系物的CYP依赖性去甲基化，而不是来自PBDE的羟基化。
There are growing concerns about the increase in hyperthyroidism in pet cats due to exposure to organo-halogen contaminants and their hydroxylated metabolites. This study investigated the blood contaminants polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) and their hydroxylated and methoxylated derivatives (OH-PCBs, OH-PBDEs, and MeO-PBDEs), in pet dogs and cats. We also measured the residue levels of these compounds in commercially available pet foods. Chemical analyses of PCBs and OH-PCBs showed that the OH-PCB levels were 1 to 2 orders of magnitude lower in cat and dog food products than in their blood, suggesting that the origin of OH-PCBs in pet dogs and cats is PCBs ingested with their food. The major congeners of OH-/MeO-PBDEs identified in both pet food products and blood were natural products (60H-/MeO-BDE47 and 2'OH-/MeO-BDE68) from marine organisms. In particular, higher concentrations of 60H-BDE47 than 2'OH-BDE68 and two MeO-PBDE congeners were observed in the cat blood, although MeO-BDEs were dominant in cat foods, suggesting the efficient biotransformation of 60H-BDE47 from 6MeO-BDE47 in cats. We performed in vitro demethylation experiments to confirm the biotransformation of MeO-PBDEs to OH-PBDEs using liver microsomes. The results showed that 6MeO-BDE47 and 2'MeO-BDE68 were demethylated to 60H-BDE47 and 2'OH-BDE68 in both animals, whereas no hydroxylated metabolite from BDE47 was detected. The present study suggests that pet cats are exposed to MeO-PBDEs through cat food products containing fish flavors and that the OH-PBDEs in cat blood are derived from the CYP-dependent demethylation of naturally occurring MeO-PBDE congeners, not from the hydroxylation of PBDEs.