多氯联苯化合物、2,3,7,8-四氯二苯并对二恶英、苯巴比妥和铁对肝脏尿卟啉原脱羧酶的影响。对卟啉症发病机制的启示。
Effects of polychlorinated biphenyl compounds, 2,3,7,8-tetrachlorodibenzo-p-dioxin, phenobarbital and iron on hepatic uroporphyrinogen decarboxylase. Implications for the pathogenesis of porphyria.
作者信息
De Verneuil H, Sassa S, Kappas A
出版信息
Biochem J. 1983 Jul 15;214(1):145-51. doi: 10.1042/bj2140145.
Abstract
Treatment of cultured chick embryo hepatocytes with phenobarbital, polychlorinated biphenyl compounds and 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in increased delta-aminolaevulinate synthase and decreased uroporphyrinogen decarboxylase activities and porphyrin accumulation; uroporphyrin and heptacarboxyporphyrin predominated. Iron had no effect on these changes. Simultaneous treatment of cultures with dioxin and phenobarbital produced a synergistic response in delta-aminolaevulinate synthase induction, uroporphyrinogen decarboxylase inhibition and porphyrin accumulation. These data suggest that an inhibitor of uroporphyrinogen decarboxylase may be generated in the liver from polychlorinated biphenyl compounds or dioxin by metabolic activation. Additionally these findings bear on the postulated role of these and related chemicals in determining the low levels of uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients.
摘要
用苯巴比妥、多氯联苯化合物和2,3,7,8-四氯二苯并对二恶英处理培养的鸡胚肝细胞，导致δ-氨基乙酰丙酸合酶活性增加、尿卟啉原脱羧酶活性降低以及卟啉积累；尿卟啉和七羧基卟啉占主导。铁对这些变化没有影响。用二恶英和苯巴比妥同时处理培养物，在δ-氨基乙酰丙酸合酶诱导、尿卟啉原脱羧酶抑制和卟啉积累方面产生协同反应。这些数据表明，尿卟啉原脱羧酶的抑制剂可能通过代谢活化在肝脏中由多氯联苯化合物或二恶英产生。此外，这些发现与这些及相关化学物质在迟发性皮肤卟啉症患者中导致尿卟啉原脱羧酶活性水平降低的假定作用有关。
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