Turunen M, Dallner G
Department of Biochemistry, Stockholm University, Sweden.
Chem Biol Interact. 1998 Nov 6;116(1-2):79-91. doi: 10.1016/s0009-2797(98)00082-9.
The effect of di(2-ethylhexyl)phthalate (DEHP) on the induction of peroxisomes and the content of ubiquinone in the liver was studied in rats between 25 and 496 days of age. During this period, peroxisomal beta-oxidation of fatty acids was greatly decreased but it could be induced many-fold in all ages. The ubiquinone (UQ) content was increased upon induction 6-fold in the first weeks of life, but the extent of this elevation continuously narrowed and no induction could be observed in the oldest animals, even after prolonged treatment with the plasticizer. In contrast, the treatment decreased the amount of liver cholesterol in all age groups. Treatment with this peroxisomal inducer increased the biosynthesis of UQ while the breakdown rate was found to be unaffected, as the half-life of this lipid was 103 and 106 h in control and treated rats, respectively. These results indicate that treatment with peroxisomal inducers increases the liver UQ content by increasing the rate of biosynthesis and that this effect is not apparent in aged rats.
研究了邻苯二甲酸二（2-乙基己基）酯（DEHP）对25至496日龄大鼠肝脏中过氧化物酶体诱导及泛醌含量的影响。在此期间，脂肪酸的过氧化物酶体β-氧化作用大幅降低，但在所有年龄段都能被诱导增加数倍。在生命的最初几周，诱导后泛醌（UQ）含量增加了6倍，但这种升高的程度持续缩小，即使在用增塑剂长期处理后，最年长的动物中也未观察到诱导现象。相反，该处理降低了所有年龄组的肝脏胆固醇含量。用这种过氧化物酶体诱导剂处理增加了UQ的生物合成，而分解速率未受影响，因为在对照大鼠和处理大鼠中，这种脂质的半衰期分别为103小时和106小时。这些结果表明，用过氧化物酶体诱导剂处理可通过增加生物合成速率来提高肝脏UQ含量，且这种作用在老年大鼠中不明显。
