Yamamoto A, Kawashima Y
Faculty of Pharmaceutical Sciences, Josai University, Keyakidai, Sakado, Saitama 350-02, Japan.
Biochem J. 1997 Jul 15;325 ( Pt 2)(Pt 2):429-34. doi: 10.1042/bj3250429.
The feeding of perfluorodecanoic acid (PFDA) to male rats at a dietary concentration of 0.005% (w/w) for 7 days resulted in a marked increase in the activity of microsomal stearoyl-CoA desaturation in the liver. This increase in the overall desaturation activity was due to the induction of terminal desaturase among the components comprising the desaturation system. In contrast, PFDA inhibited desaturation in vitro, seemingly due to interference with electron transport through the desaturation system. Accordingly, PFDA can be an inducer and also an inhibitor of delta9-desaturation. PFDA feeding enhanced the conversion of radioactive stearic acid into oleic acid in the liver in vivo, indicating that the induction of delta9-desaturase by PFDA functions in vivo. PFDA feeding increased the mass of octadecenoic acid (C18:1) in the liver and the proportion of C18:1 in microsomal lipid. A highly significant linear correlation existed between the microsomal desaturase activity and the proportion of C18:1 in microsomal lipid when compared using rats in five different physiological states: control, PFDA-fed, p-chlorophenoxyisobutyric acid (clofibric acid)-fed, starved and starved/refed. These results suggest that the increase in the hepatic level of C18:1 caused by feeding of PFDA to rats can be explained by the common concept of regulation, i.e. the hepatic level of C18:1 is under the control of delta9-desaturase. The dietary administration of PFDA also increased the content of cytochrome P-450 and the activity of 7-ethoxycoumarin O-de-ethylase in the liver.
以0.005%（w/w）的膳食浓度给雄性大鼠喂食全氟癸酸（PFDA）7天，导致肝脏微粒体硬脂酰辅酶A去饱和酶的活性显著增加。整体去饱和活性的这种增加是由于去饱和系统组成成分中末端去饱和酶的诱导。相比之下，PFDA在体外抑制去饱和，这似乎是由于其干扰了通过去饱和系统的电子传递。因此，PFDA可以是Δ9-去饱和的诱导剂，也是抑制剂。喂食PFDA可增强体内肝脏中放射性硬脂酸向油酸的转化，表明PFDA对Δ9-去饱和酶的诱导在体内起作用。喂食PFDA增加了肝脏中十八碳烯酸（C18:1）的含量以及微粒体脂质中C18:1的比例。当使用处于五种不同生理状态的大鼠（对照、喂食PFDA、喂食对氯苯氧异丁酸（氯贝酸）、饥饿和饥饿/再喂食）进行比较时，微粒体去饱和酶活性与微粒体脂质中C18:1的比例之间存在高度显著的线性相关性。这些结果表明，给大鼠喂食PFDA导致肝脏中C18:1水平升高可以用共同的调节概念来解释，即肝脏中C18:1的水平受Δ9-去饱和酶的控制。膳食给予PFDA还增加了肝脏中细胞色素P-450的含量以及7-乙氧基香豆素O-脱乙基酶的活性。
