Faculty of Pharmaceutical Sciences, Josai University, Sakado, Saitama, Japan.
Biol Pharm Bull. 2011;34(6):856-64. doi: 10.1248/bpb.34.856.
Alterations by perfluorinated fatty acids (PFCAs) with a chain length of 6-9 carbons in the fatty acid profile of hepatic lipids of mice were investigated. The characteristic changes caused by all the PFCAs examined were increases in the contents and proportions of oleic acid (18 : 1), palmitoleic acid (16 : 1) and 8,11,14-eicosatrienoic acid (20 : 3) in hepatic lipids. Hepatic contents of palmitic acid were also increased by the treatments with the PFCAs. These effects were almost dependent on the hepatic concentrations of PFCA molecules regardless of their carbon chain length. Perfluorooctanoic acid elevated the expressions of mRNA encoding acetyl-CoA carboxylase, fatty acid synthase, malic enzyme, stearoyl-CoA desaturase (SCD) (SCD1 and 2), chain elongase (ELOVL5), Δ6 desaturase (Fads2), 1-acylglycerophosphocholine acyltransferase (LPCAT) (LPCAT3). The four PFCAs examined induced microsomal SCD and LPCAT in hepatic concentration-dependent manners regardless of carbon chain length. One linear regression line was confirmed between LPCAT activity and hepatic concentration of PFCA at wide range of the concentration, whereas the induction of SCD was saturable at relatively low concentration of PFCAs. These results suggest (i) that PFCAs with a chain length of 6-9 carbons change the fatty acid profile of hepatic lipids by increasing contents and proportions of 16 : 1, 18 : 1 and 20 : 3, (ii) that these alterations in fatty acid profile are caused by up-regulation of SCD, de novo fatty acid synthesis, chain elongase and Δ6 desaturase and (iii) that the mechanism underlying SCD induction is, in part, mediated through peroxisome proliferator-activated receptor α.
研究了链长为 6-9 个碳原子的全氟脂肪酸 (PFCAs) 对小鼠肝脂脂肪酸谱的影响。所有检查的 PFCAs 引起的特征变化是肝脂中油酸 (18:1)、棕榈油酸 (16:1) 和 8,11,14-二十碳三烯酸 (20:3) 的含量和比例增加。肝脂中的棕榈酸含量也因 PFCAs 的处理而增加。这些影响几乎取决于肝内 PFCAs 分子的浓度,而与碳链长度无关。全氟辛酸还能提高乙酰辅酶 A 羧化酶、脂肪酸合酶、苹果酸酶、硬脂酰辅酶 A 去饱和酶 (SCD)(SCD1 和 2)、链延长酶 (ELOVL5)、Δ6 去饱和酶 (Fads2)、1-酰基甘油磷酸胆碱酰基转移酶 (LPCAT) (LPCAT3) 的 mRNA 表达。在所检查的四种 PFCAs 中,无论碳链长度如何,都以肝浓度依赖的方式诱导微粒体 SCD 和 LPCAT。在广泛的浓度范围内,LPCAT 活性与 PFCA 的肝浓度之间证实了一条线性回归线,而 SCD 的诱导在相对较低的 PFCAs 浓度下达到饱和。这些结果表明:(i) 链长为 6-9 个碳原子的 PFCAs 通过增加 16:1、18:1 和 20:3 的含量和比例来改变肝脂的脂肪酸谱;(ii) 脂肪酸谱的这些变化是由 SCD、从头脂肪酸合成、链延长酶和 Δ6 去饱和酶的上调引起的;(iii) SCD 诱导的机制部分是通过过氧化物酶体增殖物激活受体-α介导的。