Laposata M, Prescott S M, Bross T E, Majerus P W
Proc Natl Acad Sci U S A. 1982 Dec;79(24):7654-8. doi: 10.1073/pnas.79.24.7654.
We have developed an essential fatty acid-deficient cell line from a parental cell line, HSDM1C1, which metabolizes arachidonic acid to prostaglandin E2 (PGE2). This cell line, designated EFD-1, is depleted of arachidonate, is unable to synthesize PGE2 in response to bradykinin, and has changes in fatty acid composition characteristic of tissues from animals with essential fatty acid deficiency. Within 15 min of repletion by arachidonate, the ability to synthesize PGE2 is restored. Linoleate also is able to restore PGE2 synthesis, indicating that deficient cells contain both the rate-limiting delta 6 desaturase enzyme and the delta 5 desaturase enzyme, which are required to form arachidonate. When parental cells are incubated in lipid-free medium, there is rapid induction of the ability to convert linoleate to arachidonate. Arachidonate prevents this induction, suggesting that icosanoid precursor availability controls the rate of arachidonate formation.
我们从亲代细胞系HSDM1C1中培育出了一种必需脂肪酸缺乏的细胞系,该亲代细胞系可将花生四烯酸代谢为前列腺素E2(PGE2)。这种细胞系命名为EFD-1,缺乏花生四烯酸,对缓激肽无反应,无法合成PGE2,并且其脂肪酸组成具有必需脂肪酸缺乏动物组织的特征性变化。在补充花生四烯酸后的15分钟内,合成PGE2的能力得以恢复。亚油酸也能够恢复PGE2的合成,这表明缺乏的细胞同时含有形成花生四烯酸所需的限速δ6去饱和酶和δ5去饱和酶。当将亲代细胞在无脂质培养基中孵育时,将亚油酸转化为花生四烯酸的能力会迅速诱导产生。花生四烯酸可阻止这种诱导,这表明类二十烷酸前体的可用性控制着花生四烯酸的形成速率。