Miura Y
Lipids. 1981 Oct;16(10):721-5. doi: 10.1007/BF02535338.
Frog liver microsomes catalyzed the hydroxylation of 1-dodecanol into the corresponding omega- and (omega-1)-hydroxy derivatives. The hydroxylation rate for 1-dodecanol was much lower than that for lauric acid. Both NADPH and O2 were required for hydroxylation activity. NADH had no effect on the hydroxylation. The hydroxylating system was inhibited 49% by CO at a CO:O2 ratio of 4.0. The formation of omega-hydroxydodecanol was more sharply inhibited by CO than was the formation of (omega-1)-hydroxydodecanol, implying that more than one cytochrome P-450 was involved in the hydroxylation of 1-dodecanol and that CO has a higher affinity for the P-450 catalyzing the omega-hydroxylation. The formation of laurate during the incubation of 1-dodecanol with frog liver microsomes suggests that a fatty alcohol oxidation system is also present in the microsomes. NAD+ was the most effective cofactor for the oxidation of 1-dodecanol and NADP+ had a little effect. Pyrazole (an inhibitor of alcohol dehydrogenase) had a slight inhibitory effect on the oxidation and sodium azide (an inhibitor of catalase) had no effect.
蛙肝微粒体催化1-十二醇羟基化为相应的ω-和（ω-1）-羟基衍生物。1-十二醇的羟基化速率远低于月桂酸的羟基化速率。羟基化活性需要NADPH和O₂。NADH对羟基化没有影响。在CO:O₂比例为4.0时，羟基化系统被CO抑制49%。与（ω-1）-羟基十二烷醇的形成相比，ω-羟基十二烷醇的形成受到CO的抑制更为明显，这意味着1-十二醇的羟基化涉及不止一种细胞色素P-450，并且CO对催化ω-羟基化的P-450具有更高的亲和力。1-十二醇与蛙肝微粒体孵育期间月桂酸的形成表明微粒体中也存在脂肪醇氧化系统。NAD⁺是1-十二醇氧化最有效的辅因子，NADP⁺的作用较小。吡唑（醇脱氢酶抑制剂）对氧化有轻微抑制作用，叠氮化钠（过氧化氢酶抑制剂）没有作用。
