Donchenko G V, Metal'nikova N P, Palivoda O M
Ukr Biokhim Zh (1978). 1985 Jan-Feb;57(1):47-52.
A decrease in the CoA and acetyl-CoA amount in the rat liver tissue by 34.8 and 29.4%, respectively, as well as inhibition of the biosynthesis rate of mevalonic acid from [I-14C] acetyl-CoA in the postmitochondrial liver fraction by 17.9% as compared to the control are found against a background of E-hypovitaminosis. The last change is not associated with the inhibition of the 3-oxy-3-methylglutaryl-CoA-reductase activity and may not be one of reasons which cause the biosynthesis disturbances in the isoprenoid part of the ubiquinone molecule in this organ. alpha-Tocopherol activates the ubiquinone biosynthesis from [2-14C] sodium acetate in the liver of rats with E-hypovitaminosis under conditions of 30 min preincubation and is not efficient when added in combination with actinomycin D. Probably, such an effect of alpha-tocopherol is realized at the level of RNA synthesis and is associated with the biosynthesis activation of short-living RNA.
在维生素E缺乏症背景下,大鼠肝脏组织中辅酶A和乙酰辅酶A的含量分别降低了34.8%和29.4%,并且与对照组相比,肝脏线粒体后部分中由[I-14C]乙酰辅酶A合成甲羟戊酸的生物合成速率受到17.9%的抑制。最后一个变化与3-氧代-3-甲基戊二酰辅酶A还原酶活性的抑制无关,可能不是导致该器官中泛醌分子类异戊二烯部分生物合成紊乱的原因之一。α-生育酚在预孵育30分钟的条件下可激活维生素E缺乏症大鼠肝脏中由[2-14C]醋酸钠合成泛醌的过程,而与放线菌素D联合添加时则无效。α-生育酚的这种作用可能在RNA合成水平上实现,并且与短寿命RNA的生物合成激活有关。