Latipää P M, Kärki T T, Hiltunen J K, Hassinen I E
Biochim Biophys Acta. 1986 Feb 12;875(2):293-300. doi: 10.1016/0005-2760(86)90179-7.
The redox-mediated regulation of palmitoylcarnitine oxidation was studied in isolated rat liver mitochondria in which the mitochondrial free NADH/NAD+ ratio was controlled by graded concentrations of acetoacetate and ketomalonate in a rotenone and malonate-inhibited system in the presence of ADP. The NADH/NAD+ ratio was buffered kinetically by adjusting the concentrations of the hydrogen acceptor substances and determined by calibrated NAD(P)H fluorometry of the mitochondrial suspension. A two-fold variation in the beta-oxidation rate and a five-fold variation in the free NADH/NAD+ ratio was obtained in the presence of rotenone. A non-linear negative correlation was found between the acetyl-CoA concentration and the beta-oxidation rate and a negative correlation between the long-chain acyl-CoA concentration and the beta-oxidation rate. The data indicate that the redox state is a partial controller of the beta-oxidation rate in liver mitochondria. The contribution of acetyl-CoA, a putative regulator of beta-oxidation at the acyl-CoA thiolase step is small under the conditions used.
在离体大鼠肝线粒体中研究了氧化还原介导的棕榈酰肉碱氧化调节,在存在ADP的鱼藤酮和丙二酸抑制系统中,通过分级浓度的乙酰乙酸和酮丙二酸来控制线粒体游离NADH/NAD⁺比值。通过调节氢受体物质的浓度对NADH/NAD⁺比值进行动力学缓冲,并通过线粒体悬浮液的校准NAD(P)H荧光法测定。在存在鱼藤酮的情况下,β氧化速率有两倍的变化,游离NADH/NAD⁺比值有五倍的变化。发现乙酰辅酶A浓度与β氧化速率之间存在非线性负相关,长链酰基辅酶A浓度与β氧化速率之间存在负相关。数据表明氧化还原状态是肝线粒体中β氧化速率的部分控制因素。在所用条件下,乙酰辅酶A作为酰基辅酶A硫解酶步骤中β氧化的假定调节因子,其作用较小。