Martínez F, Espinosa-García T, Flores-Herrera O, Pardo J P
Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, D.F.
Placenta. 1993 May-Jun;14(3):321-31. doi: 10.1016/s0143-4004(05)80430-8.
Oxygen uptake in human placental mitochondria was stimulated by ATP addition. ATP-induced respiration was supported by malate, alpha-keto glutarate, and succinate, and inhibited by oligomycin and carboxytractyloside. This phenomenon was not caused by contamination with unspecific phosphatases or alkaline phosphatase, since NaF, L-phenyl alanine, or P1, P5-di-(adenosine-5') pentaphosphate failed to inhibit oxygen uptake induced by ATP. The stimulation of respiration was caused by an ATPase activity tightly bound to mitochondria, which yields ADP that is responsible for the oxygen uptake. The stimulation was not an uncoupling effect because ATP addition produced a transition between state 3 and 4 of respiration, indicating that ATP was not released from mitochondria.
添加ATP可刺激人胎盘线粒体对氧气的摄取。ATP诱导的呼吸作用由苹果酸、α-酮戊二酸和琥珀酸支持,并受到寡霉素和羧基鱼藤酮的抑制。这种现象并非由非特异性磷酸酶或碱性磷酸酶污染所致,因为氟化钠、L-苯丙氨酸或P1、P5-二(腺苷-5')五磷酸均未能抑制ATP诱导的氧气摄取。呼吸作用的刺激是由紧密结合在线粒体上的ATP酶活性引起的,该活性产生的ADP负责氧气摄取。这种刺激不是解偶联效应,因为添加ATP会导致呼吸状态3和状态4之间的转变,这表明ATP并未从线粒体中释放出来。