Atlante A, Seccia T M, Marra E, Minervini G M, Vulpis V, Pirrelli A, Passarella S
Centro di Studio sui Mitocondri e Metabolismo Energetico, CNR, Bari, Italy.
FEBS Lett. 1996 Nov 4;396(2-3):279-84. doi: 10.1016/0014-5793(96)01114-3.
In this study we have investigated hydroxyproline transport in rat heart mitochondria and, in particular, in heart left ventricle mitochondria isolated from both spontaneously hypertensive and Wistar-Kyoto rats. Hydroxyproline uptake by mitochondria, where its catabolism takes place, occurs via a carrier-mediated process as demonstrated by the occurrence of both saturation kinetics and the inhibition shown by phenylsuccinate and the thiol reagent mersalyl. In any case, hydroxyproline transport was found to limit the rate of mitochondrial hydroxyproline catabolism. A significant change in Vmax and Km values was found in mitochondria from hypertensive/hypertrophied rats in which the Km value decreases and the Vmax value increases with respect to normotensive rats, thus accounting for the increase of hydroxyproline metabolism due to its increased concentration in a hypertrophic/hypertensive state.
在本研究中，我们研究了大鼠心脏线粒体中羟脯氨酸的转运，特别是从自发性高血压大鼠和Wistar-Kyoto大鼠分离的心脏左心室线粒体中的羟脯氨酸转运。线粒体摄取羟脯氨酸（其分解代谢发生在此处）是通过载体介导的过程进行的，饱和动力学的出现以及苯琥珀酸盐和硫醇试剂汞撒利所显示的抑制作用证明了这一点。无论如何，发现羟脯氨酸转运限制了线粒体羟脯氨酸分解代谢的速率。在高血压/肥大大鼠的线粒体中发现Vmax和Km值有显著变化，其中与正常血压大鼠相比，Km值降低而Vmax值增加，从而解释了在肥大/高血压状态下由于羟脯氨酸浓度增加导致其代谢增加的原因。
