The effect of oxidative injury on hepatocellular influx of leucine in the rat

David G. Le Couteur , Laurent P. Rivory, Susan M. Pond
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引用次数: 2

Abstract

The hepatocellular influx of leucine was investigated in the perfused rat liver using the multiple indicator-dilution technique. The cellular influx of leucine was saturable and the Km and Vmax values were 5.3 ± 1.8 mM and 194 ± 25 nmol/s/g of liver, respectively. These were similar to those reported in cell membrane preparations. Previous studies have indicated that oxidative injury impairs the activity of membrane transporters. Perfusion with 10 mM hydrogen peroxide for 3 min caused a significant reduction in leucine influx from 7.4 ± 1.4 nmol/s/g of liver to 4.6 ± 1.0 nmol/s/g of liver (P = 0.007) with a perfusate leucine concentration of 0.13 μM. This was not associated with any significant change in the extracellular volume (0.31 ± 0.08 ml/g of liver vs. 0.32 ± 0.01 ml/g of liver). This confirms that oxidative injury in the liver is associated with impairment of membrane transport and extends the observation to the transport of leucine.

氧化损伤对大鼠肝细胞亮氨酸内流的影响
采用多指标稀释法研究了大鼠灌注肝脏中亮氨酸的肝细胞内流。亮氨酸的细胞内流是饱和的,肝脏Km和Vmax分别为5.3±1.8 mM和194±25 nmol/s/g。这些与在细胞膜制备中报道的相似。以往的研究表明,氧化损伤会损害膜转运蛋白的活性。10 mM过氧化氢灌注3 min后,肝脏亮氨酸内流从7.4±1.4 nmol/s/g显著降低至4.6±1.0 nmol/s/g (P = 0.007),灌注亮氨酸浓度为0.13 μM。这与细胞外体积的任何显著变化无关(肝脏为0.31±0.08 ml/g,肝脏为0.32±0.01 ml/g)。这证实了肝脏氧化损伤与膜转运障碍有关,并将观察扩展到亮氨酸的转运。
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