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Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency

机译:在消化蛋白质缺陷背景下毒性损伤瘤肝粉煤中酸瘤代谢指标

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It is known that citrulline is converted into arginine in the series of metabolic transformations. Results of our previous studies showed that acetaminophen-induced toxic injury on the background of the alimentary deprivation of protein is accompanied by a decrease in arginine level in rat hepatocytes, but citrulline liver metabolism at these conditions remains incompletely clear. In this work, the content of citrulline in the rat liver mitochondrial and cytosolic fractions and the activity of citrulline-degrading enzymes – argininosuccinate synthase and argininosuccinate lyase were investigated. It was found that in the mitochondrial fraction a maximal reduction of the citrulline levels occurred after administration of acetaminophen toxic doses regardless of the protein amount in the ration, while in the cytosolic fraction the alimentary protein deficiency was a key factor in decreasing the activity of argininosuccinate synthase and arginino-succinate lyase. The data obtained indicated the disturbances of the urea cycle functioning and explained the decrease of L-arginine level in hepatocytes in conditions of acetaminophen-induced toxic injury against the background alimentary protein deficiency.
机译:众所周知,在一系列代谢转化中将瓜氨酸转化为精氨酸。我们以前的研究结果表明,对蛋白质的消化剥夺背景的乙酰氨基酚诱导的毒性损伤伴随着大鼠肝细胞的精氨酸水平降低,但这些条件下的瓜氨酸肝脏代谢仍然不完全清楚。在这项工作中,研究了大鼠肝线粒体和细胞溶质分数中的瓜氨酸的含量以及瓜氨酸降解酶 - 氨基氨基铵合酶和精氨酸琥珀酸裂解酶的活性。发现在线粒体级分中,无论在对乙酰氨基酚毒性剂量施用乙酰氨基酚毒性剂量的情况下,在对乙酰氨基酚毒性剂量的情况下发生的最大降低,而在胞质粒子级分中,消化蛋白质缺乏是降低氨基膦酸的活性的关键因素合成酶和阿糖氨基 - 琥珀酸盐酶。所获得的数据表明了尿素循环功能的干扰,并解释了对乙酰氨基酚诱导的毒性损伤条件的肝细胞中L-精氨酸水平的降低。

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