Arnaud Alexandra, López-Pedrosa José María, Torres María Isabel, Gil Angel
R&D Department, Abbott Laboratories, Ross Products Division, Granada, Spain.
J Pediatr Gastroenterol Nutr. 2003 Aug;37(2):124-31. doi: 10.1097/00005176-200308000-00008.
Chronic diarrhea during early infancy is characterized by intestinal mucosal injury, and as a consequence, the mitochondrial system of oxidation and reduction and energy production is altered. Since dietary nucleotides have been associated with the process of intestinal mucosal repair in rats with chronic diarrhea, the aim of this study was to examine the effects of dietary nucleotides on the functioning of mucosal mitochondria.
Weanling rats were fed with a semipurified synthetic diet (C) or the same diet in which carbohydrates were substituted by lactose (L), resulting in chronic diarrhea. During recovery, rats were fed with the semipurified synthetic diet (LC) or the same diet supplemented with nucleotides (LN). The activities of adenosine triphosphate synthase (ATPase), cytochrome c oxidase, citrate synthase, and malate dehydrogenase were measured in mitochondria from ileum and colon mucosa.
These enzymatic activities rose in rats with chronic diarrhea, possibly to compensate for the drastic decline in adenosine triphosphate (ATP) synthesis. Dietary nucleotide supplementation allowed normalizing of the activities of ATPase (C: 0.37 +/- 0.16 microg/min/mg protein; L: 0.68 +/- 0.25 microg/min/mg protein; LC: 0.60 +/- 0.20 microg/min/mg protein; LN: 0.42 +/- 0.22 microg/min/mg protein), citrate synthase (C: 0.12 +/- 0.05 mM/min/mg protein; L: 0.21 +/- 0.07 mM/min/mg protein; LC: 0.21 +/- 0.06 mM/min/mg protein; LN: 0.12 +/- 0.02 mM/min/mg protein), and malate dehydrogenase (C: 0.77 +/- 0.48 mM/min/mg protein; L: 3.08 +/- 0.85 mM/min/mg protein; LC: 2.11 +/- 0.44 mM/min/mg protein; LN: 1.13 +/- 0.51 mM/min/mg protein) in the ileum mitochondria of the diarrheic rats. In colonic mucosa, mitochondrial enzymatic activities were restored after eliminating lactose from the diet.
These results suggest that dietary nucleotides promote earlier restoration of the ileal mitochondrial function after chronic diarrhea.
婴儿早期的慢性腹泻以肠黏膜损伤为特征,因此,氧化还原和能量产生的线粒体系统会发生改变。由于膳食核苷酸与慢性腹泻大鼠的肠黏膜修复过程有关,本研究的目的是检测膳食核苷酸对黏膜线粒体功能的影响。
给断奶大鼠喂食半纯化合成饮食(C组)或用乳糖替代碳水化合物的相同饮食(L组),从而导致慢性腹泻。在恢复期间,给大鼠喂食半纯化合成饮食(LC组)或添加了核苷酸的相同饮食(LN组)。测定回肠和结肠黏膜线粒体中三磷酸腺苷合酶(ATP酶)、细胞色素c氧化酶、柠檬酸合酶和苹果酸脱氢酶的活性。
这些酶活性在慢性腹泻大鼠中升高,可能是为了补偿三磷酸腺苷(ATP)合成的急剧下降。补充膳食核苷酸可使腹泻大鼠回肠线粒体中ATP酶(C组:0.37±0.16微克/分钟/毫克蛋白质;L组:0.68±0.25微克/分钟/毫克蛋白质;LC组:0.60±0.20微克/分钟/毫克蛋白质;LN组:0.42±0.22微克/分钟/毫克蛋白质)、柠檬酸合酶(C组:0.12±0.05毫摩尔/分钟/毫克蛋白质;L组:0.21±0.07毫摩尔/分钟/毫克蛋白质;LC组:0.21±0.06毫摩尔/分钟/毫克蛋白质;LN组:0.12±0.02毫摩尔/分钟/毫克蛋白质)和苹果酸脱氢酶(C组:0.77±0.48毫摩尔/分钟/毫克蛋白质;L组:3.08±0.85毫摩尔/分钟/毫克蛋白质;LC组:2.11±0.44毫摩尔/分钟/毫克蛋白质;LN组:1.13±0.51毫摩尔/分钟/毫克蛋白质)的活性恢复正常。在结肠黏膜中,从饮食中去除乳糖后线粒体酶活性恢复。
这些结果表明,膳食核苷酸可促进慢性腹泻后回肠线粒体功能的早期恢复。