Domenicali M, Caraceni P, Vendemiale G, Grattagliano I, Nardo B, Dall'Agata M, Santoni B, Trevisani F, Cavallari A, Altomare E, Bernardi M
Dipartimento di Medicina Interna, Cardioangiologia ed Epatologia e., Rianimatorie e dei Trapianti, University of Bologna, 40138 Bologna, Italy.
J Nutr. 2001 Jan;131(1):105-10. doi: 10.1093/jn/131.1.105.
Mitochondria undergo oxidative damage during reperfusion of ischemic liver. Although nutritional status affects ischemia-reperfusion injury in the liver, its effect on mitochondrial damage has not been evaluated. Thus, this study was designed to determine whether starvation influences the oxidative balance in mitochondria isolated from livers exposed to warm ischemia-reperfusion. Fed and 18- and 36-h food-deprived rats underwent partial hepatic ischemia followed by reperfusion. Mitochondria were isolated before and after ischemia and during reperfusion. Serum alanine transaminase was measured to assess liver injury. The mitochondrial concentrations of malondialdehyde, protein carbonyls and glutathione were determined as indicators of oxidative injury. Cell ultrastructure was assessed by transmission electron microscopy. Transaminase levels were greater in 18-h food-deprived than fed rats (after 120 min of reperfusion: 3872 +/- 400 vs. 1138 +/- 59 U/L, P < 0.01). Mitochondrial glutathione was lower in food-deprived than fed rats before and after ischemia, and during reperfusion. Food deprivation also was associated with significantly greater lipid and protein oxidative damage. Finally, more ultrastructural damage was observed during reperfusion in mitochondria from food-deprived rats. Prolonging the length of food deprivation to 36 h exacerbated significantly both the mitochondrial oxidative injury and the release of serum transaminases in rats (after 120 min of reperfusion: 5438 +/- 504 U/L, P < 0.01). Food deprivation was associated with greater mitochondrial oxidative injury in rat livers exposed to warm ischemia-reperfusion, and the extent of oxidative damage in mitochondria increased with the length of food deprivation.
线粒体在缺血肝脏再灌注过程中会遭受氧化损伤。尽管营养状况会影响肝脏的缺血再灌注损伤，但其对线粒体损伤的影响尚未得到评估。因此，本研究旨在确定饥饿是否会影响从经历热缺血再灌注的肝脏中分离出的线粒体的氧化平衡。对喂食的大鼠以及禁食18小时和36小时的大鼠进行部分肝脏缺血，然后再灌注。在缺血前后以及再灌注期间分离线粒体。测量血清丙氨酸转氨酶以评估肝损伤。测定线粒体中丙二醛、蛋白质羰基和谷胱甘肽的浓度作为氧化损伤的指标。通过透射电子显微镜评估细胞超微结构。禁食18小时的大鼠的转氨酶水平高于喂食的大鼠（再灌注120分钟后：3872±400 vs. 1138±59 U/L，P<0.01）。在缺血前后以及再灌注期间，禁食大鼠的线粒体谷胱甘肽含量均低于喂食的大鼠。禁食还与脂质和蛋白质氧化损伤显著增加有关。最后，在禁食大鼠的线粒体再灌注期间观察到更多的超微结构损伤。将禁食时间延长至36小时会显著加剧大鼠的线粒体氧化损伤和血清转氨酶的释放（再灌注120分钟后：5438±504 U/L，P<0.01）。饥饿与热缺血再灌注的大鼠肝脏中线粒体氧化损伤加重有关，并且线粒体氧化损伤的程度随着禁食时间的延长而增加。
