Sano W, Watanabe F, Tamai H, Furuya E, Mino M
Department of Pediatrics, Osaka Medical College, Japan.
Gastroenterology. 1995 Jun;108(6):1785-92. doi: 10.1016/0016-5085(95)90141-8.
BACKGROUND/AIMS: Several groups have reported that administration of fructose-1,6-bisphosphate (FBP) reduces ischemic injury. The aim of this study was to determine the protective effect of FBP on the impairment of mitochondrial oxidative phosphorylation by ischemia-reperfusion injury in the rat liver.
The respiratory control ratio (RCR) and the adenine nucleotide content of mitochondria isolated from ischemic and reperfused livers with or without FBP treatment were measured.
In FBP-treated livers, the cellular adenosine triphosphate level was restored to more than 50% of normal after 120 minutes of reperfusion following 120 minutes of ischemia, whereas that of control livers only reached 15% of normal. The RCR and the adenine nucleotide content of mitochondria isolated from FBP-treated livers were significantly higher than those of mitochondria from control livers after ischemia and reperfusion. FBP strongly suppressed the formation of lipid peroxides during reperfusion. In vitamin E-deficient rats, the RCR decreased markedly during reperfusion, but FBP protected the mitochondria against reperfusion injury.
FBP has a protective effect against ischemia-reperfusion injury on the liver and especially preserves the oxidative phosphorylation capacity of hepatic mitochondria.
背景/目的：多个研究小组报告称，给予1,6-二磷酸果糖（FBP）可减轻缺血性损伤。本研究的目的是确定FBP对大鼠肝脏缺血再灌注损伤所致线粒体氧化磷酸化损伤的保护作用。
测量从接受或未接受FBP治疗的缺血再灌注肝脏中分离出的线粒体的呼吸控制率（RCR）和腺嘌呤核苷酸含量。
在FBP治疗的肝脏中，缺血120分钟后再灌注120分钟，细胞三磷酸腺苷水平恢复至正常水平的50%以上，而对照肝脏仅达到正常水平的15%。从FBP治疗的肝脏中分离出的线粒体的RCR和腺嘌呤核苷酸含量在缺血再灌注后显著高于对照肝脏的线粒体。FBP强烈抑制再灌注期间脂质过氧化物的形成。在维生素E缺乏的大鼠中，再灌注期间RCR明显下降，但FBP保护线粒体免受再灌注损伤。
FBP对肝脏缺血再灌注损伤具有保护作用，尤其能保留肝脏线粒体的氧化磷酸化能力。
