Decrease in Mitochondrial Levels of Adenine Nucleotides and Concomitant Mitochondrial Dysfunction in Ischemic Rat Liver1

Can adenine nucleotides predict primary nonfunction of the human liver homograft?

“…This irreversibility is partially due to the loss of mitochondrial oxidative phosphorylation capacity [14,25]. In addition to a decrease in AN, PC accumulates during warm ischemia, and this plays an important role in superoxide generation after reperfusion.…”

An improved technique for isolated perfusion of rat livers and an evaluation of perfusates

“…However, after an initial rise during the first 30 min of perfusions, the amount of bile produced during perfusions without albumin was stable and significantly higher than in the presence of albumin (P < 0.0001). In our system, the extent of hepatic injury can be assessed simply by monitoring the bile flow rate as a reflection of the cellular energy status [35][36][37].…”

Identification of the Mitochondrial ATP-Mg/Pi Transporter

“…For example, the mitochondrial adenine nucleotide pool has been found to be increased in newborn liver mitochondria 3-4 times within 3-4 h after birth (35) and in adult liver mitochondria upon fasting (50,51), after glucagon treatment (50 -52), and in altered thyroid states (53). On the other hand, it is decreased by hypoxia (54) and ischemia (55), in fast growing hepatomas (56), during hibernation (57), and in copper deficiency (58). Furthermore, recent data have shown that P iinduced opening of the permeability transition pore of rat liver mitochondria is secondary to depletion of the intramitochondrial adenine nucleotide content via the ATP-Mg/P i carrier (59).…”