Videla L A, Villena M I, Donoso G, Giulivi C, Boveris A
Biochem J. 1984 Nov 1;223(3):879-83. doi: 10.1042/bj2230879.
The addition of t-butyl hydroperoxide to perfused rat liver elicited a biphasic effect on hepatic respiration. A rapid fall in liver oxygen consumption was initially observed, followed by a recovery phase leading to respiratory rates higher than the initial steady-state values of oxygen uptake. This overshoot in hepatic oxygen uptake was abolished by free-radical scavengers such as (+)-cyanidanol-3 or butylated hydroxyanisole at concentrations that did not alter mitochondrial respiration. (+)-Cyanidanol-3 was also able to facilitate the recovery of respiration, the diminution in the calculated rate of hydroperoxide utilization and the decrease in liver GSH content produced by two consecutive pulses of t-butyl hydroperoxide. It is suggested that the t-butyl hydroperoxide-induced overshoot in liver respiration is related to increased utilization of oxygen for lipid peroxidation as a consequence of free radicals produced in the scission of the hydroperoxide by cellular haemoproteins.
向灌注大鼠肝脏中添加叔丁基过氧化氢会对肝脏呼吸产生双相效应。最初观察到肝脏耗氧量迅速下降，随后是一个恢复阶段，导致呼吸速率高于初始稳态氧摄取值。肝脏氧摄取的这种过冲现象可被自由基清除剂如（+）-氰基丹酚-3或丁基化羟基茴香醚消除，其浓度不会改变线粒体呼吸。（+）-氰基丹酚-3还能够促进呼吸恢复、降低计算出的过氧化氢利用率以及减轻由连续两个叔丁基过氧化氢脉冲产生的肝脏谷胱甘肽含量的下降。有人提出，叔丁基过氧化氢诱导的肝脏呼吸过冲与细胞血红蛋白将过氧化氢裂解产生的自由基导致脂质过氧化对氧的利用增加有关。
