Tomasi A, Billing S, Garner A, Slater T F, Albano E
Chem Biol Interact. 1983 Sep 15;46(3):353-68. doi: 10.1016/0009-2797(83)90019-4.
The technique of free radical spin trapping has been applied to demonstrate the formation of free radicals produced during the metabolism of halothane by rat liver hepatocytes under hypoxic conditions. The results obtained support previous findings that reported sex differences in the metabolic activation of halothane by rats in vivo. Cell viability under hypoxic conditions, as judged by trypan blue staining and lactate dehydrogenase release, shows a correlation with the extent of metabolism of halothane as measured by electron spin resonance spectroscopy. The extent of lipid peroxidation was measured by diene conjugation, malondialdehyde production and chemiluminescence. The latter technique allowed the demonstration of lipid peroxidation during incubations of hepatocytes under aerobic conditions. The magnitude of the aerobic chemiluminescence showed a similar sex dependency to the extent of free radical formation under hypoxic conditions. Cell viability measurements show that halothane metabolism in both hypoxic and aerobic conditions can lead to cell death. Consequently, oxidative lipid damage could be a cause of cell damage, as judged by cell viability, additional to covalent binding.
自由基自旋捕捉技术已被用于证明在缺氧条件下大鼠肝脏肝细胞代谢氟烷过程中产生的自由基的形成。所获得的结果支持了先前的研究发现，即报告了大鼠体内氟烷代谢激活存在性别差异。通过台盼蓝染色和乳酸脱氢酶释放判断，缺氧条件下的细胞活力与通过电子自旋共振光谱测量的氟烷代谢程度相关。脂质过氧化程度通过二烯共轭、丙二醛生成和化学发光进行测量。后一种技术能够证明在有氧条件下肝细胞孵育过程中的脂质过氧化。有氧化学发光的强度在缺氧条件下与自由基形成程度表现出相似的性别依赖性。细胞活力测量表明，在缺氧和有氧条件下氟烷代谢均可导致细胞死亡。因此，除共价结合外，从细胞活力判断，氧化脂质损伤可能是细胞损伤的一个原因。
