Koblin D D, Watson J E, Deady J E, Stokstad E L, Eger E I
Anesthesiology. 1981 Apr;54(4):318-24. doi: 10.1097/00000542-198104000-00012.
To characterize the nitrous oxide-induced inhibition of the enzyme, methionine synthetase, we measured enzyme inactivation as a function of nitrous oxide concentration and exposure time. Mice exposed to 0.8 atm nitrous oxide exhibited more than a 50 per cent decrease in liver methionine synthetase activity within 30 min, and activity dropped to 5--25 per cent of the original value after a 4-hour exposure. Although 4-hour exposures to low nitrous oxide partial pressures (less than 0.05 atm) did not significantly alter methionine synthetase activity, higher concentrations of nitrous oxide caused a progressive inhibition over this time period. Continuous exposure to trace levels of nitrous oxide (approximately 1100 ppm) for eight to 22 days produced a small but significant reduction in liver and brain methionine synthetase activity. Methionine synthetase activity returned to control levels two to four days following inactivation. Other anesthetics (xenon, halothane, isoflurane, enflurane) did not produce inactivation.
为了描述一氧化二氮对甲硫氨酸合成酶的抑制作用,我们测量了酶失活与一氧化二氮浓度和暴露时间的关系。暴露于0.8个大气压一氧化二氮的小鼠在30分钟内肝脏甲硫氨酸合成酶活性下降超过50%,暴露4小时后活性降至原始值的5% - 25%。虽然在低一氧化二氮分压(低于0.05个大气压)下暴露4小时不会显著改变甲硫氨酸合成酶活性,但在此时间段内较高浓度的一氧化二氮会导致逐渐抑制。连续暴露于痕量水平的一氧化二氮(约1100 ppm)八至二十二天会使肝脏和大脑甲硫氨酸合成酶活性出现小幅但显著的降低。失活后两至四天,甲硫氨酸合成酶活性恢复到对照水平。其他麻醉剂(氙气、氟烷、异氟烷、恩氟烷)不会导致失活。