Nishizaki Y
Biochim Biophys Acta. 1976 Dec 6;449(3):368-75. doi: 10.1016/0005-2728(76)90148-1.
Acid-base triggered luminescence in relation to slow delayed light emission (greater than 3 s) was studied in chloroplasts. After analyzing their time courses, the acid-base induced luminescence curve was found to return to the original curve of delayed light emission. Peaks of the acid-base triggered luminescence induced after various darkness periods following preillumination decreased parallel to the time course of delayed light emission without base treatment. 3-(3,4-Dichlorophenyl)-1,1-dimethylurea enhanced both the delayed light emission and acid-base induced luminescence, while carbonyl cyanide m-chlorophenylhydrazone inhibited both. Several photophosphorylat ion uncouplers inhibited the acid-base induced luminescence wtihout any substantial effect on the delayed light emission. It is concluded that the acid-base triggered luminescence is not caused by the reversionof electrons from remote intermediates on the reducing side of Photosystem II. The possibility of the presence of an activation pathway for the acid-base triggered luminescence which differs from that of the delayed light emission is also discussed.
研究了叶绿体中与缓慢延迟发光(大于3秒)相关的酸碱触发发光。在分析其时间进程后,发现酸碱诱导的发光曲线恢复到延迟发光的原始曲线。预照光后在不同黑暗期诱导的酸碱触发发光的峰值,与未经碱处理的延迟发光的时间进程平行下降。3-(3,4-二氯苯基)-1,1-二甲基脲增强了延迟发光和酸碱诱导的发光,而羰基氰化物间氯苯腙则两者都抑制。几种光合磷酸化解偶联剂抑制了酸碱诱导的发光,而对延迟发光没有任何实质性影响。得出的结论是,酸碱触发发光不是由光系统II还原侧远程中间体的电子逆转引起的。还讨论了存在不同于延迟发光的酸碱触发发光激活途径的可能性。