摘要
作用于质子通道的抑制剂(TPT,DCCD和OM)对与叶绿体中质子跨膜传导失去联系的甲醇活化的类囊体膜上或离体的CF1—ATP酶活性无抑制作用,其主要作用部位在质子通道CF_0上。TPT和 DCCD能恢复残缺膜积贮H_in^+、重建△pH和△ψ,使其电子流从解联状态回到复与叶绿体基础电子流相一致的水平。低浓度TPT即可部分恢复残缺膜的DLE,而DCCD需较高的浓度。低浓度TPT对叶绿体DLE有明显促进作用,而高浓度TPT和 DCCD有抑制作用。OM对这些功能都没有明显影响。推测OM可能作用于CF_0与CF_1的连接处,TPT的作用部位可能与光系统Ⅱ的水氧化质子释放部位有联系。
The effects of triphenyltin chloride (TPT),
dicyclohexylcarbodiimide (DCCD) and oligo-
anycin (OM), which act on the proton channel
of H^+ -ATPase complex, on proton conduction
and relative steps in chloroplasts have been
studied. They have no obvious effects on the
thylakoid membrane-bound or isolated CF_1-
ATPase activity activated by methanol (Table 1,
Fig. 1), which have no association with proton
translocation across membrane. TPT and
DCCD decrease the intensity of delayed light
amission(DLE) in chloroplasts at higher con-
centration, while TPT increases DLE distinc-
tively at lowcr concentration. OM has no ob-
vious effect (Fig. 2). TPT and DCCD enable
the depleted thylakoid membrane (DTM) to
reconstitute ?pH (Fig. 3), to retard the decay
of electrochromic absorption at 515 nm (Fig. 4),
to restore the H_(in)^+ accumulation (Fig. 5) and
to decrease the electron flow from uncoupled
state to the level of basal state in chloroplasts
(Fig. 6). TPT can obviously restore the DLE
of DTM, while DCCD can partially restore it
only at high concentration and the ustored DLE
has different characteristics from those in chlo-
roplasts (Fig.7). OM has no effect on DTM.
As the action site of DCCD has been known,
we speculate the action site of OM may be on
the connection place between CF_0 and CF_1,
and that of TPT may have relation to the proton
release site of water splitting of Photosystem Ⅱ.
基金
国家自然科学基金
关键词
叶绿体
三苯基锡
寡霉素
chloroplasts
H^+-ATPase
depleted thylakoid membrane
proton channel
triphenyltin chloride
dicyclohexylcarbodiimide
oligomycin