【摘要】 铜离子对PS Ⅱ电子传递有明显的抑制作用,并且不能被加入人工电子供体DPC而恢复电子传递。铜离子表现出对胰蛋白酶消化叶绿体膜后使PS Ⅱ电子传递所受抑制有加成作用,并且铜离子又可拮抗胰蛋白酶对被DCMU阻止的PS Ⅱ电子传递的部分恢复作用。因而推测铜离子在PS Ⅱ的作用部位是在DPC供电子处至PS Ⅱ作用中心之间,其作用方式可能在于钝化了参与PS Ⅱ电子传递的膜蛋白。用SDS-PAGE对叶绿体膜蛋白的分离结果,也符合于这一假设。更多还原

【Abstract】 The PSⅡ electron transport was significantly inhibited by Cu²⁺ treatment, and the rate of electron transport could not be restored by the addition of the artificial electron donor DPC. Cu²⁺ also accelerated the inhibition of PSⅡ electron transport by trypsin, after digestion of thylakoid membrane by the enzyme. Furthermore, Cu²⁺ antagonized the partial restoration by trypsin of PSⅡ electron transport inhibited by DCMU. Hence it is suggested that the action site of Cu²⁺ may be located between the water-splitting enzyme on the oxidizing side of PSⅡ and PSⅡ reaction center. The mode of its action may be due to inactivation of the membrane protein involved in PSⅡ electron transport. The results of the densitometric scans of chlorophyll-protein complexes resolved by SDS-PAGE are in accordance with this supposition.更多还原