Department of Plant Molecular Physiology, University of Hawaii at Manoa, Honolulu, Hawaii 96822.
Plant Physiol. 1992 Aug;99(4):1354-61. doi: 10.1104/pp.99.4.1354.
Induction of zeaxanthin formation and the associated nonphotochemical quenching in iodoacetamide-treated, non-CO(2)-fixing intact chloroplasts of Lactuca sativa L. cv Romaine is reported. The electron transport needed to generate the required DeltapH for zeaxanthin formation and nonphotochemical quenching are ascribed to the Mehler-ascorbate peroxidase reaction. KCN, an inhibitor of ascorbate peroxidase, significantly affected these activities without affecting linear electron transport to methyl viologen or violaxanthin deepoxidase activity. At 1 millimolar KCN, zeaxanthin formation and DeltapH were inhibited 60 and 55%, respectively, whereas ascorbate peroxidase activity was inhibited almost totally. The KCN-resistant activity, which apparently was due to electron transport mediated by the Mehler reaction alone, however, was insufficient to support a high level of nonphotochemical quenching. We suggest that in vivo, as CO(2) fixation becomes limiting, the Mehler-peroxidase reaction protects photosystem II against the excess light by supporting the electron transport needed for zeaxanthin-dependent nonphotochemical quenching and concomitantly scavenging H(2)O(2). Ascorbate is essential for this process to occur.
碘乙酰胺处理的不固定 CO2 的莴苣完整叶绿体中,诱导玉米黄质形成和与之相关的非光化学猝灭的现象被报道。玉米黄质形成和非光化学猝灭所需的 DeltapH 所需的电子传递归因于 Mehler-抗坏血酸过氧化物酶反应。KCN,抗坏血酸过氧化物酶的抑制剂,显著影响这些活性而不影响到甲基紫精的线性电子传递或紫黄质脱环氧化酶活性。在 1 毫摩尔 KCN 时,玉米黄质形成和 DeltapH 分别被抑制 60%和 55%,而抗坏血酸过氧化物酶活性几乎被完全抑制。然而,显然是由于 Mehler 反应介导的电子传递,KCN 抗性活性不足以支持高水平的非光化学猝灭。我们认为,在体内,随着 CO2 固定变得有限,Mehler-过氧化物酶反应通过支持玉米黄质依赖性非光化学猝灭所需的电子传递并同时清除 H2O2,来保护光系统 II 免受过量光的影响。抗坏血酸对于这一过程的发生是必不可少的。