Institute of General Botany of the Johannes Gutenberg University, Saarstr. 21, D-6500, Mainz, FRG.
Photosynth Res. 1990 Jun;24(3):237-43. doi: 10.1007/BF00032311.
In a previous paper it was shown that photoinhibition of reaction centre II of spinach thylakoids was predominantly caused by the degradation of D1-protein. An initial inactivation step at the QB-site was distinguished from its breakdown. The present paper deals with the question as to whether this loss of QB-function is caused by oxygen radical attack. For this purpose the photoinhibition of thylakoids was induced at 20°C in the presence of either superoxide dismutase and catalase or the antioxidants glutathione and ascorbic acid. This resulted in comparable though not total protection of D1-protein, photochemistry and fluorescence from photoinhibition. The combined action of both the enzymatic and the non-enzymatic radical scavenging systems brought about an even more pronounced protective effect against photoinhibition than did either of the two systems singularly at saturating concentrations. The results signify a major contribution of activated oxygen species to the degradation process of D1-protein and the related phenomena of photoinhibition. Thylakoids treated with hydroxyl radicals generated through a Fenton reaction showed a loss of atrazine binding sites, electron transport capacity and variable fluorescence in a similar manner, though not to the same extent, as usually observed following photoinhibitory treatment.
在之前的一篇论文中表明,菠菜类囊体反应中心 II 的光抑制主要是由于 D1 蛋白的降解引起的。在 QB 位区分了初始失活步骤及其分解。本文探讨了 QB 功能丧失是否是由氧自由基攻击引起的。为此,在 20°C 下,在超氧化物歧化酶和过氧化氢酶或抗氧化剂谷胱甘肽和抗坏血酸的存在下诱导类囊体的光抑制。这导致 D1 蛋白、光化学和荧光对光抑制的保护作用相当,但不如两种系统在饱和浓度下单独使用时那样完全。结果表明,活性氧物种对 D1 蛋白的降解过程以及相关的光抑制现象有很大的贡献。通过芬顿反应产生的羟基自由基处理的类囊体以类似但并非相同的方式表现出阿特拉津结合位点、电子传递能力和可变荧光的丧失,尽管不如通常在光抑制处理后观察到的那样严重。