CEBAS-CSIC, Department of Plant Nutrition, Campus Universitario de Espinardo, Espinardo, Murcia, Spain.
J Plant Physiol. 2012 Nov 15;169(17):1719-27. doi: 10.1016/j.jplph.2012.07.013. Epub 2012 Aug 31.
Based on previous results in which oxidative metabolism was suggested as a possible inducer of blossom-end rot (BER), the main questions addressed here were whether calcium deficiency is the main factor that induces BER or whether this physiological disorder a general stress-related phenomenon? Tomato plants were grown under optimal or deficient calcium concentrations. Only the application of 0.1mM calcium resulted in BER induction, although only half of the fruits grown under this treatment had this disorder. Having fruits showing or not showing BER in the same plant and treatment provided us with a powerful tool that we used to investigate whether calcium deficiency operates alongside another mechanism in the induction of BER. Whether or not this other mechanism was the one controlling BER incidence was also investigated. We performed a complete study of the oxidative metabolism in the pericarp of healthy fruits and in the healthy portion of BER-affected fruits. Calcium deficiency led to an induction of NADPH oxidase, superoxide dismutase, dehydro- and monodehydroascorbate reductase, and to an inhibition of catalase, ascorbate peroxidase and glutathione reductase, with a concomitant accumulation of hydrogen peroxide and an increase in lipid peroxidation. While the ascorbate redox state was not affected by calcium deficiency, the glutathione redox state was markedly reduced. We conclude that calcium deficiency fundamentally affected the activity of the ascorbate-glutathione enzymes, with special importance to the inhibition of GR, which lead to a reduction of the glutathione redox state. This could cause the breakdown of cellular homeostasis, the inhibition of other enzymes responsible for H(2)O(2) detoxification, and ultimately an increase of lipid peroxidation. Therefore, BER is defined here as the visual symptom of a massive lipid peroxidation event caused by the breakdown of cellular glutathione homeostasis.
基于先前的研究结果表明氧化代谢可能是导致枯梢果腐病（BER）的一个原因，这里主要探讨的问题是钙缺乏是否是导致 BER 的主要因素，还是这种生理紊乱是一种与一般应激相关的现象？番茄植株在最佳钙浓度或缺钙浓度下生长。只有应用 0.1mM 钙才会导致 BER 的诱导，尽管只有一半在这种处理下生长的果实有这种失调。在同一植株和处理下既有表现出 BER 的果实，也有不表现出 BER 的果实，这为我们提供了一个有力的工具，用于研究钙缺乏是否与 BER 诱导中的另一种机制同时起作用。我们还研究了这种其他机制是否是控制 BER 发病率的机制。我们对健康果实的果皮和 BER 影响的健康部分的氧化代谢进行了全面研究。钙缺乏导致 NADPH 氧化酶、超氧化物歧化酶、脱氢和单脱氢抗坏血酸还原酶的诱导，以及过氧化氢酶、抗坏血酸过氧化物酶和谷胱甘肽还原酶的抑制，同时伴随着过氧化氢的积累和脂质过氧化的增加。虽然钙缺乏不影响抗坏血酸的氧化还原状态，但谷胱甘肽的氧化还原状态明显降低。我们的结论是，钙缺乏从根本上影响了抗坏血酸-谷胱甘肽酶的活性，特别是抑制了 GR，这导致了谷胱甘肽氧化还原状态的降低。这可能导致细胞内稳态的崩溃，抑制其他负责 H2O2 解毒的酶，最终导致脂质过氧化的增加。因此，BER 在这里被定义为细胞内谷胱甘肽内稳态破坏导致的大量脂质过氧化事件的可见症状。
