Ozone-induced oxidative stress: Mechanisms of action and reaction

Ozone-induced oxidative stress: Mechanisms of action and reaction
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DOI:
10.1034/j.1399-3054.1997.1000207.x
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发表时间:
1997-06-01
影响因子:
6.4
通讯作者:
Arteca, RN
Arteca, RN
中科院分区:
生物学2区
文献类型:
--
作者:
Pell, EJ;Schlagnhaufer, CD;Arteca, RN

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本文综述了几种可能解释臭氧(O-3)对植物叶片伤害的模型。臭氧通过产生活性氧的细胞壁和质膜进入细胞。如果O-3的浓度非常高,就会发生不受调节的细胞死亡。另外,活性氧或随后的反应产物可以作为调控植物反应的激发子。这些受调控的反应包括乙烯的诱导,乙烯可以作为后续反应的主要信号或促进者。探讨了光合基因的调控抑制和几丁质酶和β -1,3-葡聚糖酶的诱导在程序性细胞死亡中的作用。在o -3诱导细胞修复或细胞保护的背景下,讨论了抗氧化剂、木质素化酶和谷胱甘肽- s转移酶的诱导。第二种模式被假定用来解释低水平的O-3对叶片加速衰老的诱导。o -3诱导的细胞核反应可能导致叶绿体氧化应激增加的概念被认为是加速核酮糖- 1,15 -二磷酸羧化酶/加氧酶(Rubisco)降解速率的机制。讨论了O-3诱导Rubisco丢失的机制及其与叶面加速衰老的关系。
In this review we explore several models which might explain ozone (O-3)-induced injury to plant foliage. Ozone enters the cell through the wall and plasma membrane where active oxygen species are generated. If the concentration of O-3 is very high, unregulated cell death will occur. Alternatively, the active oxygen species, or succeeding reaction products, may serve as elicitors of regulated plant responses. These regulated responses include the induction of ethylene which could serve as a primary signal for - or a facilitator of - subsequent responses. The role of regulated suppression of photosynthetic genes and induction of chitinases and beta-1,3-glucanase in programmed cell death is explored. Induction of antioxidants, enzymes of lignification and glutathione-S-transferase are discussed in the context of O-3-induced cell repair or cell protection. A second model is postulated to explain induction of accelerated foliar senescence by low levels of O-3. The notion that O-3-induced elicitation of responses in the nucleus might lead to increased oxidative stress in the chloroplast is considered as a mechanism for accelerating the rate of degradation of ribulose-1, 15-bisphosphate carboxylase/oxygenase (Rubisco). The mechanisms by which O-3 induces loss of Rubisco, and the relationship to accelerated foliar senescence are discussed.