Abstract
A huge amount of studies highlighted the importance of high ascorbic acid (AA) content in ozone tolerance, yet the relationship between them appears more complex than a simple direct correlation. Sometimes the connection is clear, for example, two Arabidopsis mutants defective in the main AA biosynthetic pathway (vtc mutants) were identified by means of their ozone sensitivity. However, some low-AA containing mutants are relatively tolerant, suggesting that AA location/availability could be more relevant than total content. A clear distinction should also be made between ozone tolerance obtained when AA content is increased by experimental supplementation (exogenous AA), and the physiological role of plant-synthesized AA (endogenous AA), whose amount is apparently subjected to tight regulation. Recent findings about the role of AA in signal transduction and epigenetic regulation of gene expression open new routes to further research.
Highlights
The origin of research on plant ozone (O3 ) sensitivity dates back to the late 1950s, when a leaf spot disease known as weather fleck was identified as caused by ozone [1]
We present here some considerations on the relationship between ascorbic acid (AA) and plant ozone tolerance, without the pretension of offering a complete and exhaustive review of the wide literature addressing the mechanisms of plant ozone tolerance
Many accurate studies clearly showed that higher AA content is not the only possible mechanism involved in ozone tolerance [4,16], and that the AA/ozone relationship is more complex than one might expect on the basis of a simple interaction between reactive oxygen species (ROS) and antioxidants facing each other
Summary
The origin of research on plant ozone (O3 ) sensitivity dates back to the late 1950s, when a leaf spot disease known as weather fleck was identified as caused by ozone [1]. Several papers supported the view of a direct correlation between AA content and ozone tolerance [3,4]. Over the years and decades, this notion has led to the conclusion that ozone tolerance in a given plant species or cultivar could be somewhat anticipated on the basis of its AA content [5]. Many accurate studies clearly showed that higher AA content is not the only possible mechanism involved in ozone tolerance [4,16], and that the AA/ozone relationship is more complex than one might expect on the basis of a simple interaction between reactive oxygen species (ROS) and antioxidants facing each other. What is the relationship between exogenous (experimentally supplied) and endogenous (synthesized by the plant) AA in O3 tolerance? Some relevant points will be critically discussed starting from a few basic questions: Is AA content always directly related to ozone tolerance? Is AA cellular location involved in ozone tolerance? What is the relationship between exogenous (experimentally supplied) and endogenous (synthesized by the plant) AA in O3 tolerance? What do we know about the mechanisms of AA-mediated tolerance? Recent data about AA involvement in the epigenetic control of gene expression opened the way to so far unexplored possibilities of explaining contrasting results obtained in decades of experimental work
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