Increasing tolerance to ozone by elevating foliar ascorbic acid confers greater protection against ozone than increasing avoidance.
Ascorbic acid (Asc) is the most abundant antioxidant in plants and serves as a major contributor to the cell redox state. Exposure to environmental ozone can cause significant damage to plants by imposing conditions of oxidative stress. We examined whether increasing the level of Asc through enhanced Asc recycling would limit the deleterious effects of environmental oxidative stress. Plants overexpressing dehydroascorbate reductase (DHAR), which results in an increase in the endogenous level of Asc, were exposed to acute or chronic levels of ozone. DHAR-overexpressing plants had a lower oxidative load, a lower level of oxidative-related enzyme activities, a higher level of chlorophyll, and a higher level of photosynthetic activity 24 h following an acute exposure (2 h) to 200 ppb ozone than control plants, despite exhibiting a larger stomatal area. Reducing the size of the Asc pool size through suppression of DHAR expression had the opposite effect. Following a chronic exposure (30 d) to 100 ppb ozone, plants with a larger Asc pool size maintained a larger stomatal area and a higher oxidative load, but retained a higher level of photosynthetic activity than control plants, whereas plants suppressed for DHAR had a substantially reduced stomatal area, but also a substantially lower level of photosynthetic activity. Together, these data indicate that, despite a reduced ability to respond to ozone through stomatal closure, increasing the level of Asc through enhanced Asc recycling provided greater protection against oxidative damage than reducing stomatal area.
Chen
Zhong
Z
Department of Biochemistry, University of California, Riverside, California 92521-0129, USA.
Gallie
Daniel R
DR
D001205:Ascorbic Acid / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D007700:Kinetics; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism; D010126:Ozone / Q000037:antagonists & inhibitors / Q000494:pharmacology* / Q000633:toxicity; D010788:Photosynthesis / Q000187:drug effects; D030821:Plants, Genetically Modified / Q000187:drug effects / Q000201:enzymology; D014026:Nicotiana / Q000187:drug effects / Q000201:enzymology*
D010126:Ozone; D010088:Oxidoreductases; C020666:glutathione dehydrogenase (ascorbate); D005978:Glutathione; D001205:Ascorbic Acid