The study focuses on the interaction between reactive oxygen species and hormones that regulate the programmed cell death in plants of Melissa officinalis exposed to ozone. Interaction between hormone and redox signaling pathways has been investigated in ozone-stressed (200 ppb, 5 h) lemon balm to verify if the response resembles the biotic defense reactions. In comparison to controls, plants exhibited foliar injury and the cell death was induced by (1) biphasic production of hydrogen peroxide and superoxide radical; (2) hormonal regulation of ozone-induced lesion formation with a significant production of ethylene, salicylic, jasmonic and abscisic acid; (3) ozone degradation to reactive oxygen species and their detoxification by some enzymatic (such as superoxide dismutase) and non-enzymatic antioxidant systems (such as ascorbic acid, glutathione and carotenoids), that worked in cooperation without providing a defense against free radicals (such as confirmed by the modification of the antioxidant properties of leaf tissue). This integrated view showed that reactive oxygen species interact with hormonal signaling pathway regulating cell death and the sensitivity of lemon balm to ozone.

No abstract

Physiological and biochemical responses to ozone (O) (150 ppb, 8 h day, 35 consecutive days) of two Italian provenances (Piedmont and Tuscany) of Fraxinus excelsior L. were evaluated, with special attention to the role of phenylpropanoids. Our results indicate (i) the high O sensitivity especially of Piedmont provenance (in terms of visible injury, water status, and photosynthetic apparatus); (ii) although the intra-specific sensitivity to O between provenances differs (mainly due to different stomatal behaviors since only Tuscany plants partially avoided the uptake of the pollutant gas), both provenances showed detoxification and defense mechanisms; (iii) the crucial participation of phenylpropanoids, with a key role played by flavonoids (especially quercitrin): among this class of metabolites, isoquercitrin is the principal player in the lower O sensitivity of Tuscany plants, together with lignins; (iv) although coumarins (typical compounds of Fraxinus) were severely depressed by O, isofraxidin was triggered suggesting a key role in reactive oxygen species (ROS) detoxification, as well as trans-chalcone. Furthermore, the different behavior of verbascoside and oleuropein among provenances lead us to speculate on their influence in the tentatively repair or acclimation shown by Piedmont plants at the end of the exposure. Finally, the intra-specific O sensitivity may be also due to de novo peaks triggered by O not yet associated to some chemicals.

No abstract

Liriodendron tulipifera (known as the tulip tree) is a woody species that has been previously classified as sensitive to ozone (O) in terms of visible leaf injuries and photosynthetic primary reactions. The objective of this work is to give a thorough description of the detoxification mechanisms that are at the basis of O sensitivity. Biochemical and molecular markers were used to characterize the response of 1-year-old saplings exposed to O (120 ppb, 5 h day, for 45 consecutive days) under controlled conditions. O effects resulted in a less efficient metabolism of Halliwell-Asada cycle as confirmed by the diminished capacity to convert the oxidized forms of ascorbate and glutathione in the reduced ones (AsA and GSH, respectively). The reduced activity of AsA and GSH regenerating enzymes indicates that de novo AsA biosynthesis occurred. This compound could be a cofactor of several plant-specific enzymes that are involved in the early part of the phenylpropanoid and flavonoid biosynthesis pathway, as confirmed by the significant rise of PAL activity (+75%). The induction of the defence-related secondary metabolites (in particular, rutin and caffeic acid were about threefold higher) and the concomitant increase in transcript levels of PAL and CHS genes (+120 and 30%, respectively) suggest that L. tulipifera utilized this route in order to partially counteract the O-induced oxidative damage.