In this review we explore several models which might explain ozone (O3)-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 O3 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 β-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 O3-induced cell repair or cell protection. A second model is postulated to explain induction of accelerated foliar senescence by low levels of O3. The notion that O3-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-1,5-bisphosphate carboxylase/oxygenase (Rubisco). The mechanisms by which O3 induces loss of Rubisco, and the relationship to accelerated foliar senescence are discussed.
|Original language||English (US)|
|Number of pages||10|
|State||Published - Jun 1 1997|
All Science Journal Classification (ASJC) codes
- Plant Science
- Cell Biology