Ruth Grene Alscher

Differential response of Cu,Zn superoxide dismutases in two pea cultivars during a short-term exposure to sulfur dioxide

Pea cultivars Progress and Nugget have been shown previously to be differentially sensitive with respect to apparent photosynthesis in a short-term exposure to 0.8 μl/l SO2. One possible contributing factor to the relative insensitivity of apparent photosynthesis of Progress to SO2 is an increase in superoxide dismutase (SOD) activities. We show here that both chloroplastic and cytoplastic Cu,Zn-SOD proteins increased in Progress on exposure to sulfur dioxide whereas both proteins decreased in Nugget. The increase in cytosolic Cu,Zn-SOD protein was greater than that of chloroplastic Cu,Zn-SOD protein. Using a gene-specific probe for the plastid SOD, northern blot analysis revealed an initial decrease in transcript abundance of the chloroplastic Cu,Zn-SOD gene in Progress on exposure to SO2 with an eventual recovery to pre-exposure levels. The transcript levels of the chloroplastic Cu,Zn-SOD decreased in Nugget over the time period of the exposure. These results suggest that a combination of translational and post-translational mechanisms may be involved in SO2-induced changes in cytosolic and plastidic Cu,Zn-SODs in pea.

Physiological, Biochemical and Molecular Effects of Sulfur Dioxide

Summary Damage of leaves due to air pollutants such as sulfur dioxide is mediated through the production of reactive oxygen species. The site of action of sulfur dioxide is the chloroplast and deleterious effects on foliar tissue depend on light and photosynthetic electron transport. Protection may be afforded, in part, by components of the antioxidant (photo)scavenging cycle. Relative resistance to sulfur dioxide and cross-resistance to other oxidative stresses which originate in the chloroplast have been correlated, in many cases, with elevated levels of various antioxidant proteins and/or substrates. Recent studies utilizing differentially sensitive cultivars, antioxidant enzyme analyses which differentiate between specific isoforms at the gene and protein levels, and plants genetically engineered to alter the expression of specific antioxidant isozymes, have provided new insights into the mechanisms of resistance to sulfur dioxide and other stresses. These data suggest that complex regulatory mechanisms function at both the gene and protein level to coordinate antioxidant responses and that a critical role is played by organellar localization and inter-compartment coordination. An involvement of a strong developmental component in resistance is indicated.

Prospects for Increasing Stress Resistance of Plant Peroxisomes

Any circumstance in which cellular redox homeostasis is disrupted can lead to oxidative stress, or the generation of reactive oxygen species or ROS (Asada, 1994). Orchestrated defense/antioxidant processes ensue in response to the imposition of stress (Figure 1). Functional roles of these responses include the protection of redox-sensitive enzymatic processes, the preservation of membrane integrity and the protection of DNA and proteins (Scandalios, 1997). Redox-sensitive regulatory enzymes such as fructose-1, 6-bisphosphatase (FbPase) can be protected from oxidation/inactivation by the action of antioxidants such as glutathione. Plant cells respond defensively to oxidative stress by removing the ROS and maintaining antioxidant defense compounds at levels that reflect ambient environmental conditions (Scandalios, 1997). The mechanisms that act to adjust antioxidant levels to afford protection include changes in antioxidant gene expression.