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SUMMARY Atmospheric pollution by the oxides of nitrogen, NO and NO2, can cause reductions in growth but rarely visible injury. This review considers their uptake into foliage, as well as their subsequent metabolism and physiology, and attempts to explain why these gases are often phytotoxic. The combined stresses of resisting cellular acidification, enhanced levels of nitrite (and ammonia), and the direct interference of the free radical ('N=O) with critical enzymes, reaction centres and regulatory mechanisms are thought to be the main reasons why oxides of nitrogen, especially NO, inhibit growth. If other air pollutants such as SO2 are also present with NO or NO2 then free radical‐induced injury, similar to that caused by O3 alone, also occurs.

Glutathione (GSH), a major antioxidant in most aerobic organisms, is perceived to be particularly important in plant chloroplasts because it helps to protect the photosynthetic apparatus from oxidative damage. In transgenic tobacco plants overexpressing a chloroplast-targeted ␥ -glutamylcysteine synthetase ( ␥ -ECS), foliar levels of GSH were raised threefold. Paradoxically, increased GSH biosynthetic capacity in the chloroplast resulted in greatly enhanced oxidative stress, which was manifested as light intensity-dependent chlorosis or necrosis. This phenotype was associated with foliar pools of both GSH and ␥ -glutamylcysteine (the immediate precursor to GSH) being in a more oxidized state. Further manipulations of both the content and redox state of the foliar thiol pools were achieved using hybrid transgenic plants with enhanced glutathione synthetase or glutathione reductase activity in addition to elevated levels of ␥ -ECS. Given the results of these experiments, we suggest that ␥ -ECS-transformed plants suffered continuous oxidative damage caused by a failure of the redox-sensing process in the chloroplast. INTRODUCTIONPlants, like all aerobic organisms, possess an array of hydrophilic and lipophilic antioxidants, such as glutathione, ascorbic acid (vitamin C), phenolic isoflavanoid compounds, ␣ -tocopherol (vitamin E), and the carotenoids, including the xanthophylls (Fryer, 1993; Mullineaux and Creissen, 1996). The reduced forms of these compounds, together with antioxidant enzymes, scavenge reactive oxygen species (ROS) and other products of oxidative reactions. These enzymes include subcellular compartment-specific isoforms of superoxide dismutase (SOD), catalase, ascorbate peroxidase (APX), glutathione S -transferase/glutathione peroxidase (GST/GPX), dehydroascorbate reductase, monodehydroascorbate free radical reductase, and glutathione reductase (GR). Several reduction-oxidation (redox) cycles that scavenge ROS in different subcellular compartments and that involve these enzymes and antioxidants have been proposed (e.g., the ascorbate-GSH cycle). The reducing equivalents for these reactions are derived ultimately from photosynthetic electron transport (Foyer and Halliwell, 1976; Mullineaux and Creissen, 1997). Thus, the degree of reduction of major antioxidant pools is generally considered to reflect the redox status of the tissue in question and is consequently an indicator of oxidative stress.Glutathione, either as GSH or as GSSG (glutathione disulfide; oxidized glutathione), is regarded as a key component of antioxidant defenses in most aerobic organisms, including plants (Foyer et al., 1997). However, the high (i.e., millimolar) concentration of GSH in the chloroplast (Foyer and Halliwell, 1976; Law et al., 1983; Bielawski and Joy, 1986) is in apparent conflict with its proposed roles: the regeneration of ascorbate (Foyer and Halliwell, 1976), reduction of lipid hydroperoxides (Mullineaux et al., 1998), and regulation of chloroplast gene expression by thiol-mediated modulation of RNA polymeras...

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SummaryA pea glutathione reductase cDNA was expressed in tobacco. Three classes of construct were used which gave a range of elevated levels of glutathione reductaee (GR) activity in the cytosol (GR32), chloroplasts (GR36), or in both chloroplasts and mitochondria (GR46}. In some transgenic progeny (T z) from self-fertilized GR32 and GR36 primary transformants, having approximately twofold elevation of GR activity as compared with recessive siblings, there was an amelioration of the effect on leaf discs of up to 15 pM paraquat. However, lines with similarly elevated levels of GR activity showed no decreased sensitivity to the herbicide. None of the GR32 and GR36 lines was less sensitive to ozone. Conversely, 1"2 progeny of GR46 lines, with greater than 4.5-fold elevations of GR activity, showed no reduced sensitivity to paraquat but two out of four of these lines were less sensitive to ozone fumigation. The differential response to stress cosegregated with the presence of the transgene but there was no relationship between the degree of stress response and the level of GR activity. There was an elevation in the total glutathione pool in all lines showing increased GR activity but there was no change in the ratio of oxidized to reduced glutathione. These results demonstrate that the mechanisms of protection against ozone and paraquat are different although both can be mediated by elevated GR activity.