The defense potential of glutathione-ascorbate dependent detoxification pathway to sulfur dioxide exposure in Tagetes erecta.

Sulfur dioxide (SO2) exposure is associated with increased risk of various damages to plants. However, little is known about the defense response in ornamental plants. In this study, an artificial fumigation protocol was carried out to study the defense potential of the glutathione (GSH)-ascorbate (AsA) dependent detoxification pathway to SO2 exposure in Tagetes erecta. The results show that when the plants were exposed to different doses of SO2 (0, 15, 30, 50 or 80 mg m(-3)) for different times (6, 12, 18, 24 or 33 h), SO2 induced oxidative stress was confirmed by the increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and relative conductivity of membrane (RC) in a dose-dependent manner for different exposure times. However, the increased levels for H2O2, MDA and RC were not significant vis-a-vis the control when SO2 doses and exposure times were lower than 15 mg m(-3)/33 h, 30 mg m(-3)/24 h or 50 mg m(-3)/12 h (p>0.05). The results could be explained by the increases in the content of reduced form of glutathione (GSH), total glutathione (TGSH), ascorbate (AsA), ratio of GSH/GSSG (oxidized form of glutathione), activities of ascorbate peroxidase (APX), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione S-transferases (GST). On the other hand, exposure to higher doses of SO2 and longer exposure times, the values of the GSH-AsA dependent antioxidative indices decreased significantly (p<0.01), manifested by increased levels of H2O2. Furthermore, the levels of H2O2, MDA and RC varied little when SO2 doses and exposure times reached a 'critical' value (50 mg m(-3)/24 h). The defense ability of T. erecta to SO2 reached nearly extremity. To summarize, the response of T. erecta to elevated SO2 was related to higher H2O2 levels. GSH-AsA dependent detoxification pathway played an important role in against SO2-induced toxicity, although the defense response could not sufficiently alleviate oxidative damage when SO2 doses and exposure times reached critical value.