Chlorophyll a and carotenoids of spinach began to be destroyed 2 to 3 hr after fumigation with 2 ppm SO2 under light, whereas chlorophyll b was undamaged during 8 hr of exposure to SO2. Pheophytin a was not affected by the fumigation. When disks excised from leaves fumigated with SO2 at 2 ppm for 2 hr were illuminated, chlorophyll a and carotenoids were broken down, while they were not destroyed in darkness. The destruction of these pigments was suppressed under nitrogen. Chlorophyll a destruction was inhibited by l,2-dihydroxybenzene-3,5-disulfonate (tiron), hydro-quinone and ascorbate, but not by l,4-diazabicyclo-[2,2,2]-octane (DABCO), methio-nine, histidine, benzoate and formate. Chlorophyll a destruction was inhibited by phenazine methosulfate but stimulated by methyl viologen. Addition of superoxide dismutase (SOD) to the homogenate of SO2-fumigated leaves inhibited the chlorophyll a destruction. The activity of endogenous SOD was reduced to 40% by 2-hr fumigation before the loss of chlorophyll was observed. These results suggest that chlorophyll a destruction by SO2 was due to superoxide radicals (O2−). Moreover, malondialdehyde (MDA), a product of lipid peroxidation, was formed in SO2-fumigated leaves. MDA formation was inhibited by tiron, hydroquinone and DABCO but not by benzoate and formate. MDA formation was increased by D2O. These results suggest that lipid peroxidation in SO2-fumigated leaves was due to singlet oxygen 1O2 produced from O2−.
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Shimazaki et al. (1980) studied this question.