Active oxygen participation in chlorophyll destruction and lipid peroxidation in SO2-fumigated leaves of spinach |
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Authors: | Shimazaki, Ken-ichiro Sakaki, Takeshi Kondo, Noriaki Sugahara, Kiyoshi |
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Affiliation: | Division of Environmental Biology, National Institute for Environmental Studies Yatabe, Ibaraki 305, Japan |
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Abstract: | Chlorophyll a and carotenoids of spinach began to be destroyed2 to 3 hr after fumigation with 2 ppm SO2 under light, whereaschlorophyll 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 for2 hr were illuminated, chlorophyll a and carotenoids were brokendown, while they were not destroyed in darkness. The destructionof these pigments was suppressed under nitrogen. Chlorophylla 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. Chlorophylla destruction was inhibited by phenazine methosulfate but stimulatedby methyl viologen. Addition of superoxide dismutase (SOD) tothe homogenate of SO2-fumigated leaves inhibited the chlorophylla destruction. The activity of endogenous SOD was reduced to40% by 2-hr fumigation before the loss of chlorophyll was observed.These results suggest that chlorophyll a destruction by SO2was due to superoxide radicals (O2). Moreover, malondialdehyde (MDA), a product of lipid peroxidation,was formed in SO2-fumigated leaves. MDA formation was inhibitedby tiron, hydroquinone and DABCO but not by benzoate and formate.MDA formation was increased by D2O. These results suggest thatlipid peroxidation in SO2-fumigated leaves was due to singletoxygen 1O2 produced from O2. (Received May 15, 1980; ) |
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