In chloroplasts isolated from SO2-fumigated leaves at 2.0 ppm, electron flow from water to 2,6-dichloroindophenol (DCIP) was inhibited, but the electron flow from reduced DCIP to methyl viologen was not affected. Neither diphenylcarbazide nor MnCl2 could restore the activity of the DCIP-Hill reaction of SO2-injured chloroplasts. Electron flows, from water to ferricyanide or to silicomolybdic acid, were inhibited in a degree similar to that of the DCIP-Hill reaction. The rate of carotenoid photobleaching in the presence of carbonyl cyanide-m-chlorophenylhydrazone was suppressed and paralleled the inhibition of the DCIP-Hill reaction. In SO2-injured chloroplasts, the variable part of the fluorescence transient was diminished, and the fluorescence yield lowered by SO2 was increased with 3-(3′, 4′-dichlorophenyl)-l, l-dimethylurea (DCMU) or more pronouncedly by incubating the sample with sodium dithionite. However, the yield could not recover to the level found in non-fumigated chloroplasts. With SO2 fumigation, the time required to reach steady-state level of fluorescence became longer in the absence of DCMU, but was not altered in the presence of DCMU. The pool size of the primary electron acceptors decreased with SO2 fumigation. We concluded that SO2 inactivated the primary electron donor or the reaction center itself. The mode of SO2 action in the electron transport chain is discussed.
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Shimazaki et al. (1980) studied this question.