Abstract

Ample evidence exists that the phytotoxic action of sulfur dioxide in plants is initiated and propagated by impairment of their thioredoxin systems, which by their redox status control the light-dark regulation and productivity of chloroplast metabolism. We have shown that oxidized thioredoxin reacts readily with sulfite ions under sulfitolysis of its exposed disulfide bond and formation of an inactive S-sulfonyl thioredoxin. Accumulation of such modified proteins is suggested to mark the specific threshold concentration of SO2 toxicity in a plant. The adverse effects are potentiated intracellularly by an induction of excess H2O2 synthesis which will oxidize additional SH groups and make them susceptible to further sulfitolysis and incapacitation.

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