Several herbicides mediate phototoxic responses, acting as secondary phototoxins in plants. Bipyridinium herbicides, like paraquat (methyl viologen) act as electron acceptors of Photosystem I and the subsequent rapid autooxidation of the paraquat anion radical creates O-. The hydroxyl radical formed in the subsequent Fenton chemistry is the primary reactant causing the destruction of the photosynthetic apparatus. The herbicidal effect of carotenoid biosynthesis inhibitors, like norflurazon, is based on herbicide-induced removal of photoprotective compounds (Sandmann and Böger, 1989). Inhibitors of the plastidic pro-toporphyrinogen oxidase (diphenyl ether herbicides) cause accumulation of protoporphyrin IX on the plasmalemma where the plastidic protoporphyrinogen is translocated (Kunert and Dodge, 1989; Duke and Rebeiz, 1994), causing the accumulation of protoporphyrin IX. Herbicidal application of S-aminolevulinate, in turn, by-passes a regulatory step in porphyrin synthesis causing accumulation of photodynamically active tetrapyrroles (Rebeiz et al, 1987; Duke and Rebeiz, 1994). DCMU (diuron) and other PS II herbicides bind to the Qb site in the D1 protein of PS II (Mets and Thiel, 1989). Their primary effect is inhibition of electron flow through PS II, but several lines of evidence show that the killing of the plant finally occurs via phototoxic reactions sensitized by the chlorophylls (Pallett and Dodge, 1980).
Excess concentrations of heavy metals in the soil cause oxidative damage to plants that take up the metal ions (reviewed by Dietz et al., 1999). The damage is often light-dependent (Luna et al., 1994; Sandmann and Böger, 1980; Pätsikkä et al., 1998). Mechanisms of heavy metal phototoxicity include participation of the metal ions in Fenton chemistry (Dietz et al., 1999), inhibition of enzymes protecting against oxidative damage, and depletion of antioxidant pools (Luna et al., 1994).
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