Abstract

The nitrodiphenyl ether herbicide acifluorfen requires light for phytotoxicity even though it alone cannot absorb light. All possible major pigment systems have been implicated as the photoreceptor. We tested whether carotenoids and chlorophyll are essential for phytotoxicity. We used green-photosynthetic (mixotrophic) tomato cell cultures, etiolated cells of the same line (containing carotenoids but no chlorophyll), and carotenoid-free white cells (by continuously culturing etiolated cells on norflurazon). All three cell culture types parallel plants insofar as the first measureable effect is membrane lipoxidation. Acifluorfen at 1 μ M had little effect in darkness, but strongly inhibited growth of all cultures in 40 μmol m −2 sec −1 white light. Acifluorfen at 0.1 μ M did not affect green cells in light, but inhibited the growth of white and etiolated cells. Action spectroscopy showed that 350-nm light was the most effective wavelength inhibiting the growth of white cells with 1 μ M acifluorfen, followed by 550-nm, 450-nm, cool-white fluorescent, and 630-nm light, with only a threefold difference between 350-nm and red light. Far-red light was ineffective. These data demonstrate that in this system, chlorophyll, carotenes, cryptochrome, flavins, and phytochrome cannot be the sole photoreceptor for acifluorfen action. Our data, along with all other published findings are consistent with two hypotheses: (a) that acifluorfen interacts with other moieties to produce broad-spectrum chromophore(s) that react(s) with oxygen, forming active-oxygen species in the light; (b) that acifluorfen stimulates the accumulation of chromophoric photodynamic molecules.

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