Previous reports have suggested the primary mode of action of the allelochemical hydroquinone involves disruption of root cell membrane transport. Here we report the effects of hydroquinone on common bean (Phaseolus vulgaris) plants. Growth of leaves, roots and stems were all inhibited by 14 day exposure to 0.01 mM or 0.25 mM hydroquinone. Chlorophyll fluorescence (Fv/Fm) was inhibited by 0.25 mM hydroquinone. The membrane potential of P. vulgaris root cortex cells briefly hyperpolarized and subsequently slowly transiently depolarized upon abrupt exposure to a range of hydroquinone concentrations. Both the hyperpolarization and depolarization were concentration dependent but appeared saturable. Root cells exposed to 0.03 mM hydroquinone hyperpolarized 3.4 mV (+/- 0.6 s.e.) 3 minutes after the start of exposure then depolarized 36.7 mV (+/- 3.9) with no effect evident after 24 hours. Individual recordings showed a response to as little as 0.001 mM hydroquinone. Exposure of P. vulgaris root cells to arbutin, a nontoxic monoglucoside of hydroquinone, produced a similar but much smaller (approximately 25%) electrical response. Exposure of root cells of Antennaria microphylla, a known allelopathic source (donor plant) of hydroquinone, also produced a much smaller hyperpolarization and depolarization response. It is concluded that the electrical response to hydroquinone by P. vulgaris root cells and the changes in membrane transport they represent are not sufficiently large or long lasting enough to disrupt mineral and water uptake leading to plant injury. The possibility, however, that these events are related to initiation of signal transduction events leading to cell death is discussed.
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