Abstract
Representative cultivars of white bean (Phaseolus vulgaris) were treated with selected antioxidants, thiol compounds and sulfhydryl reagents and then exposed to ozone under laboratory conditions. Severity of the bronzing disorder was influenced by such treatments, as was the activity of peroxidase and lactic dehydrogenase enzymes.Dust applications of ascorbic acid and nickel-N-dibutyl dithiocarbamate markedly reduced ozone injury, the latter compound being the most effective. Decreased ozone sensitivity was also noted following treatment of a susceptible and a tolerant cultivar with cysteine hydrochloride and glutathione.The severity of bronzing was increased over that of the control plants by the application of sulfhydryl reagents, namely parachloromercuribenzoate and N-ethyl maleimide. Necrotic stipple of the upper surface of the lamina, a symptom associated with the bronzing disorder, was induced following treatment with the sulfhydryl reagents without exposure to ozone.Ozone fumigation increased peroxidase activity and decreased lactic dehydrogenase activity. Similar effects were observed following treatment with parachloromercuribenzoate. Neither enzyme showed response to the application of cysteine hydrochloride.The role of protein sulfhydryls is discussed in relation to ozone damage and the bronzing disorder.
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