| The industrial processes and human activities increase heavy metal release into the soil. As ahighly toxic heavy metal element in soil, cadmium (Cd) can be easily absorbed by plants andenriched in edible parts of plants. Through the food chain, Cd enters human body and threatenshuman health. Increasing evidence has shown that salicylic acid (SA) is involved in plantresponses to various adverse stresses including heavy metal Cd. However, SA-relatedmechanism in plant response to Cd is less understood. In addition, the most related studies areperformed just by application of SA to plants or measuring the endogenous SA levels in plants,while the studies with endogenous SA-altering plant mutants are scarce.To evaluate the role of endogenous SA in plant response to Cd stress, Arabidopsis wild type(Columbia) and its SA-altering mutants snc1(suppressor of npr1-1, constitutive) with high SAlevel, transgenic line nahG with low SA level and npr1-1(nonexpressor of PR gene) with SAsignaling blockage were used in this study. All the tested plants were randomly divided intofour groups including a control group and three Cd stress groups treated with50μmol/L,100μmol/L and150μmol/L of CdCl2, respectively. After7days of Cd exposure, all the plants wereharvested, collecting the data of dry weight, content of chlorophyll and malondialdehyde(MDA), enzyme activities of superoxide dismutase (SOD), peroxidase (POD) and Catalase(CAT), proline contents and electrolyte leakage in leaves. The effects of Cd exposure on theSOD, POD and CAT isozymes were studied by polyacrylamide gel electrophoresis (PAGE).Results showed that Cd stress caused all plants growth retardation with a dose-effectrelationship relative to control. However, compared to wild type plants, a greater growthinhibition occurred in snc1, while a less inhibition was observed in nahG and npr1-1plants.Cd-induced growth inhibition was associated with the cellular lipid peroxidation, as indicatedby significant accumulation of MDA (a product of membrane lipid peroxidation) and highelectrolyte leakage rates compared to control. However, as compared to wild type plants, thesnc1plants generated more MDA, and nahG and npr1-1plants produced less MDA. Thechanges of electrolyte leakage were coincident with the MDA levels in all the plants under Cdstress. In the present study, exposure to150μmol/L of CdCl2caused the most serious lipidperoxidation in all the tested plants regardless of the SA levels or signaling. The investigation ofantioxidative enzymes and their isozymes showed that Cd exposure increased the activities ofSOD and POD, decreased the activities of CAT in all the plants. Among which, the mostincreased extents in SOD or POD were occurred in snc1plants, and the least in nahG andnpr1-1plants, which further demonstrated that the snc1plants were more sensitive and nahGand npr1-1plants more tolerant to Cd stress than wild type plants due to these enzymes arenormally induced to some extent by oxidative damages. The Cd-caused damage was alsoindicated by the decreased chlorophyll contents, with the more extent being observed in snc1plants and less in nahG and npr1-1plants relative to the wild type plants. Cd exposureincreased the contents of soluble sugar and free proline in all the tested plants, with the leastmagnitude existing in snc1plants.Taken together, these data showed that Cd-induced plants growth inhibition was associatedwith the oxidative damage. Among the tested plants, snc1plants with high SA levels wereaffected most significantly, while the transgenic line nahG with low SA level and npr1-1plantswith SA signaling blockage were the least. Although the antioxidative enzymes SOD and PODincreased upon Cd exposure, they were insufficient to remove oxidative stress, especially in snc1plants. The accumulations of soluble sugar and proline in the tested plants were positivelyrelated to their tolerance to Cd stress. |
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