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      Insights into cadmium induced physiological and ultra-structural disorders in Juncus effusus L. and its remediation through exogenous citric acid.

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          Abstract

          This study appraised cadmium (Cd) toxicity stress in wetland plant Juncus effusus, and explored its potential for Cd phytoextraction through chelators (citric acid and EDTA). Cadmium altered morphological and physiological attributes of J. effusus as reflected by growth retardation. Citric acid in the presence of 100 μM Cd significantly countered Cd toxicity by improving plant growth. Elevated Cd concentrations reduced translocation factor that was increased under application of both chelators. Citric acid enhanced Cd accumulation, while EDTA reduced its uptake. Cadmium induced oxidative stress modified the antioxidative enzyme activity. Both levels of citric acid (2.5 and 5.0 mM) and lower EDTA concentration (2.5 mM) helped plants to overcome oxidative stress by enhancing their antioxidative enzyme activities. Cadmium damaged the root cells through cytoplasmic shrinkage and metal deposition. Citric acid restored structure and shape of root cells and eliminated plasmolysis; whereas, EDTA exhibited no positive effect on it. Shoot cells remained unaffected under Cd treatment alone or with citric acid except for chloroplast swelling. Only EDTA promoted starch accumulation in chloroplast reflecting its negative impact on cellular structure. It concludes that Cd and EDTA induce structural and morphological damage in J. effusus; while, citric acid ameliorates Cd toxicity stress.

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          Author and article information

          Journal
          J. Hazard. Mater.
          Journal of hazardous materials
          1873-3336
          0304-3894
          Feb 15 2011
          : 186
          : 1
          Affiliations
          [1 ] Institute of Crop Science, Zhejiang University, Hangzhou, China.
          Article
          S0304-3894(10)01461-5
          10.1016/j.jhazmat.2010.11.037
          21159423
          e98ebf7c-708a-4d0a-8a76-01a85d585305
          Copyright © 2010 Elsevier B.V. All rights reserved.
          History

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