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Silicon-mediated genotoxic alterations in Brassica juncea under arsenic stress: A comparative study of biochemical and molecular markers
Authors:Afsana PRAVEEN  Chandana PANDEY  Ehasanullah KHAN  Medha PANTHRI and Meetu GUPTA
Institution:Ecotoxicogenomics Laboratory, Department of Biotechnology, Jamia Millia Islamia, New Delhi 110025(India)
Abstract:Arsenic (As), one of the most harmful toxicant at the global level, severely affects plant metabolism when taken up. Interestingly, the presence of silicon (Si) as a fertilizer in As-contaminated soil is an effective strategy to decrease As accumulation in plants. Brassica juncea (var. Varuna) were grown hydroponically to investigate the role of Si at biochemical and molecular levels under arsenite (As3+) stress. Seedlings of B. juncea were exposed to As3+, Si, and a combination of both elements. Our data demonstrated that seedlings exposed to As3+ showed an inhibition in shoot length, chlorophyll, carotenoid, and protein, while co-application of Si improved these growth parameters. Silicon supplementation reduced As accumulation in shoot. Increase/decrease was observed in stress-related parameters (cysteine and proline), antioxidant enzymes (superoxide dismutase, ascorbate peroxidase, and catalase), and oxidative stress markers (malondialdehyde and H2O2), which were improved upon co-application of Si as compared to As3+ alone treatment. Random amplified polymorphic DNA (RAPD) is a suitable biomarker assay for plants for assessing the genotoxicity. Seven RAPD primers produced a total of 39 and 48 bands in the leaves of the untreated and treated seedlings, respectively. The RAPD band-profiles and genomic template stability were consistent with other growth and physiological parameters. In conclusion, the genotoxic alterations along with the biochemical parameters indicate that the exposure to Si mitigates As3+-induced oxidative stress by improving the stress-related parameters and antioxidant system in B. juncea.
Keywords:antioxidant enzyme  genomic template stability  genotoxicity  polymorphism  RAPD
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