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Plant Physiology and Biochemistry 2020-Sep

Carbon dot induces tolerance to arsenic by regulating arsenic uptake, reactive oxygen species detoxification and defense-related gene expression in Cicer arietinum L

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
Vibhuti Chandrakar
Bhumika Yadu
Jyoti Korram
Manmohan Satnami
Amit Dubey
Meetul Kumar
S Keshavkant

Atslēgvārdi

Abstrakts

The scientific and technological applications of one of the nanomaterials viz.; carbon dot (C-dots), having extraordinary properties, is becoming an emerging and ongoing research area in recent times. In the present study, we have evaluated the effectiveness of C-dots in reducing arsenic (As) toxicity by analyzing physiological, biochemical and molecular parameters in Cicer arietinum L. The results revealed that As decreased the germination rate, growth, biomass, and membrane stability of the cell to a significant extent. Further, As was taken up by the growing seeds which eventually caused cell death. Levels of reactive oxygen species (ROS), stress markers (malondialdehyde), activities of defensive enzymes (glutathione-S-transferase and pyrroline-5-carboxylate synthetase) and non-enzymatic antioxidant contents (proline and glutathione) were increased under As stress. Moreover, As treatment resulted in the up-regulation of expressions of NADPH oxidase and defense-related genes in Cicer arietinum L. However, application of C-dots along with As improved the germination and growth of Cicer arietinum L. Exogenous application of C-dots, enhanced the expressions of defense-related genes and, contents of proline and glutathione, thereby causing considerable reductions in ROS, and malondialdehyde levels. Overall, this study suggests the possible involvement of C-dots in lowering the toxic effects of As on biomass by reducing As uptake and, inducing the activities/gene expressions and contents of enzymatic and non-enzymatic antioxidants.

Keywords: Arsenic; Carbon dot; Cicer arietinum L.; Gene expression; Nanomaterials; Oxidative damage; Reactive oxygen species.

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