Modulation of salt stress in paddy field cyanobacteria with exogenous application of gibberellic acid: growth behavior and antioxidative status.

UNLABELLED

The present study explores the possible function of gibberellic acid (GA: 20 µM) in reducing salt (NaCl) induced toxicity in two diazo-trophic cyanobacteria i.e. and . The physiological and biochemical parameters viz. growth, photosynthetic pigments (chlorophyll , carotenoids, and phycocyanin), photosynthetic and respiratory rates, oxidative stress biomarkers (superoxide radicle, hydrogen peroxide, and malondialdehyde contents) antioxidant activities (superoxide dismutase, peroxidase, catalase, and glutathione-S-transferase) and non-enzymatic antioxidants were studied under both the doses i.e. 40 mM (LC 10) and  mM (LC 30) of NaCl. The growth, photosynthetic pigments and photosynthetic rate were found to be declined under concentration-dependent manner of NaCl. Contrastingly, the respiratory rate, oxidative stress biomarkers, and the activity of antioxidant enzymes i.e. superoxide dismutase (SOD), peroxidases (POD), catalase (CAT), and glutathione-S-transferase (GST) together with contents of non-enzymatic antioxidants (proline and cysteine) were found to increase in the test cyanobacteria. PSII photochemistry in both the cyanobacteria was negatively affected showing an inhibitory effect of NaCl on JIP parameters, while an enhancement effect was noticed in the values related to energy flux parameters. Further, the addition of GA to the growth medium caused an alleviating effect as it completely mitigated NaCl toxicity induced by a lower dose i.e. 40 mM of NaCl, while it partially alleviated the growth and photosynthetic parameters of 80 mM NaCl stressed cyanobacteria. Supplementation of GA significantly reduced the contents of oxidative stress tested cyanobacteria due to an improved antioxidant system (increased activities of enzymatic and non-enzymatic antioxidants) as evident from the biochemical analysis. In brief, our findings reflect the possible role of GA as a potential modulator of salt toxicity.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s12298-022-01266-5.