Abstract
In the present study, the potential role of hydrogen peroxide (H2O2) and nitric oxide (NO) has been well recorded in the induction of cadmium (Cd) stress tolerance in cyanobacteria. In this regard, H2O2 and SNP (sodium nitroprusside, NO donor), were applied to Nostoc muscorum and Anabaena sp. exposed to Cd (6 µM) stress, to analyze different physiological and biochemical parameters. Results revealed that treatment of Cd reduced the growth, pigment contents, photosynthetic oxygen yield and performance of PS II photochemistry (decreased chlorophyll a fluorescence parameters, i.e., ФPo, Ψo, ФEo, PIABS along with Fv/Fo and increased the energy flux parameters, i.e., ABS/RC, TRo/RC, ETo/RC, DIo/RC along with Fo/Fv. Similarly, uptake of nitrate (NO3 -) and nitrite (NO2 -), as well as the activities of nitrate and ammonia assimilating enzymes along with carbohydrate content, were severely affected by Cd toxicity and notwithstanding this, glutamate dehydrogenase (GDH) activity exhibited reverse trend. Exogenous application of a very low dose (1 µM) of H2O2 (only for 3 h) and NO (SNP; 10 µM) notably counteracted Cd-induced toxicity. Nevertheless, the positive impact of H2O2 got reversed under the treatment of PTIO (NO scavenger) and LNAME (inhibitor of nitric oxide synthase; NOS) while NO could work efficiently even in the presence of NAC (H2O2 scavenger) and DPI (inhibitor of NADPH oxidase); hence indicated towards the H2O2 mediated NO signaling in averting Cd induced toxicity in test cyanobacteria. In conclusion, current finding demonstrated a positive cross-talk between H2O2 and NO for providing tolerance to cyanobacteria against Cd stress.