Crosstalk mechanism of hydrogen sulfide and nitric oxide in regulating the nickel induced toxicity of cyanobacteria Nostoc muscorum and Anabaena sp.

The present study examined the interactive role of hydrogen sulfide (H₂S) and nitric oxide (NO) in alleviation of nickel (Ni) induced toxicity on growth, photosynthetic pigments, PS II photochemistry, and impact on oxidative stress biomarkers and antioxidant defense systems of cyanobacteria, i.e., Nostoc muscorum and Anabaena sp., respectively. To substantiate the potential function of H₂S [as sodium hydrosulfide (NaHS); 8 µM)] and NO [as sodium nitroprusside (SNP); 10 µM] test organisms was exposed under 1 µM Ni stress and distinct physio-biochemical parameters was evaluated. The Ni stress declined the growth (by 19% and 23% in N. muscorum and Anabaena sp. respectively), photosynthetic pigments, photosynthetic oxygen evolution, and imbalanced the values of chlorophyll a fluorescence kinetics parameters (Phi_Po, Psi_o, Phi_Eo, PI_ABS decreased together with Fv/Fo) whereas, energy flux parameters were increased (ABS/RC, TRo/RC, ETo/RC and DIo/RC). The exogenous supplementation of NaHS and SNP significantly reduced reactive oxygen species (ROS) in both the cyanobacteria and induced substantial improvement in growth and photosynthesis under Ni stress. Besides this, under NaHS and SNP treatment the activity of antioxidant enzymes like superoxide dismutase, peroxidase, catalase and glutathione-s-transferase downregulated the level of oxidative biomarkers (superoxide radicals, hydrogen peroxide and malondialdehyde equivalents). Further, the interplay role of H₂S and NO was evaluated using H₂S scavenger [hypotaurine (HT; 20 µM)] and inhibitor [propargylglycine (PAG; 50 µM)] of H₂S and scavenger of NO [2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO; 20 µM)] and NO inhibitor [NG-nitro-L-arginine methyl ester (L-NAME; 100 µM)]. The present study points towards the combined mechanism with downstream signaling of H₂S on NO mediated response in alleviation of Ni induced toxicity in rice field cyanobacteria.