Calcium mediated nitric oxide responses: Acquisition of nickel stress tolerance in cyanobacterium Nostoc muscorum ATCC 27893.

Calcium (Ca2+) and nitric oxide (NO) are potentially active and multitasking signaling molecules which are known to regulate abiotic stresses in plants, but their interactive role in the acquisition of metal stress tolerance in cyanobacteria remains elusive. In current study the signaling role of Ca2+ (800 µM) and NO (10 µM SNP) on key physiological and biochemical attributes of the agriculturally and economically important cyanobacterium Nostoc muscorum ATCC 27893 subjected to Ni stress (2 µM) was examined. Results revealed that Ni at elevated level caused severe damages to the test organism but exogenous supplementation of Ca2+ and NO efficiently mitigated its toxic effects and up-regulated the growth, pigment contents, rate of photosynthesis (whole cell oxygen evolution and Chl a fluorescence indices: Kinetic traits: ΦP0, Ψ0, ΦE0 and PIABS, along with Fv/F0), nitrogen metabolism (NO3‾ and NO2‾ uptake, nitrate:NR and NiR; and ammonia:GS and GOGAT; assimilating enzymes), and boosted the enzymatic (SOD, POD, CAT and GST) along with non-enzymatic (proline, cysteine and NP-SH) antioxidants. Whereas the increased values of energy flux traits: (ABS/RC, TR0/RC, DI0/RC and ET0/RC) along with F0/Fv, rate of respiration, oxidative stress biomarkers (SOR, H2O2 and MDA), and activity of GDH enzyme exhibited lowering trends with application of Ca2+ and NO. Further, addition of EGTA (Ca2+ scavenger) and PTIO (NO scavenger) reversed the positive impacts of Ca2+ and NO and worsened the toxicity of Ni on test cyanobacterium, but the damages were more pronounced under PTIO application that demonstrated Ca2+ mediated signaling role of NO in Ni toxicity alleviation.

Cytokinin alleviates cypermethrin toxicity in Nostoc muscorum by involving nitric oxide: Regulation of exopolysaccharides secretion, PS II photochemistry and reactive oxygen species homeostasis.

Growth of the most important nitrogen fixing cyanobacterium Nostoc muscorum is reported to be badly affected by the application of insecticides. To overcome their damaging effects, several strategies are being used. Out of these, some works on kinetin (KN, a synthetic cytokinin) has been recognized that it can overcome toxicity of insecticides in cyanobacteria. Besides this, it is now known that every hormone needs certain second messengers such as nitric oxide (NO) for its action. But implication of NO in KN-mediated regulation of insecticide toxicity is yet to be investigated. Hence in the current study, we have investigated the possible involvement of NO in KN-mediated regulation of cypermethrin toxicity in the cyanobacterium Nostoc muscorum. Cypermethrin decreased growth of Nostoc muscorum which was accompanied by decreased pigment contents and altered photosystem II (PS II) photochemistry that resulted in inhibition of photosynthetic process but KN significantly ameliorated cypermethrin toxicity. Cypermethrin induced production of free radicals (in-vivo and in-vitro) and weakened defensive mechanism (enzymatic and non-enzymatic defense system) which was restored by KN. Further, the results revealed that NG-nitro-l-arginine methyl ester (l-NAME, an inhibitor of nitric oxide synthase) worsened the effect of cypermethrin toxicity even in the presence of KN while 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO, a scavenger of NO) reversed KN-mediated amelioration even in the presence of sodium nitroprusside (SNP, an NO donor), suggesting that endogenous NO is required for mitigation of cypermethrin toxicity. Overall, our results first time show that endogenous NO is essential for KN-mediated mitigation of cypermethrin toxicity in the Nostoc muscorum.

Regulation of insecticide toxicity by kinetin in two paddy field cyanobacteria: Physiological and biochemical assessment.

The imprudent agricultural practices are leading to an increasing load of pesticides in agricultural fields. Thus, there is a need to minimize the harmful effect of pesticides by adopting sustainable strategies. In the recent past decade, kinetin, a plant synthetic hormone, has been reported as a pesticide toxicity alleviator in higher plants. But its role in mitigating pesticide toxicity in cyanobacteria is still limited. Thus, in current study an attempt has been made to investigate the potential of kinetin in regulating cypermethrin, an insecticide, induced toxicity in Anabaena PCC 7120 and Nostoc muscorum ATCC 27893. Cypermethrin (Cyp1; 2 µg ml-1 and Cyp2; 4 µg ml-1) showed negative impact on growth, photosynthetic pigments, photosynthetic O2-evolution and primary photochemistry of PS II (Phi_P0, Psi_0, Phi_E0) resulting in decrease in performance index (PIABS). However, under similar conditions, increases in energy flux parameters (ABS/RC, TR0/RC, ET0/RC and DI0/RC) were noticed. Cypermethrin at both the doses enhanced the level of oxidative stress biomarkers (SOR, H2O2, and MDA equivalent contents) despite of increased antioxidant enzymatic activity (SOD, POD, CAT and GST).Under similar condition, cypermethrin at tested doses caused substantial decrease in non-enzymatic antioxidant contents (proline, cysteine and NP-SH). Nevertheless, kinetin treatment attenuated cypermethrin induced oxidative stress by further up-regulating the activity of enzymatic antioxidants and by enhancing the contents of non-enzymatic antioxidants. Thus, with the application of kinetin improved photochemistry of PS II and growth yield of both the cyanobacteria were observed even in the presence of cypermethrin. Current results establish that cypermethrin induces toxicity on photosynthesis, photosynthetic pigments and growth, and this effect was more pronounced in Anabaena PCC 7120 than Nostoc muscorum ATCC 27893. Furthermore, the potential role of kinetin in mitigating the toxicity of cypermethrin in both the cyanobacteria provides an insight to be used in paddy fields for sustainable agricultural practices.

Pretilachlor toxicity is decided by discrete photo-acclimatizing conditions: Physiological and biochemical evidence from Anabaena sp. and Nostoc muscorum.

The current study was undertaken to elucidate the impact of the herbicide pretilachlor (3 µg ml-1 and 6 µg ml-1) on cyanobacteria, Nostoc muscorum ATCC 27893 and Anabaena sp. PCC 7120 under three levels of photoacclimatization (suboptimum, 25 µmol photon m-2 s-1; optimum, 75 µmol photon m-2 s-1; and supra-optimum, 225 µmol photon m-2 s-1) by analyzing certain physiological (biomass accumulation, photosynthesis, Chl a fluorescence and respiration) and biochemical parameters (photosynthetic pigments‒ chlorophyll a, carotenoids and phycocyanin; reactive oxygen species‒ O2•¯, H2O2, lipid peroxidation; antioxidant system‒ superoxide dismutase, peroxidise, catalase and glutathione-S-transferase). The light conditioning played the most prominent role in deciding the extent of herbicide toxicity on both the tested cyanobacteria as the maximum toxicity was observed in suboptimum light acclimatized cyanobacterial cells corroborated by the least growth in the same cells. The impact of pretilachlor treatment on photosystem II photochemistry viz. φP0, Ñ°0, φE0, PIABS, ABS/RC, TR0/RC, ET0/RC and DI0/RC was also altered by light acclimatization. The percent rise in oxidative stress markers (SOR and H2O2) and consequent lipid peroxidation (MDA equivalents) were also highest in suboptimum light acclimatized cells exposed to pretilachlor which could not be prospered with compatible antioxidant performance. Conversely, supra-optimum light acclimatized cells of both the cyanobacteria was found to accelerate the activities of all the studied enzymes and thus able to counterbalance the pretilachlor toxicity and supported the healthier growth.