scholarly journals 5-Aminolevulinic Acid-induced Salt Tolerance in Strawberry: Possible Role of Nitric Oxide on Interception of Salty Ions in Roots

2020 ◽  
Author(s):  
Shasha He ◽  
Yuyan An ◽  
Hao Yang ◽  
Rongqiang Cao ◽  
Quan Tang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Salt Tolerance ◽  
Aminolevulinic Acid ◽  
Culture Solution ◽  
Gene Expressions ◽  
Protein Amino Acid ◽  
No Donor ◽  
Upward Transport ◽  
Plant Salt Tolerance ◽  
Whole Plants

Abstract Background: 5-Aminolevunic acid (ALA), as a natural non-protein amino acid and the first essential precursor of tetrapyrrole biosynthesis in all living bodies, has been suggested to improve salt tolerance of plants. In the previous work, we reported that ALA induces H2O2 accumulation in roots of strawberry, which is involved in up-regulating Na+ transporter gene expressions to intercept Na+ in roots with less upward transport. However, the signal route is not clear.Results: In this study, we propose that nitric oxide (NO) is involved in ALA signaling cascade. Therefore, we applied sodium nitrosylpentacy (SNP, NO donor), Na2WO4 (NO biosynthetic inhibitor), and 2, 4-carboxyphenyl-4, 4, 5, 5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO, NO scavenger) to the culture solution when strawberry (Fragaria × ananassa Duch. cv. ‘Benihoppe’) was stressed by 100 mmol L-1 NaCl with or without exogenous ALA. The results reveal that salinity greatly impaired plant growth while 10 mg L-1 ALA or 10 µM SNP ameliorated the inhibition. When 5 µM Na2WO4 or cPTIO was co-treated, the ALA-improved salt tolerance was almost completely eliminated. This suggests that ALA-improved salt tolerance is dependent on NO presence. We found that salinity caused NO, H2O2, Na+ and Cl- increases in the whole plants, while ALA induced additional increases in roots but significant depressions in leaves. These tissue-specific responses to ALA are important for plant salt tolerance. Conclusion: We propose that the regulation of ALA in roots is critical, which is mediated through NO and then H2O2 signal to up-express genes related with Na+ and Cl- transport, selectively retaining Na+ and Cl- in roots with less upward transport. The hypothesis can reasonably explain how ALA-treated plants cope with toxic ions under salinity.

scholarly journals Patellin1 negatively regulates plant salt tolerance by attenuating nitric oxide accumulation in Arabidopsis

2019 ◽  
Vol 14 (12) ◽  
pp. 1675472
Author(s):  
Xia Sun ◽  
Yufen Zhuang ◽  
Honghui Lin ◽  
Huapeng Zhou
Keyword(s):  
Nitric Oxide ◽  
Salt Tolerance ◽  
Plant Salt Tolerance

scholarly journals Identification of Foliar Salt Tolerance of Woody Perennials Using Chlorophyll Fluorescence

HortScience ◽  
2005 ◽  
Vol 40 (6) ◽  
pp. 1892-1897 ◽  
Author(s):  
G.C. Percival
Keyword(s):  
Chlorophyll Fluorescence ◽  
Salt Tolerance ◽  
Laboratory Tests ◽  
Woody Perennials ◽  
Laboratory Conditions ◽  
Whole Plant ◽  
Leaf Necrosis ◽  
Plant Salt Tolerance ◽  
Whole Plants ◽  
Inexpensive Procedure

Aims of this investigation were to determine whether chlorophyll fluorescence values obtained from excised leaves of woody perennials subjected to salinity stress under laboratory conditions provided a measurable indicator of whole plant salinity tolerance. Laboratory tests consisted of measurements of the ratio of variable to maximal chlorophyll fluorescence (Fv/Fm) performed on excised leaves taken from thirty woody perennials following immersion in salt solutions ranging from concentrations of 2% to 7%. Based on reductions in Fv/Fm of excised leaves following salinity treatments plants were ranked in order of tolerance. Whole plants of six of the thirty species tested were then subjected to a foliar applied salt at a concentration of 7% and placed under glass for 14 weeks. Damage to, and recovery of whole plants from salt damage as measured by chlorophyll fluorescence, leaf necrosis and chlorophyll content mirrored tolerance ranking of excised leaves under laboratory conditions. In addition, based on reductions in plant growth at the cessation of the experiment, salt tolerance followed a similar order as that obtained from Fv/Fm values of excised leaves. Results indicate that testing of excised leaf material of woody perennials under laboratory conditions using chlorophyll fluorescence offers a potentially quick, reliable and inexpensive procedure that can provide a useful means of estimating whole plant salt tolerance.

Acute depletion of heme by succinylacetone alters vascular responses but does not induce hypertension

2008 ◽  
Vol 86 (9) ◽  
pp. 613-619 ◽  
Author(s):  
Jonathan Soong ◽  
Michael A. Adams ◽  
Kanji Nakatsu
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Aminolevulinic Acid ◽  
Critical Role ◽  
High Dose ◽  
Compensatory Mechanisms ◽  
Irreversible Inhibitor ◽  
Synthesis Inhibitor ◽  
Vascular Effects ◽  
No Donor

Heme plays a critical role in blood pressure regulation because it is required by a number of enzymes that synthesize vascular modulators, including nitric oxide (NO), carbon monoxide (CO), guanosine 3′,5′-cyclic monophosphate (cGMP), endothelium-derived hyperpolarizing factor (EDHF), and prostacyclin. The goal of this study was to examine the vascular effects of a short-term depletion of heme achieved through administration of the heme-synthesis inhibitor succinylacetone (SA), an irreversible inhibitor of aminolevulinic acid dehydratase (ALAD). Rats were depleted of heme by using a 4-day treatment with SA. This treatment impacted hemoenzyme function, decreasing renal nitric oxide synthase (NOS) activity (as indicated by decreased in vitro NOS activity), and increasing kidney microsomal heme oxygenase (HO) activity by 27%. SA treatment also resulted in enhanced reduction in blood pressure after infusions of exogenous NO donor MAHMA NONOate (at high dose) and acetylcholine (at low doses). Nevertheless, this SA treatment was insufficient to produce an overt elevation of basal arterial pressure. This latter lack of effect may be the result of multiple compensatory mechanisms for the regulation of blood pressure.

scholarly journals Florigen governs shoot regeneration

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yaarit Kutsher ◽  
Michal Fisler ◽  
Adi Faigenboim ◽  
Moshe Reuveni
Keyword(s):  
Nitric Oxide ◽  
Shoot Regeneration ◽  
Ectopic Expression ◽  
Flowering Plants ◽  
Regeneration Capacity ◽  
No Donor ◽  
Tobacco Leaves ◽  
Age Related ◽  
Delayed Flowering

AbstractIt is widely known that during the reproductive stage (flowering), plants do not root well. Most protocols of shoot regeneration in plants utilize juvenile tissue. Adding these two realities together encouraged us to study the role of florigen in shoot regeneration. Mature tobacco tissue that expresses the endogenous tobacco florigen mRNA regenerates poorly, while juvenile tissue that does not express the florigen regenerates shoots well. Inhibition of Nitric Oxide (NO) synthesis reduced shoot regeneration as well as promoted flowering and increased tobacco florigen level. In contrast, the addition of NO (by way of NO donor) to the tissue increased regeneration, delayed flowering, reduced tobacco florigen mRNA. Ectopic expression of florigen genes in tobacco or tomato decreased regeneration capacity significantly. Overexpression pear PcFT2 gene increased regeneration capacity. During regeneration, florigen mRNA was not changed. We conclude that florigen presence in mature tobacco leaves reduces roots and shoots regeneration and is the possible reason for the age-related decrease in regeneration capacity.

Nitric Oxide Activates Leak K+ Currents in the Presumed Cholinergic Neuron of Basal Forebrain

2007 ◽  
Vol 98 (6) ◽  
pp. 3397-3410 ◽  
Author(s):  
Youngnam Kang ◽  
Yoshie Dempo ◽  
Atsuko Ohashi ◽  
Mitsuru Saito ◽  
Hiroki Toyoda ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Basal Forebrain ◽  
Reversal Potential ◽  
Soluble Guanylyl Cyclase ◽  
Outward Current ◽  
Pump Current ◽  
Atp Depletion ◽  
Equilibrium Potential ◽  
No Donor ◽  
Bath Application

Learning and memory are critically dependent on basal forebrain cholinergic (BFC) neuron excitability, which is modulated profoundly by leak K+ channels. Many neuromodulators closing leak K+ channels have been reported, whereas their endogenous opener remained unknown. We here demonstrate that nitric oxide (NO) can be the endogenous opener of leak K+ channels in the presumed BFC neurons. Bath application of 1 mM S-nitroso- N-acetylpenicillamine (SNAP), an NO donor, induced a long-lasting hyperpolarization, which was often interrupted by a transient depolarization. Soluble guanylyl cyclase inhibitors prevented SNAP from inducing hyperpolarization but allowed SNAP to cause depolarization, whereas bath application of 0.2 mM 8-bromoguanosine-3′,5′-cyclomonophosphate (8-Br-cGMP) induced a similar long-lasting hyperpolarization alone. These observations indicate that the SNAP-induced hyperpolarization and depolarization are mediated by the cGMP-dependent and -independent processes, respectively. When examined with the ramp command pulse applied at –70 mV under the voltage-clamp condition, 8-Br-cGMP application induced the outward current that reversed at K+ equilibrium potential ( EK) and displayed Goldman-Hodgkin-Katz rectification, indicating the involvement of voltage-independent K+ current. By contrast, SNAP application in the presumed BFC neurons either dialyzed with the GTP-free internal solution or in the presence of 10 μM Rp-8-bromo-β-phenyl-1,N2-ethenoguanosine 3′,5′-cyclic monophosphorothioate sodium salt, a protein kinase G (PKG) inhibitor, induced the inward current that reversed at potentials much more negative than EK and close to the reversal potential of Na+-K+ pump current. These observations strongly suggest that NO activates leak K+ channels through cGMP-PKG-dependent pathway to markedly decrease the excitability in BFC neurons, while NO simultaneously causes depolarization by the inhibition of Na+-K+ pump through ATP depletion.

Nitric oxide preconditioning regulates endothelial monolayer integrity via the heat shock protein 90-soluble guanylate cyclase pathway

2007 ◽  
Vol 292 (2) ◽  
pp. H893-H903 ◽  
Author(s):  
Galina N. Antonova ◽  
Connie M. Snead ◽  
Alexander S. Antonov ◽  
Christiana Dimitropoulou ◽  
Richard C. Venema ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Cell Injury ◽  
Soluble Guanylate Cyclase ◽  
Heat Shock Protein 90 ◽  
Protective Effects ◽  
No Donor ◽  
Spermine Nonoate

Large (pathological) amounts of nitric oxide (NO) induce cell injury, whereas low (physiological) NO concentrations often ameliorate cell injury. We tested the hypotheses that pretreatment of endothelial cells with low concentrations of NO (preconditioning) would prevent injury induced by high NO concentrations. Apoptosis, induced in bovine aortic endothelial cells (BAECs) by exposing them to either 4 mM sodium nitroprusside (SNP) or 0.5 mM N-(2-aminoethyl)- N-(2-hydroxy-2-nitrosohydrazino)-1,2-ethylenediamine (spermine NONOate) for 8 h, was abolished by 24-h pretreatment with either 100 μM SNP, 10 μM spermine NONOate, or 100 μM 8-bromo-cGMP (8-Br-cGMP). Repair of BAECs following wounding, measured as the recovery rate of transendothelial electrical resistance, was delayed by 8-h exposure to 4 mM SNP, and this delay was significantly attenuated by 24-h pretreatment with 100 μM SNP. NO preconditioning produced increased association and expression of soluble guanyl cyclase (sGC) and heat shock protein 90 (HSP90). The protective effect of NO preconditioning, but not the injurious effect of 4 mM SNP, was abolished by either a sGC activity inhibitor 1H-[1,2,4]oxadiazolo-[4,3- a]quinoxalin-1-one (ODQ) or a HSP90 binding inhibitor (radicicol) and was mimicked by 8-Br-cGMP. We conclude that preconditioning with a low dose of NO donor accelerates repair and maintains endothelial integrity via a mechanism that includes the HSP90/sGC pathway. HSP90/sGC may thus play a role in the protective effects of NO-generating drugs from injurious stimuli.

Inducible nitric oxide synthase augments injury elicited by oxidative stress in rat cardiac myocytes

1998 ◽  
Vol 274 (1) ◽  
pp. C245-C252 ◽  
Author(s):  
Junsuke Igarashi ◽  
Masashi Nishida ◽  
Shiro Hoshida ◽  
Nobushige Yamashita ◽  
Hiroaki Kosaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiac Myocytes ◽  
Myocardial Injury ◽  
No Production ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
No Donor ◽  
Oxide Synthase ◽  
Gpx Activity

The effects of nitric oxide (NO) produced by cardiac inducible NO synthase (iNOS) on myocardial injury after oxidative stress were examined. Interleukin-1β induced cultured rat neonatal cardiac myocytes to express iNOS. After induction of iNOS,l-arginine enhanced NO production in a concentration-dependent manner. Glutathione peroxidase (GPX) activity in myocytes was attenuated by elevated iNOS activity and by an NO donor, S-nitroso- N-acetyl-penicillamine (SNAP). Although NO production by iNOS did not induce myocardial injury, NO augmented release of lactate dehydrogenase from myocyte cultures after addition of H2O2(0.1 mM, 1 h). Inhibition of iNOS with Nω-nitro-l-arginine methyl ester ameliorated the effects of NO-enhancing treatments on myocardial injury and GPX activity. SNAP augmented the myocardial injury induced by H2O2. Inhibition of GPX activity with antisense oligodeoxyribonucleotide for GPX mRNA increased myocardial injury by H2O2. Results suggest that the induction of cardiac iNOS promotes myocardial injury due to oxidative stress via inactivation of the intrinsic antioxidant enzyme, GPX.

scholarly journals Vasoactive intestinal peptide stimulates mucus secretion, but nitric oxide has no effect on mucus secretion in the ferret trachea

2006 ◽  
Vol 101 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Jung-Soo Kim ◽  
Kosuke Okamoto ◽  
Shinobu Arima ◽  
Bruce K. Rubin
Keyword(s):  
Nitric Oxide ◽  
Receptor Antagonist ◽  
Vasoactive Intestinal Peptide ◽  
Mucus Secretion ◽  
Cell Secretion ◽  
Mucin Secretion ◽  
No Donor ◽  
Peptide Analog ◽  
Dose Dependent ◽  
Vip Receptor

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are neurotransmitters involved in the regulation of bronchial and pulmonary vascular tone. Published studies of the effects of VIP on airway mucus secretion have yielded conflicting results. The purpose of this study was to determine the effect of VIP on mucus secretion in the ferret trachea and if this effect was influenced by NO. We used a sandwich enzyme-linked lectin assay to measure mucin secretion and a turbidimetric assay to measure lysozyme (serous cell) secretion from ferret tracheal segments. VIP (10−7 M) increased mucin secretion over 2 h. VIP (10−9 to 10−5 M) stimulated mucin secretion in a dose-dependent fashion. VIP-induced mucin secretion was partially blocked by a VIP receptor antagonist (a chimeric VIP-pituitary adenylate cyclase-activating peptide analog, VIP receptor antagonist) at a 10-fold excess concentration. At all concentrations tested, neither NG-nitro-l-arginine methyl ester, an inhibitor of NO synthase, nor S-nitroso- N-acetyl-penicillamine, an NO donor, had any significant effect on constitutive or VIP-induced mucus secretion. We conclude that VIP-stimulated mucin and lysozyme secretion was both time dependent and dose dependent and that NO neither stimulates nor inhibits mucus secretion in the ferret trachea.

Nitric Oxide-Donating Derivatives of Chrysin Stimulate Angiogenesis and Upregulating VEGF Production

2011 ◽  
Vol 340 ◽  
pp. 363-368 ◽  
Author(s):  
Xiao Qing Zou ◽  
Yong Lan Ding ◽  
Sheng Ming Peng ◽  
Chang Ping Hu ◽  
Han Wu Deng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Therapeutic Option ◽  
Therapeutic Angiogenesis ◽  
Vegf Mrna ◽  
No Donor ◽  
Endothelial Migration ◽  
Nitric Oxide Releasing ◽  
Derivatives Of

Angiogenesis, the development of new capillaries from pre-existing vessels, requires the coordinate activation of endothelial cells, which migrate and proliferate to form functional vessels. Endothelial dysfunction and decreased nitric oxide bioavailability may underscore the impairment of angiogenesis. As such, the delivery of exogenous NO is an attractive therapeutic option that has been used to therapeutic angiogenesis. In this paper, a novel group of hybrid nitric oxide-releasing chrysin derivatives was synthesized. The results indicated that all these chrysin derivatives exhibited promotion of endothelial migration and tubulogenesis in vitro as well as stimulation angiogenesis in vivo.Furthermore, all compounds released NO upon incubation with phosphate buffer at pH 7.4 and enhanced VEGF secretion and VEGF mRNA expression of endothelial cells. These hybrid ester NO donor prodrugs offer a potential drug design concept for the development of therapeutic or preventive agents for angiogenesis deficiency due to ischemic diseases.

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