scholarly journals Effects of Nitric Oxide On The Growth of The Marine Microalgae And The Parameters of Carbonate Chemistry

2021 ◽  
Author(s):  
Li Peifeng ◽  
Zhao Min ◽  
Liu Chunying ◽  
Yang Guipeng
Keyword(s):  
Nitric Oxide ◽  
Cell Density ◽  
Culture Media ◽  
Red Tide ◽  
Skeletonema Costatum ◽  
Marine Microalgae ◽  
Marine Phytoplankton ◽  
Carbonate System ◽  
No Donor ◽  
Low Concentrations

Abstract Nitric oxide (NO) is a non-traditional regulator for the growth of plant and phytoplankton. This study monitored the growth of five marine phytoplankton species, namely, Platymonas helgolandica var. tsingtaoensis, Platymonas subcordiformis, Skeletonema costatum, Gymnodinium sp., and Prorocentrum donghaiense, and examined the parameters of the carbonate system in the culture media after adding different concentrations of NO and sodium nitroprusside (SNP, NO donor) solutions. The different concentrations of exogenous NO had various roles in the growth of these microalgae. The two food algae,namely, P. helgolandica var. tsingtaoensis, P. subcordiformis, and three red tide algae, namely S. costatum, Gymnodinium sp., and P. donghaiense showed different responses to the same NO concentration. The red tide algae were more sensitive to exogenous NO than the food algae. NO with the concentration of 1.4 × 10− 6 mol L− 1 had the optimum stimulatory effect on the growth of the microalgae, the cell density increased by 9.8 ~ 38.3%. SNP solution with the concentration of 100 µmol L− 1 inhibited the growth of the two food algae, the cell density decreased by 38.8 ~ 84.3%. Meanwhile, 10 µmol L− 1 SNP solution additions to the three red tide algae declined the cell density by 95.3 ~ 99.9%. Low concentrations of SNP (0.1 µmol L− 1 for the two food algae and 0.01 µmol L− 1 for the red tide algae) promoted the growth of microalgae slightly. Different concentrations of exogenous NO could also influence parameters of the carbonate system in the culture media. NO participates in the regulation of marine microalgae photosynthesis, which may influence the parameters of carbonate system.

Pola Pertumbuhan, Biomassa Dan Kandungan Protein Kasar Kultur Skeletonema costatum Skala Massal Dengan Konsentrasi Kalium Nitrat Berbeda

2018 ◽  
Vol 7 (2) ◽  
pp. 75
Author(s):  
Diyah Putri Ambarwati ◽  
Ervia Yudiati ◽  
Endang Supriyantini ◽  
Lilik Maslukah
Keyword(s):  
Stationary Phase ◽  
Protein Content ◽  
Cell Density ◽  
Growth Pattern ◽  
Crude Protein ◽  
Culture Media ◽  
Skeletonema Costatum ◽  
Potassium Nitrate ◽  
Mass Scale ◽  
Crude Protein Content

Mikroalga Skeletonema costatum merupakan pakan alami yang mengandung nutrisi yang diperlukan untuk budidaya perikanan. Modifikasi media kultur merupakan salah satu upaya optimalisasi produktivitas sekaligus meningkatkan kadar proteinnya. Penelitian ini bertujuan untuk mengetahui pengaruh pemberian KNO3 dengan berbagai konsentrasi terhadap pola pertumbuhan, biomassa dan kandungan protein kasar. Metode penelitian yang digunakan adalah metode eksperimen Rancangan Acak Lengkap, dengan lima konsentrasi KNO3 (A: 25; B:50; C:75; D:100 dan E:125 ppm) yang diulang sebanyak tiga kali. Inokulum awal adalah satu ton,103 sel/mL. Saat mencapai fase stasioner, kultur massal S. costatum dipanen dan dikeringkan. Kandungan protein kasar dianalisis menggunakan metode Kjeldahl. Hasil penelitian terhadap kepadatan menunjukkan bahwa perlakuan terbaik dicapai pada konsentrasi KNO3 125 ppm (498,88. 103 sel/mL) diikuti D (316,94. 10³ sel/mL), C (313,81.10³ sel/mL), B (246,56. 10³ sel/mL) dan A (195,60. 10³ sel/mL). Terdapat perbedaan fase stasioner pada masing-masing perlakuan yaitu A:32; B:28; C: 37; D:32; E:36 jam. Biomass rata-rata yang dihasilkan pada tiap perlakuan sesuai dengan pola kepadatan sel yaitu E: 8,60, D:7,85, C:6,43, B:5,91 dan A:5,44 g. Analisa terhadap kandungan protein kasar menunjukkan tidak adanya perbedaan antar perlakuan (P>0,05). Pemberian KNO3 terbukti dapat meningkatkan kepadatan sel dan berpengaruh terhadap pola pertumbuhan dan biomassa, namun kandungan protein kasar tidak meningkat. Growth, Biomass and Rough Protein Content of Skeletonema costatum Mass Scale with Different Concentration of Potassium Nitrate (KNO3) Skeletonema costatum is natural microalgae which rich in nutrient. An effort to optimize the protein content was done by modifying the culture media. This research is aimed to find out the effect of various concentration of KNO3 addition to the growth pattern, biomass and crude protein content. The Completely Randomized Design with five treatment KNO3 (A: 25; B:50; C:75; D:100 dan E:125 ppm) in three replication were applied. The starting innoculum was one tonne, 103 cel/mL. The microalgae was harvested at stationary phase and the dried. The crude protein was analised by Kjeldahl methods. The results of cell density showed that the best concentration was E (498,88. 103 cells/mL), D (316,94. 10³ cells/mL), C (313,81.10³ cells/mL), B (246,56. 10³ cells/mL) and A (195,60. 10³ cells/mL) respectively. The stationary phase in every treatment was reached at different time A:32; B:28; C: 37; D:32; E:36 hr. The average biomass were at similar pattern to the cell density (E:8,60, D:7,85, C:6,43, B:5,91 and A:5,44 g). On the other hand, the crude protein content were not significantly different (P>0,05). It is concluded that the KNO3 addition enhanced the cell density, growth pattern, biomass. The protein content was remain similar. 

scholarly journals Nitric Oxide as a Signaling Factor To Upregulate the Death-Specific Protein in a Marine Diatom, Skeletonema costatum, during Blockage of Electron Flow in Photosynthesis

2008 ◽  
Vol 74 (21) ◽  
pp. 6521-6527 ◽  
Author(s):  
Chih-Ching Chung ◽  
Sheng-Ping L. Hwang ◽  
Jeng Chang
Keyword(s):  
Nitric Oxide ◽  
18S Rrna ◽  
Skeletonema Costatum ◽  
Electron Flow ◽  
Specific Protein ◽  
Marine Diatom ◽  
Mrna Levels ◽  
No Donor ◽  
Secondary Messenger ◽  
Light Manipulation

ABSTRACT To determine the physiological functions of a novel death-specific protein gene, Skeletonema costatum DSP-1 (ScDSP-1) in a marine diatom, Skeletonema costatum, the mRNA abundance of ScDSP-1 was measured in cultures subjected to light manipulation and treatments with various chemicals. When cells were transferred to a dim light intensity of 15 μmol m−2 s−1, ScDSP-1 mRNA levels showed a transient increase of 1 to 17.2 μmol (mol 18S rRNA)−1 in 60 h. Furthermore, treatments with the photoinhibitors 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB) resulted in high ScDSP-1 mRNA levels, which reached 943 and 72 μmol (mol 18S rRNA)−1, respectively. Treatment with the nitric oxide (NO) donor diethylamine nitric oxide also induced ScDSP-1 expression, and this inducible expression was inhibited by the NO scavenger hemoglobin. Additionally, the expression of ScDSP-1 mRNA elicited by DCMU and DBMIB was efficiently reduced when cultures were pretreated with the cell-penetrating NO scavenger 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. In contrast, treatment with another photoinhibitor, paraquat, had no effect on ScDSP-1 expression. Our results indicated that NO is the crucial secondary messenger which signals the expression of ScDSP-1 when electron flow between photosystem II and photosystem I is blocked in S. costatum cells. In addition, the discovery of a similar gene, ScDSP-2, is briefly described.

Differential Mechanisms Underlying the Modulation of Delayed-Rectifier K+ Channel in Mouse Neocortical Neurons by Nitric Oxide

2006 ◽  
Vol 95 (4) ◽  
pp. 2167-2178 ◽  
Author(s):  
Nian-Lin R. Han ◽  
Jian-Shan Ye ◽  
Albert Cheung Hoi Yu ◽  
Fwu-Shan Sheu
Keyword(s):  
Nitric Oxide ◽  
K Channel ◽  
Delayed Rectifier ◽  
Open Probability ◽  
No Donor ◽  
Whole Cell ◽  
Low Concentrations ◽  
Cgmp Signaling ◽  
Voltage Dependent ◽  
High Concentrations

The modulatory effects of nitric oxide (NO) on voltage-dependent K+ channels are intricate. In our present study, the augmentation and reduction of K+ currents by NO donor S-nitro- N-acetylpenicillamine (SNAP) and pure dissolved NO was observed in dissociated neurons from mice neocortex with both whole cell and cell-attached patch clamp. By using a specific electrochemical sensor, the critical concentrations of NO that increased or reduced the channel activities were accurately quantified. Low concentrations of SNAP (20 μM) or NO solution (0.1 μM) enhanced whole cell delayed rectifier K+-current ( IK) and left the fast inactivating A current ( IA) unchanged. However, high concentrations of SNAP (100 μM) and NO (0.5 μM) reduced both IK and IA currents. In cell-attached experiments, a significant increase in channel open probability (NP0) was observed when using low concentrations of SNAP or NO. High concentrations of SNAP or NO dramatically decreased NP0. The increase in channel activities by low concentrations of SNAP was abolished in the presence of either inhibitors of soluble guaylate cyclase or inhibitors of cGMP-dependent protein kinase G, suggesting a link to the NO-cGMP signaling cascade. The reduction of channel activities by high concentrations of SNAP was reversed by the reducing agent dithiothreitol, implying a redox reaction mechanism. Thus both NO-cGMP signaling and a redox mechanism are involved in the modulation of IK channel activity for neuron excitability.

Effects of Exogenous Nitric Oxide at Different Concentrations on the Photosynthesis of Pinus koraiensis Sieb. Et Zucc. Seedlings

2011 ◽  
Vol 183-185 ◽  
pp. 422-426
Author(s):  
Xiao Xue Wei ◽  
De Wen Li ◽  
Jing Hua Yu ◽  
Yuan Gang Zu
Keyword(s):  
Nitric Oxide ◽  
Pinus Koraiensis ◽  
Photosynthetic Parameters ◽  
Gas Exchange Parameters ◽  
No Donor ◽  
Chlorophyll Contents ◽  
Compensation Irradiance ◽  
Low Concentrations ◽  
Exogenous Nitric Oxide ◽  
Exchange Parameters

In the study, the gas exchange parameters and chlorophyll contents in the needles of Pinus koraiensis Sieb. et Zucc. exposed to exogenous nitric oxide (NO) were determined. The Pinus koraiensis Sieb. et Zucc. seedlings were treated with sodium nitroprusside (SNP), a NO donor, at 5 different concentrations ranging from 0 mM to 1 mM. The result showed that at different concentrations exogenous NO had different effects on the photosynthetic parameters and photosynthetic pigments. The content of chlorophyll was maximal in the treatment with SNP at 0.01 mM. At low concentrations (0.1 mM) SNP significantly increased the photosynthetic rate (PN) and decreased the Respiration rate (RD) and Compensation irradiance (IC) of the needles (p<0.05). The experiment proved that at low concentrations exogenous NO signals increased the photosynthesis of Pinus koraiensis Sieb. et Zucc. seedlings. The present results suggested that the lower concentrations SNP might decrease the level of reactive oxygen species (ROS) and promote the growth of the Pinus koraiensis Sieb. et Zucc.

scholarly journals L-Arginine Enhances Protein Synthesis by Phosphorylating mTOR (Thr 2446) in a Nitric Oxide-Dependent Manner in C2C12 Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
Ruxia Wang ◽  
Hongchao Jiao ◽  
Jingpeng Zhao ◽  
Xiaojuan Wang ◽  
Hai Lin
Keyword(s):  
Nitric Oxide ◽  
Protein Synthesis ◽  
Culture Media ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
C2c12 Cells ◽  
Dependent Manner ◽  
No Donor ◽  
Nos Inhibitor ◽  
Oxide Synthase

Muscle atrophy may arise from many factors such as inactivity, malnutrition, and inflammation. In the present study, we investigated the stimulatory effect of nitric oxide (NO) on muscle protein synthesis. Primarily, C2C12 cells were supplied with extra L-arginine (L-Arg) in the culture media. L-Arg supplementation increased the activity of inducible nitric oxide synthase (iNOS), the rate of protein synthesis, and the phosphorylation of mTOR (Thr 2446) and p70S6K (Thr 389). L-NAME, an NOS inhibitor, decreased NO concentrations within cells and abolished the stimulatory effect of L-Arg on protein synthesis and the phosphorylation of mTOR and p70S6K. In contrast, SNP (sodium nitroprusside), an NO donor, increased NO concentrations, enhanced protein synthesis, and upregulated mTOR and p70S6K phosphorylation, regardless of L-NAME treatment. Blocking mTOR with rapamycin abolished the stimulatory effect of both L-Arg and SNP on protein synthesis and p70S6K phosphorylation. These results indicate that L-Arg stimulates protein synthesis via the activation of the mTOR (Thr 2446)/p70S6K signaling pathway in an NO-dependent manner.

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.

Sign in / Sign up

Export Citation Format

Share Document