CO2 laser enhances the chilling tolerance of wheat seedlings by stimulating NO synthesis

2016 ◽  
Vol 96 (5) ◽  
pp. 796-807
Author(s):  
Yi-ping Chen ◽  
Qiang Liu ◽  
Dong Chen
Keyword(s):  
Nitric Oxide ◽  
Laser Irradiation ◽  
Sodium Tungstate ◽  
Chilling Stress ◽  
Chilling Tolerance ◽  
The Other ◽  
Control Group ◽  
Wheat Seedlings ◽  
Oxide Synthase ◽  
Protein Treatment

To investigate the mechanism by which laser irradiation enhances the chilling tolerance of wheat seedlings, seeds were exposed to different treatments, and biochemical parameters were measured. Compared with the control group, chilling stress (CS) led to an increase in the concentrations of malondialdehyde (MDA) and H2O2, and decreases in the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), catalase (CAT), peroxidase (POD), and nitric oxide synthase (NOS), and the concentrations of nitric oxide (NO) and protein. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), sodium tungstate (ST), and NG-nitro-L-arginine methyl ester (L-NAME) followed by CS resulted in further increases in the concentrations of MDA and H2O2 and further decreases in the other parameters. However, treatment with PTIO, ST, and L-NAME followed by laser irradiation had the opposite effects on these parameters. When the seeds were treated with PTIO, ST, and L-NAME followed by laser and CS, the concentrations of MDA and H2O2 were significantly lower and the other parameters were higher than in the PTIO, ST, and L-NAME plus CS groups. These results suggest that CO2 laser irradiation enhances the chilling tolerance of wheat seedlings by stimulating endogenous NO synthesis.

scholarly journals Physiological and transcriptome changes induced by exogenous putrescine in anthurium under chilling stress

2020 ◽  
Vol 61 (1) ◽  
Author(s):  
Xiangli Sun ◽  
Zebin Yuan ◽  
Bo Wang ◽  
Liping Zheng ◽  
Jianzhong Tan ◽  
...  
Keyword(s):  
Antioxidant Activities ◽  
Chilling Stress ◽  
Chilling Tolerance ◽  
Membrane Lipid ◽  
Control Group ◽  
Qrt Pcr ◽  
Differential Gene ◽  
Anthurium Andraeanum ◽  
Chilling Response

Abstract Background Chilling stress is the major factor limiting plant productivity and quality in most regions of the world. In the present study, we aimed to evaluate the effects of putrescine (Put) and polyamine inhibitor d-arginine (d-arg) on the chilling tolerance of anthurium (Anthurium andraeanum). Results Anthurium seedlings were pretreated with five different concentrations of Put solution or d-arg solution. Subsequently, the seedlings were subjected to chilling stress at 6 °C for 3 days, followed by a recovery at 25 °C for 1 day. Relative permeability of the plasma membrane, as well as physiological and morphologic parameters was assessed during the experiments. Additionally, transcriptome sequencing and patterns of differential gene expression related to chilling response were analyzed by qRT-PCR in 1.0 mM Put-treated and untreated anthurium seedlings. Results indicated that the supplementation of exogenous Put decreased the extent of membrane lipid peroxidation and the accumulation of malondialdehyde (MDA), promoted the antioxidant activities and proline content and maintained the morphologic performances compared with the control group. This finding indicated that the application of exogenous Put could effectively decrease the injury and maintain the quality of anthurium under chilling conditions. In contrast, the treatment of d-arg exhibited the opposite effects, which confirmed the effects of Put. Conclusions This research provided a possible approach to enhance the chilling tolerance of anthurium and reduce the energy consumption used in anthurium production.

Selective iNOS Inhibition Attenuates Acetylcholine- and Bradykinin-induced Vasoconstriction in Lipopolysaccharide-exposed Rat Lungs 

1999 ◽  
Vol 91 (6) ◽  
pp. 1724-1724 ◽  
Author(s):  
Lars G. Fischer ◽  
Damian J. Horstman ◽  
Klaus Hahnenkamp ◽  
Nancy E. Kechner ◽  
George F. Rich
Keyword(s):  
Nitric Oxide ◽  
Exhaled Nitric Oxide ◽  
Control Group ◽  
Biochemical Engineering ◽  
Inos Inhibitor ◽  
Nos Inhibitor ◽  
Inos Inhibitors ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Dose Dependent

Background Nonselective nitric oxide synthase (NOS) inhibition has detrimental effects in sepsis because of inhibition of the physiologically important endothelial NOS (eNOS). The authors hypothesized that selective inducible NOS (iNOS) inhibition would maintain eNOS vasodilation but prevent acetylcholine- and bradykinin-mediated vasoconstriction caused by lipopolysaccharide-induced endothelial dysfunction. Methods Rats were administered intraperitoneal lipopolysaccharide (15 mg/kg) with and without the selective iNOS inhibitors L-N6-(1-iminoethyl)-lysine (L-NIL, 3 mg/kg), dexamethasone (1 mg/kg), or the nonselective NOS inhibitor Nomega-nitro-L-arginine methylester (L-NAME, 5 mg/kg). Six hours later, the lungs were isolated and pulmonary vasoreactivity was assessed with hypoxic vasoconstrictions (3% O2), acetylcholine (1 microg), Biochemical Engineering, and bradykinin (3 microg). In additional lipopolysaccharide experiments, L-NIL (10 microM) or 4-Diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, 100 microM), a selective muscarinic M3 antagonist, was added into the perfusate. Results Exhaled nitric oxide was higher in the lipopolysaccharide group (37.7+/-17.8 ppb) compared with the control group (0.4+/-0.7 ppb). L-NIL and dexamethasone decreased exhaled nitric oxide in lipopolysaccharide rats by 83 and 79%, respectively, whereas L-NAME had no effect. In control lungs, L-NAME significantly decreased acetylcholine- and bradykinin-induced vasodilation by 75% and increased hypoxic vasoconstrictions, whereas L-NIL and dexamethasone had no effect. In lipopolysaccharide lungs, acetylcholine and bradykinin both transiently increased the pulmonary artery pressure by 8.4+/-2.0 mmHg and 35.3+/-11.7 mmHg, respectively, immediately after vasodilation. L-NIL and dexamethasone both attenuated this vasoconstriction by 70%, whereas L-NAME did not. The acetylcholine vasoconstriction was dose-dependent (0.01-1.0 microg), unaffected by L-NIL added to the perfusate, and abolished by 4-DAMP. Conclusions In isolated perfused lungs, acetylcholine and bradykinin caused vasoconstriction in lipopolysaccharide-treated rats. This vasoconstriction was attenuated by administration of the iNOS inhibitor L-NIL but not with L-NAME. Furthermore, L-NIL administered with lipopolysaccharide preserved endothelium nitric oxide-dependent vasodilation, whereas L-NAME did not.

scholarly journals Preventive Effect of Lactobacillus Plantarum CQPC10 on Activated Carbon Induced Constipation in Institute of Cancer Research (ICR) Mice

2018 ◽  
Vol 8 (9) ◽  
pp. 1498 ◽  
Author(s):  
Jing Zhang ◽  
Xianrong Zhou ◽  
Benshou Chen ◽  
Xingyao Long ◽  
Jianfei Mu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Activated Carbon ◽  
Nitric Oxide Synthase ◽  
Lactobacillus Plantarum ◽  
Quantitative Polymerase Chain Reaction ◽  
Inhibitory Effect ◽  
Lactobacillus Bulgaricus ◽  
Control Group ◽  
Expression Levels ◽  
Oxide Synthase

Chinese Paocai is a traditional fermented food containing an abundance of beneficial microorganisms. In this study, the microorganisms in Szechwan Paocai were isolated and identified, and a strain of lactic acid bacteria (Lactobacillus plantarum CQPC10, LP-CQPC10) was found to exert an inhibitory effect on constipation. Microorganisms were isolated and identified via 16S rDNA. Activated carbon was used to induce constipation in a mouse model and the inhibitory effect of LP-CQPC10 on this induced constipation was investigated via both pathological sections and qPCR (quantitative polymerase chain reaction). A strain of Lactobacillus plantarum was identified and named LP-CQPC10. The obtained results showed that, as compared to the control group, LP-CQPC10 significantly inhibited the amount, weight, and water content of faeces. The defecation time of the first tarry stool was significantly shorter in LP-CQPC10 groups than in the control group. The activated carbon progradation rate was significantly higher when compared to the control group and the effectiveness was improved. LP-CQPC10 increased the serum levels of MTL (motilin), Gas (gastrin), ET (endothelin), AchE (acetylcholinesterase), SP (substance P), and VIP (vasoactive intestinal peptide), while decreasing the SS (somatostatin) level. Furthermore, it improved the GSH (glutathione) level and decreased the MPO (myeloperoxidase), MDA (malondialdehyde), and NO (nitric oxide) levels. The results of qPCR indicated that LP-CQPC10 significantly up-regulated the mRNA expression levels of c-Kit, SCF (stem cell factor), GDNF (glial cell-derived neurotrophic factor), eNOS (endothelial nitric oxide synthase), nNOS (neuronal nitric oxide synthase), and AQP3 (aquaporin-3), while down-regulating the expression levels of TRPV1 (transient receptor potential cation channel subfamily V member 1), iNOS (inducible nitric oxide synthase), and AQP9 (aquaporin-9). LP-CQPC10 showed a good inhibitory effect on experimentally induced constipation, and the obtained effectiveness is superior to that of Lactobacillus bulgaricus, indicating the better probiotic potential of this strain.

Effects of chronic inhibition of inducible nitric oxide synthase in hyperthyroid rats

2005 ◽  
Vol 288 (6) ◽  
pp. E1252-E1257 ◽  
Author(s):  
Isabel Rodríguez-Gómez ◽  
Rosemary Wangensteen ◽  
Juan Manuel Moreno ◽  
Virginia Chamorro ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Control Group ◽  
Hemodynamic Variable ◽  
Male Wistar Rats ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Inducible Nitric Oxide

We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphological and renal variables in hyperthyroid rats were analyzed. The following four groups ( n = 8 each) of male Wistar rats were used: control group and groups treated with AG (50 mg·kg−1·day−1, via drinking water), thyroxine (T4, 50 μg·rat−1·day−1), or AG + T4. All treatments were maintained for 3 wk. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats and morphological, plasma, and renal variables. T4 administration produced a small BP (125 ± 2, P < 0.05) increase vs. control (115 ± 2) rats. AG administration to normal rats did not modify BP (109 ± 3) or any other hemodynamic variable. However, coadministration of T4 and AG produced a marked increase in BP (140 ± 3, P < 0.01 vs. T4). Pulse pressure and HR were increased in both T4- and T4 + AG -treated groups without differences between them. Plasma NOx (μmol/l) were increased in the T4 group (10.02 ± 0.15, P < 0.05 vs. controls 6.1 ± 0.10), and AG reduced this variable in T4-treated rats (6.81 ± 0.14, P < 0.05 vs. T4) but not in normal rats (5.78 ± 0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T4.

Distribution of CD14+ macrophages, CD4+, CD8+ lymphocytes and mRNA expression of inducible nitric oxide synthase in the endometrium of repeat breeding cows

2013 ◽  
Vol 16 (3) ◽  
pp. 443-451 ◽  
Author(s):  
W. Barański ◽  
J. Kaleczyc ◽  
S. Zduńczyk ◽  
W. Podlasz ◽  
E. Długołęcka-Malinowska ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
Polymorphonuclear Neutrophils ◽  
Control Group ◽  
Inos Mrna ◽  
Oxide Synthase ◽  
Subclinical Endometritis ◽  
Inducible Nitric Oxide

Abstract The expression of CD14+ macrophages, CD4+, CD8+ lymphocytes and mRNA of inducible nitric oxide synthase (iNOS) was investigated in the endometrium of repeat breeders with subclinical endometritis [experimental group (EXP), n = 10] and healthy [control group (CTRL), n = 10] cows. The cows were selected on the basis of repeat breeding (3 unsuccessful inseminations), clinical and cytological examinations (> 10% polymorphonuclear neutrophils in uterine smears obtained by cytobrush). From all the cows endometrial biopsies were collected and the presence of CD14+, CD4+ and CD8+ cells in the endometrium was evaluated immunohistochemically using semi quantitative counting method. The mRNA expression of iNOS was determined using reverse transcription-PCR. In general, there were no significant differences between EXP and CTRL groups in the expression of CD4+ and CD8 + lymphocytes in all endometrial structures. In contrast, we observed a higher number of CD14+ macrophages in repeat breeding group compared to the control cows, however, this difference was slightly pronounced. CD14+ cells were detectable only in the stratum compactum and stratum spongiosum. The statistically significant (p ≤ 0.05) higher expression of iNOS mRNA was measured in the cows with subclinical endometritis compared to the healthy animals. Our results suggest that the increased expression of CD14+ macrophages and iNOS mRNA may be associated with embryonal mortality in repeat breeding cows with subclinical endometritis.

scholarly journals Protective Effects of Millettia Pulchra Flavonoids on Myocardial Ischemia In Vitro and In Vivo

2015 ◽  
Vol 35 (2) ◽  
pp. 516-528 ◽  
Author(s):  
Jianchun Huang ◽  
Xudong Zhang ◽  
Feizhang Qin ◽  
Yingxin Li ◽  
Xiaoqun Duan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Myocardial Ischemia ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Protective Effects ◽  
Bax Protein ◽  
Oxide Synthase

Background: Previous studies have demonstrated that Millettia pulchra flavonoids (MPF) exhibit protective effects on myocardial ischemia reperfusion injury (MI/RI) in isolated rat hearts and show anti-oxidative, anti-hypoxic and anti-stress properties. Methods: In this study, the cardioprotective effects of MPF on myocardial ischemia and its underlying mechanisms were investigated by a hypoxia/ reoxygenation (H/R) injury model in vitro and a rat MI/RI model in vivo. Results: We found that the lactate dehydrogenase (LDH) and inducible nitric oxide synthase (iNOS) activities were decreased in the MPF pretreatment group, whereas the activities of constructional nitric oxide synthase (cNOS), total nitric oxide synthase (tNOS), Na+-K+-ATPase and Ca2+-Mg2+-ATPase were significantly increased. In addition, the cardiocytes were denser in the MPF groups than in the control group. The mortality rate and apoptosis rate of cardiocytes were significantly decreased. Furthermore, pretreatment with MPF in vivo significantly improved the hemodynamics, decreased malondialdehyde (MDA) abundance, increased the activities of plasma superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decreased the expression of the Bax protein and ratio Bax/Bc1-2 ration. Conclusions: These results suggest that MPF is an attractive protective substance in myocardial ischemia due to its negative effects on heart rate and ionotropy, reduction of myocardial oxidative damage and modulation of gene expression associated with apoptosis.

scholarly journals Expression of Constitutive Nitric Oxide Synthase Isoforms in Varicose Vein Wall; Preliminary Results

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Zora Haviarová ◽  
Andrea Janegová ◽  
Pavel Janega ◽  
Štefan Durdík ◽  
Peter Kováč ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Varicose Vein ◽  
Structural Changes ◽  
Varicose Veins ◽  
Control Group ◽  
Color Analysis ◽  
Vein Wall ◽  
Oxide Synthase ◽  
Nos Isoforms

There are conflicting findings in literature about the structural changes of the primary varicose veins. NO (a potent vasodilatator) is synthesized by nitric oxide synthase (NOS). From 3 known NOS isoforms the two are constitutional: eNOS (endothelial NOS) and nNOS (neuronal NOS). 10 varicose and 10 control vein samples were processed by standard light microscopy and immuno-histochemica techniques using rabbit polyclonal antibodies against eNOS and nNOS. Antibodies expression was evaluated semiquantitatively and proved morphometrically by 2D-image analysis. total area of NOS isoforms expressions was determined by color analysis and color digital subtraction. The results showed discontinuous and significantly lower expression of both NOS isoforms the in the tunica media of varicose veins compared with the control group. For the statistical analysis the unpaired -test was used. Our results suppose lower NO levels in varicose vein wall, deducing that varicose dilatation is due to other mechanism, and they contradict the results of previously published similar works.

scholarly journals Selective Nitric Oxide Synthase Inhibitor 7-Nitroindazole Protects against Cocaine-Induced Oxidative Stress in Rat Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Vessela Vitcheva ◽  
Rumyana Simeonova ◽  
Magdalena Kondeva-Burdina ◽  
Mitka Mitcheva
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Physical Dependence ◽  
Combination Group ◽  
Control Group ◽  
Mitochondrial Activity ◽  
Antioxidant Enzyme Activities ◽  
Repeated Treatment ◽  
Oxide Synthase

One of the mechanisms involved in the development of addiction, as well as in brain toxicity, is the oxidative stress. The aim of the current study was to investigate the effects of 7-nitroindazole (7-NI), a selective inhibitor of neuronal nitric oxide synthase (nNOS), on cocaine withdrawal and neurotoxicity in male Wistar rats. The animals were divided into four groups: control; group treated with cocaine (15 mg/kg−1, i.p., 7 days); group treated with 7-NI (25 mg/kg−1, i.p., 7 days); and a combination group (7-NI + cocaine). Cocaine repeated treatment resulted in development of physical dependence, judged by withdrawal symptoms (decreased locomotion, increased salivation and breathing rate), accompanied by an increased nNOS activity and oxidative stress. The latter was discerned by an increased formation of malondialdehyde (MDA), depletion of reduced glutathione (GSH) levels, and impairment of the enzymatic antioxidant defense system measured in whole brain. In synaptosomes, isolated from cocaine-treated rats, mitochondrial activity and GSH levels were also decreased. 7-NI administered along with cocaine not only attenuated the withdrawal, due to its nNOS inhibition, but also reversed both the GSH levels and antioxidant enzyme activities near control levels.

Using endothelial nitric oxide synthase gene polymorphisms to identify intracranial aneurysms more prone to rupture in Japanese patients

2006 ◽  
Vol 105 (5) ◽  
pp. 717-722 ◽  
Author(s):  
Boris Krischek ◽  
Hidetoshi Kasuya ◽  
Hiroyuki Akagawa ◽  
Atsushi Tajima ◽  
Akira Narita ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Intracranial Aneurysms ◽  
Tandem Repeats ◽  
Japanese Patients ◽  
Control Group ◽  
Patient Sample ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Object Recent investigators found that the presence of three tandem polymorphisms of the endothelial nitric oxide synthase (eNOS) gene—promoter single nucleotide polymorphism (SNP) T-786C, intron-4 27-bp variable number of tandem repeats, and the G894T SNP in exon 7—was indicative of intracranial aneurysms more prone to rupture in a Caucasian patient sample. In the present study, the authors sought to determine whether the presence of these eNOS polymorphisms could indicate which Japanese patients with aneurysms were more endangered by a subarachnoid hemorrhage (SAH). Methods The three eNOSpolymorphisms were genotyped in 297 patients with ruptured aneurysms (RAs), 108 patients with unruptured aneurysms (UAs), and 176 healthy volunteers by using polymerase chain reaction. The distribution of the variant alleles did not differ significantly (p > 0.05) between the RA group and the UA group. The frequency of the corresponding genotypes between the two groups and a haplotype analysis did not show any significant differences. Further comparisons of the RA and UA groups with the control group did not yield any significant allele or genotype frequency differences. Conclusions These data show that the examined set of eNOS polymorphisms were not indicative of which Japanese patients with intracranial aneurysms would suffer an SAH. The presence of eNOS polymorphisms is not useful in identifying intracranial aneurysms that are more prone to rupture in a Japanese patient sample.

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