scholarly journals Evaluation of NOS2 Polymorphism in Gastric Adenocarcinoma Patients in Mazandaran Province

2021 ◽  
Author(s):  
Mahshad Hooshyar ◽  
Saeed Abedian-Kenari ◽  
Abbas Mohammadpour ◽  
Habibeh Mirmajidi ◽  
Majid Jafari-Sabet ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Cancer ◽  
Control Group ◽  
Polymorphism Analysis ◽  
Mazandaran Province ◽  
Risk Area ◽  
Chi Square ◽  
High Risk Area ◽  
North Of Iran ◽  
Oxide Synthase

Introduction: Gastric cancer is the fourth most common cancer and the second leading cause of cancer death worldwide. North of Iran is a high-risk area for gastric cancer. Nitric oxide (NO), mainly synthesized by inducible nitric oxide synthase (NOS2) in pathological conditions, plays an important role in cytotoxicity, inflammation and fibrosis. In this research we studied the effect of (rs1137933) T>C genotype on gastric cancer. Methods: This analysis was performed on 93 patients with gastric cancer who were referred to endoscopy Tuba Clinic in 2015 and 93 healthy individuals as controls. DNA extracted from peripheral blood samples was applied in PCR-RFLP (Polymerase chain reaction- restriction fragment length polymorphism) analysis to determine (rs1137933) T>C genotype. The association of the (rs1137933) T>C genotype and gastric cancer risk were analyzed by MedCalc software and (X2) Chi-square and (OR) Odds Ratio exams. Results: Frequency of TT, CT, and CC genotypes in cases was 12.61, 51.35 and 36% and 38.7, 34.4, and 26.8% in the control group. Significant association was found between (rs1137933) T>C genotype with gastric cancer chance, P<0.05, OR=2/04, 95% CI (1/37 to 3/03). Conclusion: The results of the study show that the presence of CC+CT genotypes may increase the risk of gastric cancer.  P < 0.0001, OR=4.37 (2.17 to 8.80).Therefore, investigating the (rs1137933) T>C single nucleotide polymorphism of NOS2 gene could be an appropriate molecular marker that could be used to determine individual sensitivity to gastric cancer and for designing cancer prevention programs.

scholarly journals T-786c Polymorphism in nitric oxide synthase 3 gene and Nitrit Oxide Level of Diabetic Retinopathy in Javanese Population

2015 ◽  
Vol 16 (2) ◽  
pp. 126 ◽  
Author(s):  
Putri Widelia Welkriana ◽  
S. Sunarti ◽  
Pramudji Hastuti
Keyword(s):  
Nitric Oxide ◽  
Diabetic Retinopathy ◽  
Nitric Oxide Synthase ◽  
Control Group ◽  
Case Group ◽  
Chi Square ◽  
Chi Square Test ◽  
Nitric Oxide Synthase 3 ◽  
Oxide Synthase

Complication of retinopathy in type 2 DM is caused of lower level of NO. Nitric oxide level is synthesizedfrom L-arginin in reaction that catalyze Nitric oxide synthase (NOS) 3. The T-786C mutation in NOS 3 genedecreases the expression of nitric oxide synthase (NOS) 3 so decreases NO synthesis. To investigate theassociation between T-786C polymorphism in NOS 3 gene with NO level of diabetic retinopathy patients. Thisstudy was a case control study, consist of 40 patient of type 2 diabetic with DR (case group) and 40 patient oftype 2 diabetic without DR (control group) of Javanese ethnic. The genotyping of T-786C polymorphism wasperformed by PCR-RLFP. Level of NO was measured by spectrophotometry. Chi square test and odd ratiowere used to analyze the association of the T-786C polymorphism in NOS 3 gene with DR. Differences ofNO level between TT and TC genotypes were analyzed using independent t test. The distribution of T-786Cpolymorphism in NOS 3 gene of DR subjects showed that frequency of TT genotype was 22.5% and TC genotypewas 77.5%. Non DR subjects showed the frequency of TT genotype was 50% and TC genotype was 50%, (p=0.011). Frequency of T allele in DR group was 61.25% and C allele was 38.75%, and frequency of T allele in nonDR group was 75% and C allele was 25%, (p= 0.62). Odd ratio of TC genotype was 3.444(CI; 95% : 0.964-3.735)and C allele was 1.898 (CI; 95% : 1.310-9.058). The NO level of TC genotype was 1.43+0.126 and TT genotypewas 11.27+5.87 (p=0.000). Level of NO between RD and non RD showed not different significantly (p=0.160)for retinopathy. The T-786C polymorphism of NOS 3 gene is risk factor for retinopathy in type 2 DiabetesMellitus. Individual with TC genotype of NOS 3 gene has lower level of NO than TT genotype.

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.

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.

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