Inhibition of nitric oxide generation and lipid peroxidation attenuates hemolysate-induced injury to cerebrovascular endothelium

1997 ◽  
Vol 139 (3) ◽  
pp. 240-248 ◽  
Author(s):  
A. -L. Kwan ◽  
N. J. Solenski ◽  
N. F. Kassell ◽  
K. S. Lee
2014 ◽  
Vol 306 (10) ◽  
pp. H1472-H1480 ◽  
Author(s):  
Natalia Veronez da Cunha ◽  
Phileno Pinge-Filho ◽  
Carolina Panis ◽  
Bruno Rodrigues Silva ◽  
Laena Pernomian ◽  
...  

We investigated the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic cardiovascular parameters, vascular reactivity, and endothelial cells isolated from aorta of monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body wt of MSG or equimolar saline [control (CTR)] to newborn rats. At the 60th day, the treatment was started with NG-nitro-l-arginine methyl ester (l-NAME, 20 mg/kg) or 0.9% saline. At the 90th day, after artery catheterization, mean arterial pressure (MAP) and heart rate were recorded. Plasma was collected to assess lipid peroxidation. Endothelial cells isolated from aorta were evaluated by flow cytometry and fluorescence intensity (FI) emitted by NO-sensitive dye [4,5-diaminofluoresceindiacetate (DAF-2DA)] and by ROS-sensitive dye [dihydroethidium (DHE)]. Vascular reactivity was made by concentration-response curves of acetylcholine. MSG showed hypertension compared with CTR. Treatment with l-NAME increased MAP only in CTR. The MSG induced an increase in the low-frequency (LF) band and a decrease in the high-frequency band of pulse interval. l-NAME treatment increased the LF band of systolic arterial pressure only in CTR without changes in MSG. Lipid peroxidation levels were higher in MSG and were attenuated after l-NAME. In endothelial cells, basal FI to DAF was higher in CTR than in MSG. In both groups, acetylcholine increased FI for DAF from basal. The FI baseline to DHE was higher in MSG than in CTR. Acetylcholine increased FI to DHE in the CTR group, but decreased in MSG animals. We suggest that reduced NO production and increased production of ROS may contribute to hypertension in obese MSG animals.


Author(s):  
A. Ye. Demkovych

Introduction. Activation of lipid peroxidation is one of the trigger mechanisms of periodontium injury, which is primary caused by cellular damage. Reactive oxygen and nitrogen species (RONS) are able to cause damage to a cell as well as final products of lipid peroxidation, including unsaturated aldehydes and other metabolites. Objective. The aim of the research was to determine the role of RONS and accumulation of lipid peroxidation derivatives in initial development and formation of chronical inflammatory process in periodontium. Methods. Experimental periodontitis was modeled in animals by injection of complex mixtures of microorganisms diluted in egg protein into periodontal tissues. The results of biochemical studies of free radical processes activity in blood serum were evaluated by content of diene, triene conjugates, TBA-active products and total quantity of metabolites of nitric oxide (NO2–+NO3–), which were determined on the 7th, 14th and 30th days of the experiment. Results. Generation of active forms of oxygen is more influential, providing longevity of inflammatory process. This pays attention to typical dynamics of changes in active processes of lipid peroxidation in the development and course of experimental periodontitis. The study of inflammatory process with a bacterial-immune component in the rats’ periodontal complex proved accumulation of lipid peroxidation and nitric oxide metabolites in blood serum.Conclusions. The preservation of increased lipid peroxidation and nitric oxide metabolites in blood serum of the experimental animals with acute periodontitis conduce enhance of alteration and delayed healing that result in its sequel into chronical periodontitis.


Author(s):  
Jane-Rose I. Oche ◽  
Titilayo O. Johnson ◽  
Augustina O. Akinsanmi ◽  
Kiri H. Jaryum ◽  
Timothy Francis

Aim: The aim of this study was to investigate and compare the antioxidative properties of the mistletoe plant obtained from three different host species namely Psidium guajava, Vernonia amygdalina and Moringa olifera lam. Study Design: Experimental Design Place and Duration of Study: Department of Pharmaceutical Chemistry, Faculty of Pharmaceutical Sciences and Department of Biochemistry, College of Health Sciences, University of Jos, Nigeria. Methodology: Crude methanolic leaf extracts were studied for their antioxidative properties; Iron reducing and Iron-chelating activities, Nitric oxide (NO) radical and 2,2-diphenyl 1-picrylhydrazyl (DPPH) radical scavenging activities and the lipid peroxidation and thiobarbituric acid reaction (TBAR) methods. One way ANOVA was used for the result analysis with P<.05 for significant difference. Results: Mistletoes from Psidum guajava (MSPG) had significantly higher reducing property (0.16 – 0.20mg/mL); the chelating property of Mistletoes from Moringa olifera (MSMO) was significantly lower (45.7 – 58.9%); DPPH radical scavenging activity had no significant difference; and Nitric oxide scavenging activity was significantly higher in MSPG (72.1% in 75mg/mL) than the extracts from other hosts. MSPG had significantly higher TBAR inhibition using both FeSO4 (77.8% at 125µg/mL) and Sodium nitroprusside (61.6+1.0% at 125µg/mL) with an IC50 of 30.27µg/mL . Extract of Tapinanthus globiferus leaves from Psidium guajava had more antioxidative activities in the TBARs followed by Tapinanthus globiferus leaf extract from Vernonia amygdalina (MSVA). Conclusion: From the study, mistletoes from Psidium guajava had higher antioxidant activity compared to other hosts, which probably justifies its use for treatment of cancer in traditional medicinal practice.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Gregorio Caimi ◽  
Rosalia Lo Presti ◽  
Maria Montana ◽  
Davide Noto ◽  
Baldassare Canino ◽  
...  

Our aim was to evaluate lipid peroxidation, expressed as thiobarbituric acid-reactive substances (TBARS), nitric oxide metabolites (nitrite + nitrate) expressed asNOx, and TBARS/NOxratio in a group of subjects with metabolic syndrome (MS). In this regard we enrolled 106 subjects with MS defined according to the IDF criteria, subsequently subdivided into diabetic (DMS) and nondiabetic (NDMS) and also into subjects with a low triglycerides/HDL-cholesterol (TG/HDL-C) index or with a high TG/HDL-C index. In the entire group and in the four subgroups of MS subjects we found an increase in TBARS andNOxlevels and a decrease in TBARS/NOxratio in comparison with normal controls. Regarding all these parameters no statistical difference between DMS and NDMS was evident, but a significant increase inNOxwas present in subjects with a high TG/HDL-C index in comparison with those with a low index. In MS subjects we also found a negative correlation between TBARS/NOxratio and TG/HDL-C index. Considering the hyperactivity of the inducible NO synthase in MS, these data confirm the altered redox and inflammatory status that characterizes the MS and suggest a link between lipid peroxidation, inflammation, and insulin resistance, evaluated as TG/HDL-C index.


2014 ◽  
Vol 99 (Suppl 2) ◽  
pp. A267.1-A267
Author(s):  
M Smahi ◽  
M Aribi ◽  
L Ysmaildahlok ◽  
L Hamouda ◽  
W Meziane

2020 ◽  
Vol 34 (7) ◽  
Author(s):  
Charles Antwi‐Boasiako ◽  
Gifty Boatemaah Dankwah ◽  
Robert Aryee ◽  
Charles Hayfron‐Benjamin ◽  
George Aboagye ◽  
...  

2000 ◽  
Vol 279 (6) ◽  
pp. R1949-R1955 ◽  
Author(s):  
K. A. Nath ◽  
V. Shah ◽  
J. J. Haggard ◽  
A. J. Croatt ◽  
L. A. Smith ◽  
...  

We investigated a transgenic mouse model of sickle cell disease, homozygous for deletion of mouse β-globin and containing transgenes for human βSand βS-antillesglobins linked to the transgene for human α-globin. In these mice, basal cGMP production in aortic rings is increased, whereas relaxation to an endothelium-dependent vasodilator, A-23187, is impaired. In contrast, aortic expression of endothelial nitric oxide synthase (NOS) is unaltered in sickle mice, whereas expression of inducible NOS is not detected in either group; plasma nitrate/nitrite concentrations and NOS activity are similar in both groups. Increased cGMP may reflect the stimulatory effect of peroxides (an activator of guanylate cyclase), because lipid peroxidation is increased in aortae and in plasma in sickle mice. Despite increased vascular cGMP levels in sickle mice, conscious systolic blood pressure is comparable to that of aged-matched controls; sickle mice, however, evince a greater rise in systolic blood pressure in response to nitro-l-arginine methyl ester, an inhibitor of NOS. Systemic concentrations of the vasoconstrictive oxidative product 8-isoprostane are increased in sickle mice. We conclude that vascular responses are altered in this transgenic sickle mouse and are accompanied by increased lipid peroxidation and production of cGMP; we suggest that oxidant-inducible vasoconstrictor systems such as isoprostanes may oppose nitric oxide-dependent and nitric oxide-independent mechanisms of vasodilatation in this transgenic sickle mouse. Destabilization of the vasoactive balance in the sickle vasculature by clinically relevant states may predispose to vasoocclusive disease.


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