scholarly journals NITRIC OXIDE METABOLISM FEATURES UNDER CONDITIONS OF EXPERIMENTAL INFECTED RADIATION-INDUCED SKIN INJURIES DEVELOPMENT AND THEIR TREATMENT WITH PHOTODYNAMIC THERAPY

2020 ◽  
Vol 73 (8) ◽  
pp. 1655-1658
Author(s):  
Mykola V. Krasnoselskyi ◽  
Elena S. Pushkar ◽  
Larisa I. Simonova-Pushkar ◽  
Mykhailo S. Myroshnychenko

The aim: To follow-up nitric oxide content values in rat serum at the development of Staphylococcus aureus infected radiation skin injuries and their photodynamic therapy. Materials and methods: Eighty WAG male rats were studied in an experiment. Four groups were identified for evaluation. Group 1 included unaffected intact rats (n=20). Group 2 involved rats (n=20) with a modeled radiation-induced ulcer of the skin. The rats (n=20) with a modeled radiation-induced skin ulcer followed by infecting with Staphylococcus aureus were referred to group 3. Group 4 included rats (n=20) with Staphylococcus aureus infected radiation skin ulcer exposed to photodynamic therapy. Rats of groups 1-4 were sampled for biochemical blood examination on days 7, 14, 21, 30 and 45. Total nitric oxide metabolites (nitrites and nitrates) were measured according to V.A. Metelskaya et al. method. Results: Infectious agent (Staphylococcus aureus) present in skin ulcer impairs nitric oxide metabolism in rat blood serum that manifested in decreased total nitric oxide metabolites content on day 7, followed by its increase within days 14 to 45. While photodynamic therapy exposed on the Staphylococcus aureus infected radiation skin ulcer, total nitric oxide metabolites in blood serum had increased by day 7, but days 14 to 45 level was compliant with physiological norm. Conclusions: Infecting radiation skin ulcers with Staphylococcus aureus causes impaired nitric oxide metabolism, while photodynamic therapy helps to normalize the metabolism of the above-mentioned chemical compound that can improve healing of radiation skin ulcers.

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.


2014 ◽  
Vol 115 (11) ◽  
pp. 712-717 ◽  
Author(s):  
I. D. Uspenskaya ◽  
M. V. Erzutova ◽  
L. V. Korkotashvili ◽  
S. A. Kolesov ◽  
N. Y. Shirokova

Author(s):  
I. Ya. Krynytska

<p>Background. System of nitric oxide (NO), which consists of NO, and its metabolites, is very important for<br />various biological processes. NO is signalling molecules and mediators of intracellular and intercellular interaction<br />that causes relaxation of smooth muscles of blood vessel walls, inhibits platelet aggregation and their adherence,<br />is involved in the transmission of nerve impulses, cell proliferation.<br />Objective. The aim of our research was to study the content of nitric oxide metabolites in blood serum and<br />bronchoalveolar lavage, to substantiate their role in pathogenesis of hepatopulmonary syndrome in<br />experiment.<br />Methods. The experiments were performed on 56 outbread male rats, 180-220 g in weight. The first experimental<br />model of hepatopulmonary syndrome (HPS) was made by imposition of double ligature on common<br />bile duct and its further dissection with a scalpel. The second experimental HPS model was made by 8-week intragastric<br />administration of oil solution CCl4 (400 g per 1 L), 0.5 ml per 100 g of body weight on the first day of<br />the experiment, 0.3 ml per 100 g on the third day of the experiment and then every third day until the end of the<br />experiment 0.3 ml per 100 g. A mixture of corn flour, lard and cholesterol and alcohol solution was added to the<br />standard diet of the rats.<br />Results. The total content of nitric oxide metabolites in blood serum of the rats of the experimental group<br />No.1 (on the 31st day after the common bile duct ligation) was significantly increased in 3.9 times (p1&lt;0,001) if<br />compared with the control group №1. In the rats of the 2nd experimental group (with carbon tetrachloride induced<br />cirrhosis) the total content of nitric oxide metabolites in blood serum also significantly increased in 3.1 times<br />(p1&lt;0,001). Comparison of nitric oxide metabolites content in blood serum and bronchoalveolar lavage, which<br />directly indicated about the processes in lung tissue, was great importance.<br />Conclusions. So, in rats with experimental hepatopulmonary syndrome activation of nitroxydergic process<br />by significant increase in nitric oxide metabolites in blood serum and bronchoalveolar lavage took place.<br />KEYWORDS: hepatopulmonary syndrome, nitric oxide metabolites.</p>


2016 ◽  
Vol 97 (4) ◽  
pp. 540-544
Author(s):  
N V Galeeva ◽  
V Kh Fazylov ◽  
I Kh Valeeva

Aim. To study dynamics and interrelation between final nitric oxide metabolites (nitrites) and endogenous intoxication index (medium mass molecules) in patients with chronic hepatitis C with the effect of antiviral therapy on them.Methods. The study included 99 patients with chronic hepatitis C. The combination therapy for 48 weeks in patients with genotype 1 chronic hepatitis C with pegylated interferon (peginterferon alfa-2a and alfa-2b) in combination with ribavirin and for 24 weeks with daily standard interferon alfa-2b administration in patients with virus genotypes 2 and 3 was conducted. The nitric oxide level was estimated by the content of the nearest metabolite (nitrite) in blood serum using the P.P. Golikov method. Medium mass molecules in the blood serum were determined by the N.I. Gabrielyan method.Results.In patients with chronic hepatitis C high values of nitrogen oxide metabolites and the medium mass molecules in the blood serum were revealed, whereas the level of nitroxidemia and endogenous intoxication by the values of medium mass molecules was associated with the viral replicative capacity value and alanine aminotransferase serum levels. Amid the combination antiviral therapy the nature of nitroxidergy changed with the normalization of nitrogen oxide indicators by 24 weeks and an increase to 48 weeks of treatment. There were significantly positive correlative relations between pronouncement of levels of nitric oxide metabolites and the medium mass molecules before the start of antiviral therapy (R=0.292629, pConclusion. Chronic hepatitis C promotes increase in nitrite ion content and medium mass molecules in the blood serum, their level is associated with virus replication activity and cytolysis severity; antiviral therapy has an effect on the level of endogenous intoxication with the normalization of content of the nitrite ions and medium mass molecules in blood serum by 24th week of treatment.


1997 ◽  
Vol 17 (12) ◽  
pp. 1337-1345 ◽  
Author(s):  
Koji Osuka ◽  
Yoshio Suzuki ◽  
Yasuo Watanabe ◽  
Aclan Dogan ◽  
Masakazu Takayasu ◽  
...  

The effect of interleukin-1β (IL-1β) on a cerebral artery was investigated in anesthetized dogs. Intracisternal administration of IL-1β (0.03 and 0.3 μg) dilated the canine basilar artery in a dose-dependent manner, without affecting systemic blood pressure or heart rate. The increase in diameter induced by 0.3 μg of IL-1β was 28.4% ± 13.4% of control at 2 hours and was inhibited by 30 μg of the IL-1β receptor antagonist, zinc protoporphyrin (4.5% ± 13.5%, P < 0.05). Interleukin-1β did not affect the concentration of nitric oxide metabolites in CSF. However, there was an increase in the concentration of eicosanoids in CSF, and the elevation of 6-keto-PGF1α paralleled the vasodilation. Pretreatment with 30 μg of the selective inducible cyclooxygenase (COX-2) inhibitor NS-398 also inhibited the IL-1β-induced vasodilation significantly (5.9% ± 9.4% at 2 hours, P < 0.01). Western blot analysis revealed the expression of a 68-kD COX-2-like protein in basilar artery extracts. These findings suggest that the IL-1β-induced vasodilator effect is linked to the prostaglandin cascade, predominantly to prostaglandin I2, by induction of COX-2, but not to the stimulation of nitric oxide metabolism.


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