Tag Archives: NO-synthase
Chromium picolinate prevents the development of oxidative-nitrosative stress and restores endogenous H(2)S production in the rat brain under rotenone-induced toxicity
A. O. Mykytenko1*, I. S. Hrytsenko2, A. Y. Semenchuk2, M. V. Voroniuk2,
V. V. Kovpak2, O. Y. Akimov3, K. S. Neporada1
1Department of Bioorganic and Biological Chemistry,
Poltava State Medical University, Poltava, Ukraine;
2Medical Faculty №1, Poltava State Medical University, Poltava, Ukraine;
3Department of Pathophysiology, Poltava state medical university, Poltava, Ukraine;
*e-mail: mykytenkoandrej18@gmail.com
Received: 19 December 2024; Revised: 03 March 2025;
Accepted: 25 April 2025; Available on-line: 12 May 2025
Energy deficit, mitochondrial dysfunction and oxidative stress induced by rotenone may play a decisive role in the pathogenesis of neurodegenerative disorders. Chromium picolinate has shown neuroprotective activity and efficacy in the treatment of Alzheimer’s disease The effect of chromium picolinate on the brain under the conditions of rotenone influence has not been studied, and such data could shed light on the pathogenesis of neurodegenerative diseases. The aim of the study was to determine the effect of chromium picolinate on the indices of oxidative-nitrosative stress and the content of sulfide anion and sulfites in the brain homogenate under rotenone administration to rats. Experiments were performed on 24 white, sexually mature male Wistar rats. The animals were divided into 4 groups: control group; chromium picolinate group; rotenone group; group of combined exposure to chromium picolinate and rotenone. Chromium picolinate was administered orally at a dose of 80 μg/kg per day for 21 days. Rotenon was injected subcutaneously at a dose of 1.5 mg/kg every other day. The introduction of rotenone into the body of rats was accompanied by the development of oxidative-nitrosative stress mainly due to the increased activity of NO-synthase inducible isoform, and by the decrease in the content of H2S and SO32- in brain tissue. Oral administration of chromium picolinate against the background of rotenone administration prevents the development of oxidative-nitrosative stress in brain tissue by reducing the production of reactive oxygen and nitrogen forms, promotes the restoration of arginase activity and increases the content of H2S and SO32-.
The indices of nitrogen (II) oxide system in experimental hepatopulmonary syndrome
I. Ya. Krynytska, M. I. Marushchak
I. Horbachevsky Ternopil State Medical University, Ternopil, Ukraine;
e-mail: marushchak@tdmu.edu.ua
Hepatopulmonary syndrome (HPS) is a pulmonary complication of liver disease characterized by arterial hypoxemia. Altered nitrogen (II) oxide (NO) production has also been implicated in the pathogenesis of the HPS. The present study was designed to evaluate the indices of NO system in the blood serum and lung tissue of animals with different models of hepatopulmonary syndrome. The total NOS activity was performed by monitoring the rate of conversion of L-arginine into citrulline. The total contents of NO metabolites was assessed by evaluation of their amount, which included nitrite ions that were previously presented in the sample (NO2–) and also nitrate ions reducted to nitrites (NO3–). We found a significant increase in total NOS activity in the lung tissue of Rats of both experimental groups as compared to control animals, but it was greater in the rats on the 28th day after the common bile duct ligation. The total concentration of NO2– + NO3– in the lung tissue of the rats in the experimental group N 1 also significantly increased (5.8 times) and in the rats of the experimental group with carbon – 4.5 times (P < 0.001) vs the control group. Thus, in rats with different models of hepatopulmonary syndrome the activation of nitroxydergic process by a significant increase in nitrogen (II) oxide metabolites contents and total NO synthases activity has been established. Herewith a more pronounced intensification of nitroxydergic processes was observed in rats on the 28th day after the common bile duct ligation.
The effect of agmatine on L-arginine metabolism in erythrocytes under streptozotocin-induced diabetes in rats
I. V. Ferents, I. V. Brodyak, M. Ya. Lyuta,
V. A. Burda, A. M. Fedorovych, N. O. Sybirna
Ivan Franko National University of Lviv, Ukraine;
e-mail: sybirna_natalia@yahoo.com
The effects of agmatine on oxidative and non-oxidative metabolic pathways of L-arginine were investigated both in plasma and erythrocytes under experimental diabetes mellitus. It was indicated, that agmatine prevents the development of oxidative-nitrosative stress in diabetic rats. After treatment of animals by agmatine NO-synthase methabolic pathway of L-arginine is depressed whereas arginase one increases in erythrocytes of rats with experimental diabetes mellitus.
Peculiarities of arginase and NO-synthase pathways of L-arginine metabolism in peripheral blood lymphocytes of patients with ovarian cancer
O. I. Yakubets, R. V. Fafula, D. Z. Vorobets, Z. D. Vorobets
Danylo Halytski Lviv National Medical University, Ukraine;
е-mail: vorobets@meduniv.lviv.ua
The peculiarities of arginase and NO-synthase pathways of L-arginine metabolism in peripheral blood lymphocytes of patients with ovarian cancer were studied. It was shown that the development of cancer pathology is associated with an imbalance in the NO synthesis in blood lymphocytes. The reason for such imbalance is the activation of arginase and inducible isoform of NO-synthase (iNOS) and significant inhibition of its constitutive isoform. The analysis of the kinetic properties of NOS of blood lymphocytes of patients with ovarian cancer was carried out. It was shown that the affinity constant of iNOS affinity for L-arginine is 5.4-fold lower than for eNOS of blood lymphocytes of persons in the control group. The inhibition of eNOS occurs via non-competitive type and is related to the reduction of maximum reaction rate.
Effect of anticonvulsants on the nitric oxide system
L. A. Gromov1, I. F. Belenichev2, L. G. Gonchar-Cherdakli1, G. A. Zhernovaja2
1SI Іnstitute of Pharmacology and Toxicology, National Academy of Medical Sciences of Ukraine, Kyiv;
2Zaporizhia State Medical University, Ukraine;
e-mail: llrr@ukr.net
The effect of phenobarbital, carbamazepine, valproate sodium, depakine, topiramate and lamotrigine on the content of NO and NO-synthase activity in white rat brain tissues has been studied. It was established that the action of carbamazepine, valproate sodium, topiramate and lamotrigine decreases the activity of NO-synthase and the level of NO in the brain tissues. The amount of NO does not change while NO-synthase activity increases with the introduction of phenobarbital. The involvement of nitric oxide in the mechanism of action of the studied anticonvulsant drugs is discussed.