Tag Archives: oxidative-nitrosative stress
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-.
Influence of NF-κB on the development of oxidative-nitrosative stress in the liver of rats under conditions of chronic alcohol intoxication
A. O. Mykytenko1*, O. Ye. Akimov2, G. A. Yeroshenko3, K. S. Neporada1
1Department of Bioorganic and Biological Chemistry,
Poltava State Medical University, Poltava, Ukraine;
2Department of Pathophysiology, Poltava State Medical University, Poltava, Ukraine;
3Department of Medical Biology, Poltava State Medical University, Poltava, Ukraine;
*e-mail: mykytenkoandrej18@gmail.com
Received: 05 October 2022; Revised: 15 December 2022;
Accepted: 17 February 2023; Available on-line: 27 February 2023
Alcohol-related liver disease is the most common cause of liver disease worldwide. The purpose of this work is the establishment of the influence of the transcription factor κB on the development of oxidative-nitrosative stress in the liver of rats under conditions of chronic alcohol intoxication. The experiments were performed on 24 male Wistar rats weighing 180-220 g. The animals were divided into 4 groups of 6 animals: control; animals, which were administered NF-κB inhibitor, namely ammonium pyrrolidinedithiocarbamate (PDTC) at a dose of 76 mg/kg 3 times a week; animals, on which we simulated alcoholic hepatitis and group of combination of alcoholic hepatitis and NF-κB inhibitor. We determined in rat liver homogenate the following biochemical parameters: the activity of NO synthase isoforms, superoxide dismutase and catalase activity, the concentration of malonic dialdehyde, the concentration of peroxynitrite, nitrites and nitrosothiols, concentration of sulfide anion and superoxide anion radical production. Chronic alcohol intoxication led to increased production of reactive oxygen and nitrogen species on the background of decreased antioxidant activity, thus intensifying lipid peroxidation in the liver. Blockade of the transcription factor κB during chronic alcohol intoxication despite an increase in antioxidant activity and decrease of reactive oxygen and nitrogen species production did not ameliorate oxidative damage to the liver. Blockade of activation of nuclear transcription factor κB in rat liver by PDTC reduced the risk of oxidative damage to hepatocytes, but did not reduce the risk of developing nitrosative damage to hepatocytes.