Tag Archives: H(2)S
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-.
Effect of hydrogen sulfide-releasing aspirin on esophageal and gastric mucosa compromised by stress injury
O. S. Zayachkivska1, N. S. Bula1, Ya. I. Pavlovskiy1, I. O. Pshyk-Titko1,
E. M. Gavriluk1, O. I. Grushka1, J. L. Wallace2,3
1Danylo Halytsky Lviv National Medical University, Ukraine;
2University of Calgary, Canada;
3University of Toronto, Canada;
e-mail: ozayachkivska@gmail.com
Recent data of study H2S in gastrointestinal tract has proven its potent cytoprotection on mucosal defense among acid-related diseases in the gut. The aim was to evaluate the effects of H2S-releasing aspirin derivative (ATB-340) on esophageal and gastric mucosa compromised by stress injury. Rats were treated with vehicle (control), aspirin (10 mg/kg), ATB-340 (17.5 mg/kg) single or 9 days duration, with or without induction of stress injury. Esophageal mucosa, gastric mucosa were estimated by histopathological damage scoring. Serological levels of VCAM-1, IL-6 by ELISA. ATB-340 treatment resulted in protective effect and lower grade of damage score in esophageal mucosa and gastric mucosa lesions vs effect of aspirin in single or 9 days applications. The serum levels of VCAM, IL-6 in rats who were aspirin-treated and subjected to stress-injury were higher than those in control animals. Treatment with ATB-340 produced an anti-inflammatory effect by decreasing VCAM and IL-6 vs aspirin. Cytoprotective effect of ATB-340 on esophageal mucosa and gastric mucosa was modulated by inhibiting inflammation and improving endothelial functions.