Tag Archives: rat brain
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-.
Ser-Thr phosphatases in the rat brain that dephosphorylate phospho-Ser(1291)-GluN2A subunit of glutamate receptor
R. R. Prabhu1,2
1P. G. Department of Biotechnology, Government Arts College, Thycaud P. O, Trivandrum, India;
2Rajiv Gandhi Centre for Biotechnology, Poojappura, Thycaud P. O, Trivandrum, India;
e-mail: ramyarprabhu@gmail.com
Received: 04 June 2023; Revised: 06 July 2023;
Accepted: 07 September 2023; Available on-line: 12 September 2023
N-methyl-D-aspartate receptors (NMDARs), are one of the major ionotropic glutamate receptors found in excitatory synapses which play a key role in glutamatergic synaptic transmission. The receptors are regulated by post translational modifications such as phosphorylation. One of the major receptor subunits is GluN2A which is likely to get phosphorylated in vitro at a putative site Ser1291. However, the regulation of phosphorylation of this site by kinases and phosphatases is not yet completely understood. In the present study, we have used the fusion constructs of GluN2A tagged with glutathione S-transferase (GST) as substrate for phosphorylation, purified calcium/calmodulin dependent protein kinase type II (CaMKII) and radioactive P32. We demonstrated that the site phosphorylated by αCaMKII on GluN2A was Ser1291 and that protein phosphatases 1, 2A and 2C were able to dephosphorylate this phospho-GST-GluN2A-Ser1291 in vitro. In the rat brain tissue post synaptic density and cytosolic fraction the major phosphatase responsible for dephosphorylating phospho-GluN2A-Ser1291 was protein phosphatase 1.
Plasminogen and its fragments in rat brain: a plausible role for astrocytes in angiostatin generation
A. A. Tykhomyrov1, V. S. Nedzvetsky2,3, C. A. Ağca3,
V. V. Korsa1, T. V. Grinenko1
1Palladin Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv;
2Dnipropetrovsk National University, Dnipro, Ukraine;
3Bingöl University, Bingöl, Turkey;
e-mail: artem_tykhomyrov@ukr.net
The purpose of the present study was to examine the plasminogen localization and to detect levels of its fragments (angiostatins) in various regions of rat brain as well as to establish whether rat brain astrocytes could be involved in angiostatin production. It was shown immunohistochemically that plasminogen is distributed broadly in the various brain regions, with predominant expression in meningeal layer and IV, V, and VI layers or cerebral cortex, dentate gyrus, meningeal and Purkinje cells, molecular and granular layers of cerebellum, as well as vessel walls. Angiostatin polypeptides were detected by Western blot analysis mostly in the cerebral cortex and were represented by 50 and 40-30 kDa polypeptides. In the whole cell lysates from primary cultures of rat astrocytes, immunoreactive polypeptides with Mm ~ 92, 84, 65-60, 50, 40, 38-30 kDa, corresponding to native plasminogen and a variety of its truncated products, including angiostatin polypeptides, were revealed. Incubation of astrocytes with exogenous plasminogen resulted in gradual increasing levels of some plasminogen fragments, particularly 30 kDa protein. Moreover, this polypeptide appeared to be the single angiostatin released by astrocytes in vitro. We report here for the first time that astrocytes are one of the cell types in CNS that could be responsible for angiostatin formation and releasing.
Distribution of glial fibrillary acidic protein in different parts of the rat brain under cadmium exposure
Yu. P. Kovalchuk1, I. V. Prischepa1, U. Si2, V. S. Nedzvetsky1,
Y. G. Kot2, E. E. Persky2, G. A. Ushakova1
1Oles’ Honchar Dnepropetrovsk National University, Ukraine;
2V. N. Karazin Kharkiv National University, Ukraine;
e-mail: yulka.kovalchuk.5868152@mail.ru
The chronic effects of low doses of cadmium on the distribution of soluble and filament forms of glial fibrillary acidic protein (GFAP) and their polypeptide fragments in different parts of the rat brain were investigated. Obtained results showed dose-dependent effect of cadmium on the soluble form of GFAP and more pronounced effect on the filament form and composition of the polypeptide fragments of the protein in the rat brain. Prolonged intoxication by cadmium ions in a dose of 1.0 µg/kg of body weight induced a significant decrease in soluble GFAP and an increase in the filament form in the rat brain, pointing to the development of reactive astrogliosis and the risk of neurodegeneration.