scholarly journals Kainate-induced oxidative stress and neurotoxicity in the rat brain

2005 ◽  
Vol 57 (4) ◽  
pp. 259-266 ◽  
Author(s):  
Lidija Radenovic ◽  
Vesna Selakovic

We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements took place at different times in hippocampus, forebrain cortex, striatum, and cerebellum homogenates. Free radicals including superoxide are responsible for post-lesional cytotoxicity. Neuronal cells responded to oxidative stress in kainate-induced neurotoxicity and caused the protective mechanism to increase MnSOD levels. The increase of MnSOD in distinct brain regions functionally connected via afferents and efferent suggests that these regions are affected by the injury. It implies that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity. <br><br><font color="red"><b> This article has been retracted. Link to the retraction <u><a href="http://dx.doi.org/10.2298/ABS150318027E">10.2298/ABS150318027E</a><u></b></font>

2015 ◽  
Vol 67 (2) ◽  
pp. 749-749
Author(s):  
E Editorial

This is a notice of retraction of the article: Effect of 7-nitroindazole on superoxide production and MnSOD activity in the rat brain following kainate-induced neurotoxicity, published in the Archives of Biological Sciences in 2008, Vol. 60, Issue 1. The Editor-in-Chief has been informed that this paper plagiarizes an earlier paper: Radenovic L, Selakovic V, Kartelija G, Todorovic N, Nedeljkovic M. Differential effects of NMDA and AMPA/kainate receptor antagonists on superoxide production and MnSOD activity in rat brain following intrahippocampal injection. Brain Res Bull, 2004, 64(1):85-93. The results in the article being retracted were presented as findings obtained from novel research. Inspection of the results has revealed that they were part of research already presented in the original article without appropriate justification or cross-referencing. The Editor-in-Chief considered publishing a notice of redundancy specifying the elements published previously. However, since the original article had already been autoplagiarized by the same corresponding author in the same journal (retraction DOI:10.2298/ABS150318026E), the article is being retracted in accordance with the publishing ethics of the Archives of Biological Sciences in order to preserve the integrity of scientific research. We apologize to the journal's readers that it took so long to notice this error and instigate retraction of the paper. We request our readers to contact the editorial office and editors of the journal directly should similar cases occur in the future, so that the necessary action can be taken more promptly. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0801025R">10.2298/ABS0801025R</a></b></u>


2015 ◽  
Vol 67 (2) ◽  
pp. 741-741
Author(s):  
E Editorial

This is a notice of retraction of the article: Mitochondrial superoxide production and MnSOD activity following exposure to an agonist and antagonists of ionotropic glutamate receptors in rat brain, published in the Archives of Biological Sciences in 2005, Vol. 57, Issue 1. The Editor-in-Chief has been informed that this paper plagiarizes an earlier paper: Radenovic L, Selakovic V, Kartelija G, Todorovic N, Nedeljkovic M. Differential effects of NMDA and AMPA/kainate receptor antagonists on superoxide production and MnSOD activity in rat brain following intrahippocampal injection. Brain Res Bull, 2004, 64(1):85-93. This claim is correct and almost the entire paper is a verbatim copy of the earlier one. After confirmation of this fact, the Editor-in-Chief of the Archives of Biological Sciences has decided to retract the paper immediately. We apologize to the readers of the journal that it took so many years to notice this error and to retract the paper. We request readers of the journal to directly get in touch with the editorial office and the editors of the journal for similar cases in the future, so that they can be handled promptly. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0501001R">10.2298/ABS0501001R</a></b></u>


2015 ◽  
Vol 67 (2) ◽  
pp. 743-743
Author(s):  
E Editorial

This is a notice of retraction of the article: Kainate-induced oxidative stress and neurotoxicity in the rat brain, published in the Archives of Biological Sciences in 2005, Vol. 57, Issue 4. The Editor-in-Chief has been informed that this paper plagiarizes an earlier paper: Radenovic L, Jovanovic M, Vasiljevic I, Selakovic V. Superoxide production and the activity of MnSOD in rat brain after intrahippocampal kainate-induced seizure. Neurosci Res Comm, 2004, 34(2):92-103. This claim is correct and almost the entire paper is a verbatim copy of the earlier one. After confirmation of this fact, the Editor-in-Chief of the Archives of Biological Sciences has decided to retract the paper immediately. We apologize to the readers of the journal that it took so many years to notice this error and to retract the paper. We request readers of the journal to directly get in touch with the editorial office and the editors of the journal for similar cases in the future, so that they can be handled promptly. <br><br><font color="red"><b> Link to the retracted article <u><a href="http://dx.doi.org/10.2298/ABS0504259R">10.2298/ABS0504259R</a></b></u>


2009 ◽  
Vol 27 (2) ◽  
pp. 219-224 ◽  
Author(s):  
Supriya Swarnkar ◽  
Ethika Tyagi ◽  
Rahul Agrawal ◽  
Mahendra Pratap Singh ◽  
Chandishwar Nath

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Marco Sifringer ◽  
Clarissa von Haefen ◽  
Maria Krain ◽  
Nadine Paeschke ◽  
Ivo Bendix ◽  
...  

Dexmedetomidine is a highly selective agonist ofα2-receptors with sedative, anxiolytic, analgesic, and anesthetic properties. Neuroprotective effects of dexmedetomidine have been reported in various brain injury models. In the present study, we investigated the effects of dexmedetomidine on neurodegeneration, oxidative stress markers, and inflammation following the induction of hyperoxia in neonatal rats. Six-day-old Wistar rats received different concentrations of dexmedetomidine (1, 5, or 10 µg/kg bodyweight) and were exposed to 80% oxygen for 24 h. Sex-matched littermates kept in room air and injected with normal saline or dexmedetomidine served as controls. Dexmedetomidine pretreatment significantly reduced hyperoxia-induced neurodegeneration in different brain regions of the neonatal rat. In addition, dexmedetomidine restored the reduced/oxidized glutathione ratio and attenuated the levels of malondialdehyde, a marker of lipid peroxidation, after exposure to high oxygen concentration. Moreover, administration of dexmedetomidine induced downregulation of IL-1βon mRNA and protein level in the developing rat brain. Dexmedetomidine provides protections against toxic oxygen induced neonatal brain injury which is likely associated with oxidative stress signaling and inflammatory cytokines. Our results suggest that dexmedetomidine may have a therapeutic potential since oxygen administration to neonates is sometimes inevitable.


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