Tyurin, V.A., Tyurina, Y.Y., Borisenko, G.G., Sokolova, T.V., Ritov, V.B., Quinn, P.J., Rose, M., Kochanek, P., Graham, S.H. and Kagan, V.E. (2000) Oxidative stress following traumatic brain injury in rats: Quantitation of biomarkers and detection of free radical intermediates. Journal of Neurochemistry, 75, 2178-2189.

has been cited by the following article:

• TITLE: High resolution nuclear magnetic resonance investigation of metabolic disturbances induced by focal traumatic brain injury in a rat model: a pilot study

  AUTHORS: Laurent Lemaire, François Seguin, Florence Franconi, Delphine Bon, Anne Pasco, Nadège Boildieu, Jean-Jacques Le Jeune

  KEYWORDS: TBI; 1H-NMR Spectroscopy; Metabolomic; Traumatic Brain

  JOURNAL NAME: Journal of Biomedical Science and Engineering, Vol.4 No.2, February 25, 2011

  ABSTRACT: Experimental models of traumatic brain injury (TBI) provide a useful tool for understanding the cerebral metabolic changes induced by this pathological condition. Here, we report on the time course of changes in cerebral metabolites after TBI using high-resolution proton magnetic resonance spectroscopy (NMR). Extracts from adult male Sprague-Dawley rats were subjected to fluid lateral percussion and were then examined by NMR at 3, 24 and 48 h after the injury. A metabolomic approach was carried out to identify the cerebral metabolites impacted by the TBI and their quantitative temporal changes. Lactate, valine and ascorbate were the three first metabolites to be significantly modified after TBI. The quantitative elevation for these compounds last for the entire experimental time explored. Within 24 hours post-TBI, a significant elevation in choline-derivates, alanine and glucose were also measured. On the other hand, N-acetyl aspartate, a neuronal marker, and myo- inositol, an important organic osmolyte in the mammalian brain, were not significantly impacted in the chronic phase of TBI.