SOME METABOLIC PROCESSES IN THE PATIENTS WITH LONG-TERM CONSEQUENCES OF MILD TRAUMATIC BRAIN INJURY
DOI:
https://doi.org/10.11603/ijmmr.2413-6077.2019.2.10459Keywords:
long-term consequences of mTBI, membrane-associated enzymes, metabolic processesAbstract
Background. Mild traumatic brain injury (mTBI) leads to disturbance of various metabolic processes significant in pathogenesis of the maintaining of long-term consequences after it.
The objective of the research was to analyse changes in the activity of some membrane-associated enzyme markers, which are involved in different redox reactions, reflecting main metabolic processes.
Methods. Forty-seven patients with long-term consequences of mTBI, thirty controls were enrolled. The levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase were evaluated in sera by gas-liquid chromatograph and calorimetric methods.
Results. The study revealed significant changes in metabolic processes observed for alkaline phosphatase and LDH, which were the indicators of membrane and redox processes disturbances, acidosis severity and impaired energy cell metabolism. The averages of LDH level was 662.7 versus 381.9 U/L, in the controls. The disease progression was followed by directly proportional LDH increase reaching very high values in the patients with disease duration more than 15 years (mean ±SD 144.6±16.3 versus 82.6±8.4 U/L, controls p<0.05). The long-term consequences of mTBI were characterized by statistically significant decrease of alkaline phosphatase and positive dependence (p<0.05) of it (r=+0.48) on the disease duration with the averages of alkaline phosphatase level of 152.5±11.21 versus 212.6±9.63 U/L, controls (p<0.01). The significance of changes in membrane-associated enzymes serum levels correlated with development of oxidative stress and metabolic processes dysfunction.
Conclusion. In the patients with long-term consequences of mTBI, dysregulation of enzymes activity was detected that might be a marker of nervous system energy impairment and membranes destruction.
References
Bazan NG. Second messengers derived from excitable membranes are involved in ischemic and seizure-related brain damage. Patologicheskaia fiziologiia i eksperimental'naia terapiia. 1992(4):11-6.
Brigode W, Cohan C, Beattie G, Victorino G. Alcohol in traumatic brain injury: toxic or therapeutic?. Journal of surgical research. 2019 Dec 1;244:196-204. DOI: https://doi.org/10.1016/j.jss.2019.06.043
doi.org/10.1016/j.jss.2019.06.043
Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec;414(6865):813-20.
doi: 10.1038/414813a DOI: https://doi.org/10.1038/414813a
Halliwell B, Gutteridge JC. Lipid peroxidation, oxygen radicals, cell damage, and antioxidant therapy. The Lancet. 1984 Jun 23;323(8391):1396-7. DOI: https://doi.org/10.1016/S0140-6736(84)91886-5
Huang XJ, Choi YK, Im HS, Yarimaga O, Yoon E, Kim HS. Aspartate aminotransferase (AST/GOT) and alanine aminotransferase (ALT/GPT) detection techniques. Sensors. 2006 Jul;6(7):756-82.
doi: 10.3390/s6070756 DOI: https://doi.org/10.3390/s6070756
Jenner P. Oxidative damage in neurodegenerative disease. The Lancet. 1994 Sep 17;344(8925): 796-8.
doi: 10.1016/S0140-6736(94)92347-7 DOI: https://doi.org/10.1016/S0140-6736(94)92347-7
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F. Control of energy metabolism by iodothyronines. Journal of Endocrinological Investigation. 2001 Dec 1;24(11):897-913.
doi: 10.1007/BF03343949 DOI: https://doi.org/10.1007/BF03343949
Linden DE. The P300: where in the brain is it produced and what does it tell us?. The Neuroscientist. 2005 Dec;11(6):563-76.
doi: 10.1177/1073858405280524 DOI: https://doi.org/10.1177/1073858405280524
Lekomtseva Y, Voloshyn-Gaponov I, Tatayna G. Targeting Higher Levels of Tau Protein in Ukrainian Patients with Wilson’s Disease. Neurology and therapy. 2019 Jun 1;8(1):59-68.
doi: 10.1007/s40120-019-0134-3 DOI: https://doi.org/10.1007/s40120-019-0134-3
Mayer EA, Fanselow MS. Dissecting the components of the central response to stress. Nature Neuroscience. 2003 Oct;6(10):1011-107.
doi: 10.1038/nn1003-1011 DOI: https://doi.org/10.1038/nn1003-1011
McGinn MJ, Povlishock JT. Pathophysiology of traumatic brain injury. Neurosurgery Clinics. 2016 Oct 1;27(4):397-407.
doi: 10.1016/j.nec.2016.06.002 DOI: https://doi.org/10.1016/j.nec.2016.06.002
Neuberger EJ, Abdul Wahab R, Jayakumar A, Pfister BJ, Santhakumar V. Distinct effect of impact rise times on immediate and early neuropathology after brain injury in juvenile rats. Journal of neuroscience research. 2014 Oct;92(10):1350-61.
doi: 10.1002/jnr.23401 DOI: https://doi.org/10.1002/jnr.23401
Phillips LL, Lyeth BG, Hamm RJ, Povlishock JT. Combined fluid percussion brain injury and entorhinal cortical lesion: a model for assessing the interaction between neuroexcitation and deafferentation. Journal of neurotrauma. 1994 Dec;11(6):641-56.
doi: 10.1089/neu.1994.11.641 DOI: https://doi.org/10.1089/neu.1994.11.641
Phillips LL, Lyeth BG, Hamm RJ, Reeves TM, Povlishock JT. Glutamate antagonism during secondary deafferentation enhances cognition and axo-dendritic integrity after traumatic brain injury. Hippocampus. 1998;8(4):390-401.
doi: 10.1002/(SICI)1098-1063(1998)8:4<390::AID-HIPO7>3.0.CO;2-L DOI: https://doi.org/10.1002/(SICI)1098-1063(1998)8:4<390::AID-HIPO7>3.0.CO;2-L
Phillips LL, Reeves TM. Interactive pathology following traumatic brain injury modifies hippocampal plasticity. Restorative neurology and neuroscience. 2001 Jan 1;19(3, 4):213-35.
Pryor WA. Free radicals and lipid peroxidation: what they are and how they got that way. Natural antioxidants in human health and disease. 1994 Jan 1:1-24.
doi: 10.1016/B978-0-08-057168-3.50007-2 DOI: https://doi.org/10.1016/B978-0-08-057168-3.50007-2
Rattan SI. Theories of biological aging: genes, proteins, and free radicals. Free radical research. 2006 Jan 1;40(12):1230-8.
doi: 10.1080/10715760600911303 DOI: https://doi.org/10.1080/10715760600911303
Sohal RS. Role of oxidative stress and protein oxidation in the aging process. Free Radical Biology and Medicine. 2002 Jul 1;33(1):37-44.
doi: 10.1016/S0891-5849(02)00856-0 DOI: https://doi.org/10.1016/S0891-5849(02)00856-0
Zhang P, Wang CY, Li YX, Pan Y, Niu JQ, He SM. Determination of the upper cut-off values of serum alanine aminotransferase and aspartate aminotransferase in Chinese. World Journal of Gastroenterology: WJG. 2015 Feb 28;21(8):2419-24.
doi: 10.3748/wjg.v21.i8.2419 DOI: https://doi.org/10.3748/wjg.v21.i8.2419
Zhang J, Shi C, Wang H, Gao C, Chang P, Chen X, Shan H, Zhang M, Tao L. Protective Effects of Hydrogen Sulfide on a Cell Culture Model of Traumatic Scratch Injury involving Suppression of Oxidative Stress and Upregulation of Nrf-2. The international journal of biochemistry & cell biology. 2019 Oct:105636.
doi: 10.1016/j.biocel.2019.105636 DOI: https://doi.org/10.1016/j.biocel.2019.105636
Zhang QH, Hao JW, Xiao-Jing J, Guang-Lei L, Zhou M, Yao YM. Long-lasting neurobehavioral alterations in burn-injured mice resembling post-traumatic stress disorder in humans. Experimental neurology. 2019 Nov:113084-.
doi: 10.1016/j.expneurol.2019.113084 DOI: https://doi.org/10.1016/j.expneurol.2019.113084
Zhou YF, Li WT, Han HC, Gao DK, He XS, Li L, Song JN, Fei Z. Allicin protects rat cortical neurons against mechanical trauma injury by regulating nitric oxide synthase pathways. Brain research bulletin. 2014 Jan 1;100:14-21.
doi: 10.1016/j.brainresbull.2013.10.013 DOI: https://doi.org/10.1016/j.brainresbull.2013.10.013
