THE INCREASED KINETICS OF H2O2-INDUCED CHEMILUMINESCENCE IN THE PATIENTS WITH LONG-TERM CONSEQUENCES AFTER CEREBRAL CONTUSION
DOI:
https://doi.org/10.34287/MMT.4(43).2019.4Abstract
Purpose of the study. The aim was to study in the patients with long-term consequences after cerebral contusion the intensity of spontaneous and H2O2-induced chemiluminescence in order to evaluate the early fast-flowing reactions caused by oxidative stress and associated with the formation of primary radicals such as free radical oxidations.
Materials and Methods. Forty-two patients with long-term consequences after cerebral contusion were investigated (39,04 ± 12,84 years mean age; mean onset years 32,56 ± 6,4) where both spontaneous and H2O2-induced chemiluminescences were measured directly by HPLC-chemiluminescence assay.
Results. The study have showed that sera of the investigated patients with long-term consequences after cerebral contusion have the increased H2O2-induced chemiluminescence associated with the high amplitude of «fast» burst and the tendency to increase of spontaneous chemiluminescence (p = 0,039 and p = 0,58, accordingly). Thus, the patients with longterm consequences after cerebral contusion showed the abnormal high kinetics of H2O2-induced chemiluminescence (p < 0,05). The statistically significant increase serum Н2О2-induced chemiluminescence intensity detected in examined patients (3085,6 ± 114,2 vs 669,1 ± 214,83 controls) have showed the development of certain oxidative stress processes in this category of patients associated with the increasing of primary free radical reactions and their activity were getting increased with the progression of the disease duration (p < 0,05).
Conclusions. The study provides the novel data revealing the increased kinetics of H2O2-induced chemiluminescence in the patients with long-term consequences after cerebral contusion accompanied by the tendency to increase of spontaneous chemiluminescence that may play the certain pathogenetic role.
References
Hilmer LV, Park KB, Vycheth I, Wirsching M. Cerebral contusion: an investigation of etiology, risk factors, related diagnoses, and the surgical management at a major government hospital in Cambodia. Asian J Neurosurg. 2018; 13 (1): 23–30. DOI: 10.4103/ajns.AJNS_342_16.
Butcher I, McHugh GS, Lu J et al. Prognostic value of cause of injury in traumatic brain injury: results from the IMPACT study. J Neurotrauma. 2007; 24 (2): 281–286. DOI: 10.1089/neu.2006.0030.
Laker SR. Epidemiology of concussion and mild traumatic brain injury. PM R. 2011; 3 (10 Suppl 2): S354-358. DOI: 10.1016/j.pmrj.2011.07.017.
Anthonymuthu TS, Kenny EM, Bayir H. Therapies targeting lipid peroxidation in traumatic brain injury. Brain Res. 2016; 1640 (Pt A): 57–76. DOI: 10.1016/j.brainres.2016.02.006.
Bastos EL, Romoff P, Eckert CR, Baader WJ. Evaluation of antiradical capacity by H O -hemin-Neurol Disord Drug Targets. 2018; 17 (9): 689–695. DOI: 10.2174/1871527317666180627120501.
Halliwell B, Gutteridge JM. Lipid peroxidation, oxygen radicals, cell damage, and antioxidant therapy. Lancet. 2000; 1 (8391): 1396–1397. DOI: 10.1016/s0140-6736(84)91886-5.
Rattan SI. Theories of biological aging: genes, proteins, and free radicals. Free Radic Res. 2006; 40 (12): 1230–1238. DOI: 10.1080/10715760600911303.
Chen DL, Chen TW, Chien CT, Li PC. Intravenous low redox potential saline attenuates FeCl3-induced vascular dysfunction via downregulation of endothelial H2O2, CX3CL1, intercellular adhesion molecule-1, and p53 expression. Transl Res. 2011; 157 (5): 306–319. DOI: 10.1016/j.trsl.2010.12.012. Epub 2011 Jan 25.
Gélas P, Tscharner V, Record M et al. Human neutrophil phospholipase D activation by induced luminol chemiluminescence. J Agric Food Chem. 2003; 51 (25): 7481–7488. DOI: 10.1021/jf0345189.
Hill RL, Singh IN, Wang JA, Hall ED. Time courses of post-injury mitochondrial oxidative damage and respiratory dysfunction and neuronal cytoskeletal degradation in a rat model of focal traumatic brain injury. Neurochem. Int. 2017; 111: 45–56. DOI: 10.1016/j.neuint.2017.03.015.
Hubbard WB, Joseph B, Spry M et all. Acute mitochondrial impairment underlies prolonged cellular dysfunction after repeated mild traumatic brain injuries. J Neurotrauma. 2019. 36 (8): 1252–1263. DOI: 10.1089/neu.2018.5990.
Kontorschikova KN. Lipids periokyslation at norma and pathology. Textbook. N. Novgorod. 2000, 24.
Mayer EA, Fanselow MS. Dissecting the components of central response to stress. Nature Neuroscience. 2003; 6 (10): 1011–1012. DOI: 10.1038/nn1003-1011.
Khatri N, Thakur M, Pareek V et al. Oxidative stress: major threat in traumatic brain injury. CNS N-formylmethionyl-leucylphenylalanine reveals a
two-step process for the control ofphosphatidylcholine breakdown and oxidative burst. Biochem J. 1992; 287 (Pt1): 67–72. DOI: 10.1042/bj2870067.
Prokopov V.A., Zhukov B.I., Maysoedov V.V. Methods of luminescent analysis in evaluation of structural and functional state of biological membrane at action of xenobiotic. Eksperimentalnaya i klinicheskaya meditsina. 2003; 2: 167–171.
Murr C, Baier-Bitterlich G, Fuchs D et all. Effects of neopterin-derivatives on H2O2-induced luminol chemiluminescence: mechanistic aspects. Free Radic Biol Med. 1996; 21 (4): 449–456. DOI: 10.1016/0891-5849(96)00036-6.
Zhang JR, Scherch HM, Hall ED. Direct measurementoflipidhydroperoxidesiniron-dependent spinal neuronal injury. J. Neurochem. 1996; 66 (1): 355–361. DOI: 10.1046/j.1471-4159.1996.66010355.x.
Park E, Bell JD, Baker AJ. Traumatic brain injury: can the consequences be stopped? CMAJ. 2008; 178 (9): 1163–1170. DOI: 10.1503/cmaj.080282.
