Matrix Metalloproteinase-9, Neuron-specific Enolase, S100 B and Tau Protein Levels in the Patients with Carbon monoxide Poisoning

Article ID: e080523216643 Pages: 7

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Abstract

Background: S100B, NSE, MMP-9, and Tau protein levels increase in cases causing hypoxic cell damage. The diagnosis of the severity of carbon monoxide (CO) poisoning in the early period of these parameters was studied.

Material and Methods: COHb level measurement was made using a signal capture CO-pulse oximeter (Masimo's SET Rainbow, Masimo's Co, USA) at the first admission of the patients. Then, COHb levels were confirmed by arterial blood gas(ABG) analysis. The patients were divided into two groups as mild and moderate-severe, according to their Glasgow coma scores (GCS) [Mild (14–15); Moderate (9–13) or Severe (3–8)]. The control group was composed of 16 healthy and non-smoking volunteers.

Results: The serum S100B protein and MMP-9 values at 0 hr of admission in the hospital and 3hr of treatment were not significantly different in the patient group as compared to the control group. Tau protein levels were significantly higher in the patient group at 0 and 3 hours (p> 0.05) as compared to healthy person.

Conclusion: There was no relationship between CO poisoning and MMP-9 and S100B protein levels. NSE and Tau protein were significantly higher in the patient group than the control group. Tau protein may be more useful marker as compared to neuron-specific enolase.

[1]
Güzel M, Atay E, Terzi Ö, Demir M, Erenler A, Demir M. The role of lactate and troponin-I levels in predicting length of hospital stay in patients with carbon monoxide poisoning. Clin Lab 2019; 65 (5).
[http://dx.doi.org/10.7754/Clin.Lab.2018.180929] [PMID: 31115207]
[2]
Hampson NB. Trends in the incidence of carbon monoxide poisoning in the United States. Am J Emerg Med 2005; 23(7): 838-41.
[http://dx.doi.org/10.1016/j.ajem.2005.03.014] [PMID: 16291437]
[3]
Omaye ST. Metabolic modulation of carbon monoxide toxicity. Toxicology 2002; 180(2): 139-50.
[http://dx.doi.org/10.1016/S0300-483X(02)00387-6] [PMID: 12324190]
[4]
Hopper CP, De La Cruz LK, Lyles KV, et al. Role of Carbon Monoxide in Host–Gut Microbiome Communication. Chem Rev 2020; 120(24): 13273-311.
[http://dx.doi.org/10.1021/acs.chemrev.0c00586] [PMID: 33089988]
[5]
Wright J. Chronic and occult carbon monoxide poisoning: we don’t know what we’re missing. Emerg Med J 2002; 19(5): 386-90.
[http://dx.doi.org/10.1136/emj.19.5.386] [PMID: 12204981]
[6]
Kavak N, Doğan B, Sultanoğlu H, Kavak RP, Özdemi̇r M. Clinical and magnetic resonance imaging findings of patients with acute carbon monoxide poisoning. Konuralp Tip Derg 2020; 12(3): 443-50.
[http://dx.doi.org/10.18521/ktd.735274]
[7]
Kao LW, Nañagas KA. Carbon monoxide poisoning. Emerg Med Clin North Am 2004; 22(4): 985-1018.
[http://dx.doi.org/10.1016/j.emc.2004.05.003] [PMID: 15474779]
[8]
Oliverio S, Varlet V. What are the limitations of methods to measure carbon monoxide in biological samples? Forensic Toxicol 2020; 38(1): 1-14.
[http://dx.doi.org/10.1007/s11419-019-00490-1]
[9]
Adami C, Sorci G, Blasi E, Agneletti AL, Bistoni F, Donato R. S100b expression in and effects on microglia. Glia 2001; 33(2): 131-42.
[http://dx.doi.org/10.1002/1098-1136(200102)33:2<131::AID-GLIA1012>3.0.CO;2-D] [PMID: 11180510]
[10]
Brvar M, Možina H, Osredkar J, et al. S100B protein in carbon monoxide poisoning: a pilot study. Resuscitation 2004; 61(3): 357-60.
[http://dx.doi.org/10.1016/j.resuscitation.2004.01.009] [PMID: 15172716]
[11]
Rasmussen LS, Poulsen MG, Christiansen M, Jansen EC. Biochemical markers for brain damage after carbon monoxide poisoning. Acta Anaesthesiol Scand 2004; 48(4): 469-73.
[http://dx.doi.org/10.1111/j.1399-6576.2004.00362.x] [PMID: 15025610]
[12]
Cakir Z, Aslan S, Umudum Z, et al. S-100β and neuron-specific enolase levels in carbon monoxide–related brain injury. Am J Emerg Med 2010; 28(1): 61-7.
[http://dx.doi.org/10.1016/j.ajem.2008.10.032] [PMID: 20006203]
[13]
Yardan T, Cevik Y, Donderici O, et al. Elevated serum S100B protein and neuron-specific enolase levels in carbon monoxide poisoning. Am J Emerg Med 2009; 27(7): 838-42.
[http://dx.doi.org/10.1016/j.ajem.2008.04.016] [PMID: 19683113]
[14]
Akdemir HU, Yardan T, Kati C, et al. The role of S100B protein, neuron-specific enolase, and glial fibrillary acidic protein in the evaluation of hypoxic brain injury in acute carbon monoxide poisoning. Hum Exp Toxicol 2014; 33(11): 1113-20.
[http://dx.doi.org/10.1177/0960327114521049] [PMID: 24505052]
[15]
Brvar M, Možina H, Osredkar J, Možina M, Bručan A, Bunc M. The potential value of the protein S-100B level as a criterion for hyperbaric oxygen treatment and prognostic marker in carbon monoxide poisoned patients. Resuscitation 2003; 56(1): 105-9.
[http://dx.doi.org/10.1016/S0300-9572(02)00289-7] [PMID: 12505746]
[16]
Gawlikowski T, Golasik M, Gomółka E, Piekoszewski W. Proteins as biomarkers of carbon monoxide neurotoxicity. Inhal Toxicol 2014; 26(14): 885-90.
[http://dx.doi.org/10.3109/08958378.2014.970786] [PMID: 25357234]
[17]
Johnsson P, Blomquist S, Lührs C, et al. Neuron-specific enolase increases in plasma during and immediately after extracorporeal circulation. Ann Thorac Surg 2000; 69(3): 750-4.
[http://dx.doi.org/10.1016/S0003-4975(99)01393-4] [PMID: 10750755]
[18]
Ameri M, Shabaninejad Z, Movahedpour A, et al. Biosensors for detection of Tau protein as an Alzheimer’s disease marker. Int J Biol Macromol 2020; 162: 1100-8.
[http://dx.doi.org/10.1016/j.ijbiomac.2020.06.239] [PMID: 32603732]
[19]
Hesse C, Rosengren L, Andreasen N, et al. Transient increase in total tau but not phospho-tau in human cerebrospinal fluid after acute stroke. Neurosci Lett 2001; 297(3): 187-90.
[http://dx.doi.org/10.1016/S0304-3940(00)01697-9] [PMID: 11137759]
[20]
Montaner J, Alvarez-Sabín J, Molina C, et al. Matrix metalloproteinase expression after human cardioembolic stroke: temporal profile and relation to neurological impairment. Stroke 2001; 32(8): 1759-66.
[http://dx.doi.org/10.1161/01.STR.32.8.1759] [PMID: 11486102]
[21]
Alvarez-Sabín J, Delgado P, Abilleira S, et al. Temporal profile of matrix metalloproteinases and their inhibitors after spontaneous intracerebral hemorrhage: relationship to clinical and radiological outcome. Stroke 2004; 35(6): 1316-22.
[http://dx.doi.org/10.1161/01.STR.0000126827.69286.90] [PMID: 15087562]
[22]
Akelma AZ, Celik A, Ozdemir O, et al. Neuron-specific enolase and S100B protein in children with carbon monoxide poisoning: children are not just small adults. Am J Emerg Med 2013; 31(3): 524-8.
[http://dx.doi.org/10.1016/j.ajem.2012.10.009] [PMID: 23380091]
[23]
Mena JH, Sanchez AI, Rubiano AM, et al. Effect of the modified Glasgow Coma Scale score criteria for mild traumatic brain injury on mortality prediction: comparing classic and modified Glasgow Coma Scale score model scores of 13. J Trauma 2011; 71(5): 1185-93.
[http://dx.doi.org/10.1097/TA.0b013e31823321f8] [PMID: 22071923]
[24]
Leite MC, Galland F, Brolese G, et al. A simple, sensitive and widely applicable ELISA for S100B: Methodological features of the measurement of this glial protein. J Neurosci Methods 2008; 169(1): 93-9.
[http://dx.doi.org/10.1016/j.jneumeth.2007.11.021] [PMID: 18178255]
[25]
Xue L, Wang WL, Li Y, et al. Effects of hyperbaric oxygen on hippocampal neuronal apoptosis in rats with acute carbon monoxide poisoning. Undersea Hyperb Med 2017; 44(2): 121-31.
[http://dx.doi.org/10.22462/3.4.2017.5] [PMID: 28777902]
[26]
Lakhan SE, Kirchgessner A, Tepper D, Leonard A. Matrix metalloproteinases and blood-brain barrier disruption in acute ischemic stroke. Front Neurol 2013; 4: 32.
[http://dx.doi.org/10.3389/fneur.2013.00032] [PMID: 23565108]
[27]
Montaner J, Molina CA, Monasterio J, et al. Matrix metalloproteinase-9 pretreatment level predicts intracranial hemorrhagic complications after thrombolysis in human stroke. Circulation 2003; 107(4): 598-603.
[http://dx.doi.org/10.1161/01.CIR.0000046451.38849.90] [PMID: 12566373]
[28]
Vukasovic I, Tesija-Kuna A, Topic E, Supanc V, Demarin V, Petrovcic M. Matrix metalloproteinases and their inhibitors in different acute stroke subtypes. Clin Chem Lab Med 2006; 44(4): 428-34.
[http://dx.doi.org/10.1515/CCLM.2006.079] [PMID: 16599837]
[29]
Zhong C, Yang J, Xu T, et al. Serum matrix metalloproteinase-9 levels and prognosis of acute ischemic stroke. Neurology 2017; 89(8): 805-12.
[http://dx.doi.org/10.1212/WNL.0000000000004257] [PMID: 28747453]
[30]
Abdelnaseer MM, Elfauomy NM, Esmail EH, Kamal MM, Elsawy EH. Matrix metalloproteinase-9 and recovery of acute ischemic stroke. J Stroke Cerebrovasc Dis 2017; 26(4): 733-40.
[http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.09.043] [PMID: 28063771]
[31]
Ishida H, Murata N, Tada M, et al. Determining the levels of matrix metalloproteinase-9 in portal and peripheral blood is useful for predicting liver metastasis of colorectal cancer. Jpn J Clin Oncol 2003; 33(4): 186-91.
[http://dx.doi.org/10.1093/jjco/hyg035] [PMID: 12810833]
[32]
Iizasa T, Fujisawa T, Suzuki M, et al. Elevated levels of circulating plasma matrix metalloproteinase 9 in non-small cell lung cancer patients. Clin Cancer Res 1999; 5(1): 149-53.
[PMID: 9918213]
[33]
Che B, Zhong C, Ge J, et al. Serum matrix metalloproteinase-9 is associated with depression after acute ischemic stroke. Circ J 2019; 83(11): 2303-11.
[http://dx.doi.org/10.1253/circj.CJ-19-0376] [PMID: 31564697]
[34]
Baudier J, Gentil BJ. The S100B Protein and Partners in Adipocyte Response to Cold Stress and Adaptive Thermogenesis: Facts, Hypotheses, and Perspectives. Biomolecules 2020; 10(6): 843.
[http://dx.doi.org/10.3390/biom10060843] [PMID: 32486507]
[35]
Ciccarelli R, Di Iorio P, Bruno V, et al. Activation of A1 adenosine or mGlu3 metabotropic glutamate receptors enhances the release of nerve growth factor and S-100? protein from cultured astrocytes. Glia 1999; 27(3): 275-81.
[http://dx.doi.org/10.1002/(SICI)1098-1136(199909)27:3<275::AID-GLIA9>3.0.CO;2-0] [PMID: 10457374]
[36]
Pinto SS, Gottfried C, Mendez A, et al. Immunocontent and secretion of S100B in astrocyte cultures from different brain regions in relation to morphology. FEBS Lett 2000; 486(3): 203-7.
[http://dx.doi.org/10.1016/S0014-5793(00)02301-2] [PMID: 11119704]
[37]
Donato R. Intracellular and extracellular roles of S100 proteins. Microsc Res Tech 2003; 60(6): 540-51.
[http://dx.doi.org/10.1002/jemt.10296] [PMID: 12645002]
[38]
Herrmann M, Vos P, Wunderlich MT, de Bruijn CHMM, Lamers KJB. Release of glial tissue-specific proteins after acute stroke: A comparative analysis of serum concentrations of protein S-100B and glial fibrillary acidic protein. Stroke 2000; 31(11): 2670-7.
[http://dx.doi.org/10.1161/01.STR.31.11.2670] [PMID: 11062293]
[39]
Foerch C, Niessner M, Back T, et al. Diagnostic accuracy of plasma glial fibrillary acidic protein for differentiating intracerebral hemorrhage and cerebral ischemia in patients with symptoms of acute stroke. Clin Chem 2012; 58(1): 237-45.
[http://dx.doi.org/10.1373/clinchem.2011.172676] [PMID: 22125303]
[40]
Wunderlich MT, Lins H, Skalej M, Wallesch CW, Goertler M. Neuron-specific enolase and tau protein as neurobiochemical markers of neuronal damage are related to early clinical course and long-term outcome in acute ischemic stroke. Clin Neurol Neurosurg 2006; 108(6): 558-63.
[http://dx.doi.org/10.1016/j.clineuro.2005.12.006] [PMID: 16457947]
[41]
Li L, Li J, Chai CG, Zhang JJ, Zhang SY. [Application value of BIS and S100β combined with Copeptin in patients with acute severe carbon monoxide poisoning]. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2022; 40(3): 204-8.
[PMID: 35439863]
[42]
Irazuzta JE, de Courten-Myers G, Zemlan FP, Bekkedal MYV, Rossi J III. Serum cleaved Tau protein and neurobehavioral battery of tests as markers of brain injury in experimental bacterial meningitis. Brain Res 2001; 913(1): 95-105.
[http://dx.doi.org/10.1016/S0006-8993(01)02764-0] [PMID: 11532253]
[43]
Kilicaslan I, Bildik F, Aksel G, et al. Serum tau protein level for neurological injuries in carbon monoxide poisoning. Clin Toxicol (Phila) 2012; 50(6): 497-502.
[http://dx.doi.org/10.3109/15563650.2012.698742] [PMID: 22746384]