Oxidative Stress Parameters in Posttraumatic Stress Disorder Risk Group Patients

Vladimirs Voicehovskis 1 , Gunta Ancāne 1 , Jūlija Voicehovska 2 , Grigorijs Orļikovs 2 , Jurijs Karpovs 2 , Igors Ivanovs 3 , Andrejs Šķesters 4 , Andrejs Ancāns 5 , Alise Silova 4 , Tarass Ivaščenko 1 , Jānis Micāns 6 , Normunds Vaivads 7 ,  and Larisa Umnova 2
  • 1 Department of Psychosomatic Medicine and Psychotherapy, Rīga Stradiņš University, Kapseļu iela 23, Rīga, LV-1046, LATVIA
  • 2 Internal Diseases Department, Rīga Stradiņš University, Pilsoņu iela 13, Rīga, LV-1002, LATVIA
  • 3 Rīga 1st Hospital, Bruņinieku iela 5, Rīga, 1001, LATVIA
  • 4 Biochemical Laboratory, Rīga Stradiņš University, Dzirciema iela 16, Rīga, LV-1007, LATVIA
  • 5 Department of Pathology, Rīga Stradiņš University, Pilsoņu iela 13, Rīga, LV-1002, LATVIA
  • 6 Joint Staff Medical Department, National Armed Forces, LATVIA
  • 7 3d RLC Medical Care Centre, National Armed Forces, LATVIA

Increased excitotoxity in response to stressors leads to oxidative stress (OS) due to accumulation of excess reactive oxygen/nitrogen species. Neuronal membrane phospholipids are especially susceptible to oxidative damage, which alters signal transduction mechanisms. The Contingent of International Operations (CIO) has been subjected to various extreme stressors that could cause Posttraumatic Stress Disorder (PTSD). Former studies suggest that heterogeneity due to gender, race, age, nutritional condition and variable deployment factors and stressors produce challenges in studying these processes. The research aim was to assess OS levels in the PTSD risk group in CIO. In a prospective study, 143 participants who were Latvian CIO, regular personnel, males, Europeans, average age of 27.4, with the same tasks during the mission, were examined two months before and immediately after a six-month Peace Support Mission (PSM) in Afghanistan. PCL-M questionnaire, valid Latvian language “Military” version was used for PTSD evaluation. Glutathione peroxidase (GPx), superoxide dismutase (SOD) and lipid peroxidation intensity and malondialdehyde (MDA) as OS indicators in blood were determined. Data were processed using SPSS 20.0. The MDA baseline was 2.5582 μM, which after PSM increased by 24.36% (3.1815 μM). The GPx baseline was 8061.98 U/L, which after PSM decreased by 9.35% (7308.31 U/L). The SOD baseline was 1449.20 U/gHB, which after PSM increased by 2.89% (1491.03 U/gHB). The PTSD symptom severity (total PCL-M score) baseline was 22.90 points, which after PSM increased by 14.45% (26.21 points). The PTSD Prevalence rate (PR) baseline was 0.0357, which after PSM increased by 147.06% (0.0882). We conclude that there is positive correlation between increase of OS, PTSD symptoms severity level, and PTSD PR in a group of patients with risk of PTSD - CIO. PTSD PR depends on MDA intensity and OS severity. OS and increased free radical level beyond excitotoxity, is a possible causal factor for clinical manifestation of PTSD

If the inline PDF is not rendering correctly, you can download the PDF file here.

  • Adibhatla, R. M., Hatcher, J. F. (2008). Altered lipid metabolism in brain injury and disorders. Subcell. Biochem., 49, 241-68.

  • Anonymous (2000). Diagnostic and Statistical Manual of Mental Disorders (Revised 4th edn.). American Psychiatric Association. Washington, D.C. §309.81.

  • Anwyl, R. (1991). Modulation of vertebrate neuronal calcium channels by transmitters. Brain Res. Brain Res. Rev., 16 (3), 265-281.

  • Bremner, J. D. (2002). Neuroimaging studies in post-traumatic stress disorder. Curr. Psychiatry Rep., 4 (4), 254-263.

  • Chambers, R. A., Bremner, J. D., Moghaddam, B., Southwick, S. M., Charney, D. S., Krystal, J. H. (1999). Glutamate and post-traumatic stress disorder: Towards a psychobiology of dissociation. Semin. Clin. Neuropsychiatry, 4 (4), 274-281.

  • Cortese, B. M., Phan, K. L. (2005). The role of glutamate in anxiety and related disorders. CNS Spectr., 10 (10), 820-830.

  • Del Rio, D., Stewart, A. J., Pellegrini, N. (2005). A review of recent studies on malonaldehyde as toxic molecule and biological marker of oxidative stress. Nutr. Metab. Cardiovasc. Dis., 15 (4), 316-328.

  • Esterbauer, H., Cheeseman, R. H. (1990). Determination of aldehydic lipid peroxidation products: Malonaldehyde and 4-hydroxynonenal. Methods Enzymol., 186, 407-421.

  • Ginsberg, M. D., Bogousslauvsky, J. (eds.) (1998). Cerebrovascular Disease: Pathophysiology, Diagnosis and Management. Malden: Blackwell Science. 2185 pp.

  • Hoge, C. W., Castro, C. A., Messer, S. C., McGurk, D., Cotting, D. I., Koffman, R. L. (2004). Combat duty in Iraq and Afghanistan, mental health problems, and barriers to care. New Engl. J. Med., 351 (1), 13-22.

  • Hotopf, M., Hull, L., Fear, N. T., Browne, T., Horn, O., Iversen, A., Jones, M., Murphy, D., Bland, D., Earnshaw, M., Greenberg, N., Hughes, J. H., Tate, A. R., Dandeker, C., Rona, R., Wessely, S. (2006). The health of UK military personnel who deployed to the 2003 Iraq war:Acohort study. Lancet, 367 (9524), 1731-1741.

  • Iversen, A. C., van Staden, L., Hughes, J. H., Browne, T., Hull, L., Hall, J., Greenberg, N., Rona, R. J., Hotopf, M., Wessely, S., Fear, N. T. (2009). The prevalence of common mental disorders and PTSD in the UK military: Using data from a clinical interview-based study.BMCPsychiatry, 9, 68.

  • Jourdain, P., Bergersen, L. H., Bhaukaurally, K., Bezzi, P., Santello, M., Domercq, M., Matute, C., Tonello, F., Gundersen, V., Volterra, A. (2007). Glutamate exocytosis from astrocytes controls synaptic strength. Nat. Neurosci., 10 (3), 331-339.

  • Moghaddam, B., Bolinao, M. L., Stein-Behrens, B., Sapolsky, R. (1994). Glucocortcoids mediate the stress-induced extracellular accumulation of glutamate. Brain Res., 655 (1-2), 251-254.

  • Li, Q. Y., Pedersen, C., Day, B. J., Patel, M. (2001). Dependence of excitotoxic neurodegeneration on mitochondrial aconitase inactivation. J. Neurochem., 78 (4), 746-755.

  • McDonald, S. D., Calhoun, P. S. (2010) The diagnostic accuracy of the PTSD Checklist: A critical review. Clin. Psychol. Rev., 30 (8), 976-987.

  • Milani, P., Gagliardi, S., Cova, E., Cereda, C. (2011). SOD1 Transcriptional and Posttranscriptional Regulation and Its Potential Implications in ALS. Neurol. Res. Int. Doi: 10.1155/2011/458427. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096450/

  • Miyamoto, Y., Koh, Y. H., Park, Y. S., Fujiwara, N., Sakiyama, H., Misonou, Y., Ookawara, T., Suzuki, K., Honke, K., Taniguchi, N. (2003). Oxidative stress caused by inactivation of glutathione peroxidase and adaptive responses. Biol. Chem., 384 (4), 567-574.

  • Moore, K., Roberts, L. J.2nd. (1998). Measurement of lipid peroxidation. Free Radic. Res., 28 (6), 659-671.

  • Nie, C. L., Wang, X. S., Liu, Y., Perrett, S., He, R. Q. (2007). Amyloid-like aggregates of neuronal tau induced by formaldehyde promote apoptosis of neuronal cells. BMC Neurosci., 8, 9.

  • Paglia, D. E., Valentine, W. N. (1967). Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J. Lab. Clin. Med., 70 (1), 158-169.

  • Pall, M. L. (2001). Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite. Med. Hypotheses, 57 (2), 139-145.

  • Pall, M. L. (2007). Explaining “Unexplained Illnesses”: Disease Paradigm for Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, Post-Traumatic Stress Disorder, Gulf War Syndrome and Others. New York: Informa. 150 pp.

  • Pall, M. L., Satterlee, J. D. (2001). Elevated nitric oxide/peroxynitrite mechanism for the common etiology of multiple chemical sensitivity, chronic fatigue syndrome, and posttraumatic stress disorder. Ann. N. Y. Acad. Sci., 933, 323-329.

  • Pynoos, R. S., Steinberg, A. M., Layne, C. M., Briggs, E. C., Ostrowski, S. A., Fairbank, J. A. (2009). DSM-V PTSD diagnostic criteria for children and adolescents: A developmental perspective and recommendations. J. Trauma. Stress, 22 (5), 391-398.

  • Reul, J. M., Nutt, D. J. (2008). Glutamate and cortisol-a critical confluence in PTSD? J. Psychopharmacol., 22 (5), 469-472.

  • Riddle, J. R., Smith, T. C., Smith, B., Corbeil, T. E., Engel, C. C., Wells, T. S., Hoge, C. W., Adkins, J., Zamorski, M., Blazer, D. (2007). Millennium Cohort: The 2001-2003 baseline prevalence of mental disorders in the U.S. military. J. Clin. Epidemiol., 60 (2), 192-201.

  • Sapolsky, R. M. (2000). The possibility of neurotoxicity in the hippocampus in major depression: A primer on neuron death. Biol. Psychiatry, 48 (8), 755-765.

  • Satcher, D. (2000). Mental health: A report of the Surgeon General- Executive summary. Prof. Psychol.: Res. Practice, 31 (1), 5-13.

  • Trachootham, D., Lu, W., Ogasawara, M. A., Nilsa, R. D., Huang, P. (2008). Redox regulation of cell survival. Antioxid. Redox Signal, 10 (8), 1343-1374.

  • Voicehovskis, V., Ancane, G., Voicehovska, J., Umnova, L., Skesters, A. (2011). Posttraumatic stress disorder checklist military version in Latvian language. Eur. Psychiatry, 26, 1088.

  • Watson, P., McFall, M., McBrine, C., Schnurr, P. P., Friedman, M. J., Keane, T., Hamblen, J. L. (2005). Best Practice Manual for Posttraumatic Stress Disorder (PTSD) Compensation and Pension Examinations. U.S. Dept of Veterans Affairs, Washington, D.C. 117 p.

  • Weathers, F. W., Keane, T. M., Davidson, J. (2001). Clinician-administered PTSD scale: A review of the first ten years of research. Depress. Anxiety, 13 (3), 132-156.

  • Woolliams, J. A., Wiener, G., Anderson, P. H., McMurray, C. H. (1983). Variation in the activities of glutathione-peroxidase and superoxidedismutase and in the concentration of copper in the blood in various breed crosses of sheep. Res. Vet. Sci., 34 (3), 253-256.

  • Гаврилов В. Б., Гаврилова А. Р.. Мажуль Л. М. (1987). Диализ методов определения продуктов пере кислого окисления липидов в сыворотке крови по тесту с барбитуровой кислотой [Methods of determining lipid peroxidation products in the serum using a thiobarbituric acid test].Вопросы мед. хим., 33 (1), 118-122.


Journal + Issues