Preview

General Reanimatology

Advanced search

Oxidant-Antioxidant Balance in Severe Brain Injury

https://doi.org/10.15360/1813-9779-2010-1-22

Abstract

Objective: to study the time course of changes in oxidative status parameters and their relationship with inflammation mediators in the acute period of severe brain injury (SBI). Subjects and methods. One hundred and thirteen patients aged 17—67 years were examined. The injury was closed and open in 54 (47.8%) and 59 (52.2%) patients, respectively. Severe brain contusions were observed in 47 patients, diffuse axonal lesions were seen in 2, and intracranial hematomas were present in 64 patients. The Glasgow coma scores for admission consciousness loss were 6.8±0.25. A control group comprised 23 healthy individuals. The significance of differences was estimated by Student’s test, Wilcoxon-Mann-Whitney, test, Spearman’s correlation test. Venous blood samples were used to study total oxidative activity (TOA) and total antioxidative activity (TAA), diene conjugates, lactic acid, albumin, transferrin (TF), ceruloplasmin, C-reactive protein, and lactoferrin (LF) were measured in venous blood on disease days 1, 4, 7, 10, 14, and 21. The profile of plasma cytokines (IL-1j8, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, TNF-а, and IFN-y) was studied by flow fluorometry on a Cytomics FC 500 cytofluorometer (Beckman Counlter, USA) (reagents were from Bender Medsystems, Austria). Results. In SBI, there was an increase in oxidants, a reduction in antioxidant activity, and lipid peroxidation activation, which were closely related. The oxidation coefficient (TOA/TAA) was 40 times greater than the normal values on days 7 to 10. The oxidation parameters were found to be associated with inflammation and cytokine-mediated immunological reactions. The time course of changes in the study proteins was characteristic for systemic inflammation and there was an association with oxidative processes only for ceruloplasm. TF was found to have an association with IL-5 and IL-10, which reflects its involvement in immunological reactions. The association with hypoxia was established for IL-6 and LF. Ihe elevation or LF was directly caused by the neutrophil activating factor IL-8. Conclusion. Oxidative stress is an important factor in impairing hemostasis in SBI. The processes of oxidation and antioxidation are associated with inflammation and cytokine-mediated immunological reactions. Key words: severe brain injury, oxidative stress, cytokines, acute inflammation phase proteins.

References

1. Deng Y., Thompson B. M, Gao X., Hall E. D.

2. Williams A. J., Wei H. H, Dave J. R., Tortella F. C.Acute and delayed neu-roinflammatory response following experimental penetrating ballistic brain injury in the rat. J. Neuroinflammation 2007; 4: 17.

3. Folkersma H, Breve J. J., Tilders F. J. et al.Cerebral microdialysis of interleukin (IL)-1beta and IL-6: extraction efficiency and production

4. in the acute phase after severe traumatic brain injury in rats. Acta Neurochir. (Wien) 2008; 150 (12): 1277—1284.

5. Droge W.Free radicals in the physiological control of function. Physiol. Rev. 2002; 82 (1): 94—95.

6. Hzecka J.The protective role of ceruloplasmin against the activity of free radicals in brain ischaemia. Ann. Univ. Mariae Curie Sklodowska Med. 1996; 51: 97—101.

7. Nayak C. D, Nayak D. M., Raja A., Rao A.Erythrocyte indicators of oxidative changes in patients with graded traumatic head injury. Neurol. India 2008; 56 (1): 31—35.

8. Гаврилов В. Б., Мишкорудная М. И.Спектрофотометрическое определение содержания гидроперекисей липидов в плазме крови. Лаб. дело 1983; 3: 33—36.

9. Картавенко В. И., Голиков П. П., Давыдов Б. В., Андреев А. А.Состояние перекисного окисления липидов и антиоксидантной системы у пострадавших с тяжелой сочетанной травмой. Патол. физиол. эксперим. терапия 2004; 1: 8—10.

10. Унжаков В. В., Сухотин С. К.Влияние различных методов седации у больных с острой тяжелой черепно-мозговой травмой на перекис-ное окисление липидов. Общая реаниматология 2008; IV (5): 10—13.

11. Капитонов В. М., Остапченко Д. А., Немцова Е. Р.Применение лак-тоферрина при лечении больных с тяжелой сочетанной травмой. Общая реаниматология 2009; V (5): 10—15.

12. Родоман Г. В., Шалаева Т. И., Добрецов Г. Е. и соавт.Сывороточный альбумин при синдроме системной воспалительной реакции. Анестезиология и реаниматология 2006; 2: 62—64.

13. Sengupta S., Wehbe C., Majors A. K. et al.Relative roles of albumin and ceruloplasmin in the formation of homocystine, homocysteine-cysteine-mixed disulfide, and cystine in circulation. J. Biol. Chem. 2001; 276 (50): 46896—46904.

14. Weinhold B., Bader A., Poli V., Ruther U.Interleukin-6 is necessary, but not sufficient, for induction of the human C-reactive protein gene in vivo. Biochem. J. 1997; 325 (3): 617—621.

15. Назаров П. Г.Реактанты острой фазы воспаления. СПб.: Наука; 2001.

16. Шевченко О. П., Орлова О. В., Шевченко Ф. О.Церулоплазмин. М.: Реафарм; 2005.

17. Орлов Ю. П., Долгих В. Т., Глущенко А. В. и соавт.Роль сывороточного железа в активации процессов липопероксидации при критических состояниях. Общая реаниматология 2006; II (3): 18—22.

18. Monteiro H. P., Winterbourn C. C.The superoxide-depend transfer of iron from ferritin to transferring and lactoferrin. Biochem. J. 1988; 256 (3): 923—928.

19. Britigan B. E., Serddy J. S., Hayek M. B. et al.Uptake of lactoferrin by mononuclear phagocytes inhibits ability to from hydroxyl radical and protects them from membrane autoperoxidation. J. Immunol. 1991; 147 (12): 4271—4277.

20. Галкина Е. В., Назаров П. Г., Полевщиков А. В.Влияние белков острой фазы воспаления и IL-8 на процессы трансэндотелиальной миграции нейтрофилов. Мед. иммунол. 1999; 1 (3—4): 11—12.

21. Lloyd E., Somera-Molina K., Van Eldik L. J. et al.Suppression of acute proinflammatory cytokine and chemokine upregulation by post-injury administration of a novel small molecule improves long-term neurologic outcome in a mouse model of traumatic brain injury. J. Neuroinflammation 2008; 5: 28.

22. Ozdemir D., UysalN., Gonenc S. et al.Effect of melatonin on brain oxida-tive damage induced by traumatic brain injury in immature rats. Physiol. Res. 2005; 54 (6): 631—637.

23. Turner R.J., Dasilva K. W’., O ‘Connor C. et al.Magnesium gluconate offers no more protection than magnesium sulphate following diffuse traumatic brain injury in rats. J. Am. Coll. Nutr. 2004; 23 (5): 541S—544S.


Review

For citations:


Yepifantseva N.N., Borshchikova T.I., Churlyaev Yu.A., Ratkin I.K., Nikiforova N.V., KlochkovaAbelyants S.A., Kheringson L.G. Oxidant-Antioxidant Balance in Severe Brain Injury. General Reanimatology. 2010;6(1):22. (In Russ.) https://doi.org/10.15360/1813-9779-2010-1-22

Views: 995


Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.


ISSN 1813-9779 (Print)
ISSN 2411-7110 (Online)