• Evaluation of progressive chronic hepatitis C in children according to certain markers of oxidative stress
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Evaluation of progressive chronic hepatitis C in children according to certain markers of oxidative stress

PERINATOLOGIYA I PEDIATRIYA.2014.4(60):67–71;doi10.15574/PP.2014.60.67

Evaluation of progressive chronic hepatitis C in children according to certain markers of oxidative stress

V.S. Berezenko1, R.V. Mostovenko2, M.B. Dyba1

 

1The State Institution «Institute of Pediatrics, Obstetrics and Gynecology of The National Academy of Medical Sciences of Ukraine»

2The National Children's Specialized Hospital «Ohmatdyt»

 

 

Purpose — to study the peculiarities of chronic hepatitis C progression in children according to certain markers of oxidative stress.

 

Patients and methods. Oxidative stress was determined according to the number of ketone dinitrophenylhydrozones according to Ye.Ye. Dubinina's method. The initial level of basic 2.4 ketone dinitrophenylhydrozones (spontaneous protein oxidative modification and accumulation of basic 2.4 ketone dinitrophenylhydrozones after stimulation of protein oxidative modification by the Fenton reaction environment (induced protein oxidative modification) were determined. The rate of adaptation reserve possibilities of the organism to resist oxidative stress was calculated according to the formula (spontaneous basic 2.4 ketone dinitrophenylhydrozones x 100 / induced basic 2.4 ketone dinitrophenylhydrozones).

 

Results. The progression of chronic hepatitis C in children is accompanied by the increased sensitivity of serum proteins to oxidation and the accumulation of their oxidative modifications in serum. The greatest destruction of proteins under the influence of free radicals was observed in children with markers of progressive chronic hepatitis C, as well as in those suffering from liver cirrhosis. In healthy children the initiation of protein oxidative modification processes led to an average of a 30% increase of the oxidized proteins number, while in children with chronic hepatitis C the number of protein oxidative modification products was practically twice as much, and in children with liver cirrhosis a 150% increase was observed.

 

Conclusion. The data received testify to the depletion of adaptation reserve possibilities of the organism of children suffering from chronic hepatitis C and liver cirrhosis, as well as to their reduced ability to resist oxidative stress. A comparison of adaptation reserve possibilities rate in children with chronic hepatitis C and liver cirrhosis with ultrasound markers of fibrosis was conducted. It was determined that the adaptation reserve possibilities rate <45% can be used as a diagnostic criterion for the evaluation of progressive liver fibrosis (Sp — 76%; Se — 80%).

 

Key words: children, chronic hepatitis C, liver cirrhosis, protein oxidative modification, adaptation reserve possibilities, liver fibrosis.

 

 

REFERENCES

 

 

1. Буеверов АО. 2002. Оксидативный стресс и его роль в повреждении печени. Российский журнал гастроэнтерологии, гепатологии, колопроктологии. 4: 21—25.

2. Дубинина Е, Шугалей В. 1993. Окислительная модификация белков. Успехи современной биологии. 113,1: 71—81.

3. Меерсон Ф3, Пшенникова МГ. 1988. Адаптация к стрессорным нагрузкам и физическим нагрузкам. М., Медицина: 256.

4. Губский ЮИ, Беленичев ИФ, Павлов СВ и др. 2005. Токсикологические последствия окислительной модификации белков при различных патологических состояниях (обзор литературы). Современные проблемы токсикологии. 3: 43—46.

5. Reinheckel T, Korn S, Mohring S et al. 2000. Adaptation of protein carbonyl detection to the requirements of proteome analysis demonstrated for hypoxia/reoxygenation in isolated rat liver mitochondria. Arch. Biochem. Biophys. 1; 376(1): 59—65.

6. Berlett BS, Stadtman ER. 1997. Protein oxidation in aging, disease, and oxidative stress. J Biol Chem. 15; 272(33): 20313—20316.

7. Choi J, Ou J. 2006. Mechanisms of liver injury. III. Oxidative stress in the pathogenesis of hepatitis C virus. Am J Physiol Gastrointest Liver Physiol. 290(5): 847—851. http://dx.doi.org/10.1152/ajpgi.00522.2005; PMid:16603728

8. Fujita N, Sugimoto R, Ma N et al. 2008. Comparison of hepatic oxidative DNA damage in patients with chronic hepatitis B and C. J Viral Hepatol. 15: 498—507.

9. Levine RL, Garland D, Oliver CN et al. 1990. Determination of carbonyl content in oxidatively modified proteins. Methods in Enzymol. 186: 464—478.

10. Friedman SL. 2003. Liver fibrosis — from bench to bedside. J Hepatology. 38: 38—53.

11. Friedman SL. 2005. Molecular regulation of hepatic fibrosis, an integrated cellular response to tissue injury. J Biol Chem. 275: 2247—2250.

12. de Mochel NS, Seronello S, Wang SH et al. 2010. Hepatocyte NAD(P)H oxidases as an endogenous source of reactive oxygen species during hepatitis C virus infection. Hepatology. 52(1): 47—59. http://dx.doi.org/10.1002/hep.23671; PMid:20578128 PMCid:PMC3141587

13. Fujita N, Sugimoto R, Takeo M et al. 2007. Hepcidin expression in the liver relatively low level in patients with chronic hepatitis C. Mol Med. 13: 97—104. http://dx.doi.org/10.2119/2006-00057.Fujita; PMid:17515961 PMCid:PMC1869620

14. Levine RL. 2002. Carbonyl modified proteins in cellular regulation, aging, and disease. Free Radic Biol Med. 1; 32(9): 790—796.

15. Okuda M, Li K, Beard MR et al. 2002. Mitochondrial injury, oxidative stress, and antioxidant gene expression are induced by hepatitis C virus core protein. Gastroenterology. 122: 366—375.

16. Shepard CW, Finelli L, Alter MJ. 2005. Global epidemiology of hepatitis C virus infection. Lancet Infect Dis. 5: 558—567.

17. Davies MJ, Fu S, Wang H, Dean RT. 1999. Stable markers of oxidant damage to proteins and their application in the study of human disease. Free Radic Biol Med. 27: 1151—1163.

18. Stadtman ER, Levine RL. 2000. Protein oxidation. Ann NY Acad Sci. 899: 191—208.

19. Zaltron S, Spinetti A, Biasi L. 2012. Chronic HCV infection epidemiological and clinical relevance. BMC Infect Dis. 12, Suppl 2.