2012, Number 2
<< Back Next >>
Rev Cub Gen 2012; 6 (2)
Oxidative stress markers in cuban patients having a phase I-compatible clinical phenotype of xeroderma pigmentosum
Acosta ST, Riverón FG, Hernández REW, Martínez BO, Lantigua CA
Language: Spanish
References: 25
Page: 21-25
PDF size: 390.28 Kb.
ABSTRACT
Xeroderma pigmentosum is a genodermatosis caused by defects in repairing damaged ADN. Scientific evidences have demonstrated the association between the main clinical symptoms of this disease and oxidative stress related events. The behavior of oxidative damage and antioxidative markers was evaluated at the system level in 23 Cuban patients having a clinical phenotype compatible with phase I of xeroderma pigmentosum and also in 66 apparently healthy subjects as controls. Concentrations in plasma of malonyldialdehyde, advanced protein oxidation products and free thiol groups, as well as the specific enzymatic activities of Cu/Zn dismutase superoxide and catalase were determined by the application of spectrophotometric techniques reported in the literature. An increase in malonyldialdehyde and advanced protein oxidation products, also a decrease in thiol groups and in the catalase enzymatic activity were observed in patients respect to those in the control group. No differences between groups were observed regarding dismutase superoxide activity. The studied patients exhibited an increase in oxidative damage regarding lipids and proteins, with a decrease in the antioxidative response capacity at the system level.
REFERENCES
Kraemer K. Xeroderma pigmentosum. Gene Reviews. [en línea] 2008 [fecha de acceso May 2011]. URL disponible en: 1. http://www.genetests.org
Stary A, Sarasin A. The genetics of the hereditary xeroderma pigmentosum syndrome. Biochimie. 2002;84:49-602.
Kraemer KH, Lee MM, Scott J. Xeroderma pigmentosum: cutaneous, ocular, and neurologic abnormalities in 830 published cases. 3. Archives of Dermatology. 1987;123(3):241–50.
Ulrich R. Hengge E, Steffen E. Molecular mechanism of xeroderma pigmentosum. In: Ahmad S, Hanaoka F, editors. Advances in 4. Experimental Medicine and Biology: 2009: p.1-19
Halliwel LB, Gutteridge JM. Cellular response to oxidative stress: adaptation, damage, repair, senescence and death. In Free Radi5. cal in Biology and Medicine. Oxford: Oxford University Press: 2007:p.187–267
Masaharu H. Oxidative stress in developmental brain disorders. Neuropathology. 2009;29(1):1-8.6.
Jacobs D, DeMott W, Grady H, Horvat R, Huestis D and Kasten B. Laboratory test handbook. 1st ed.Hudson. LEXI-COMP 7. INC:1996:p.19
Witko-Sarsat V, Friedlander M. Advanced oxidation protein products as novel mediators of inflammation and monocytes activation 8. in chronic renal failure. Journal of Immunology. 1998;161:2524-32.
Sedlak J, Lidsay, RH. Estimation of total protein bound and non-protein sulfhydryl group in tissue with Ellman’s reagent. Analytical 9. Biochemistry. 1968;25:192-205.
Marklund S, Marklund G. Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay 10. for superoxide dismutase. European Journal of Biochemistry.1974;47:469-74.
Aebi H. Catalase in vitro. Methods enzymology. 1984;105:121-6.11.
Blumberg J. Use of biomarkers of oxidative stress in research studies. Journal of. Nutrition.2004;134:S3188-9.12.
ILSI Europe & Antioxidant. Markers of Oxidative Damage and Antioxidant Protection: Current Status and Relevance to Disease 13. 2000 ILSI Europe Report Series August 2000. ILSI, Brussels, Belgium.
Del Rio D, Stewart AJ, Pellegrini N. A review of recent studies on malondialdehyde as toxic molecule and biological marker of 14. oxidative stress. Nutrition, Metabolism and Cardiovascular Disease. 2005;15(4):316-28.
Barja de Quiroga G. Radicales libres y antioxidants [Tesis en opción del título de doctor en Ciencias Químicas]. Madrid. 15. Universidad Complutense: 2000.
Serra JA, Domínguez RO, Marschoff ER, Guareschi EM, Famulari AL, Boveris A. A systemic oxidative stress associated with the 16. neurological diseases of aging. Neurochemical Research. 2009;34:212-32.
Bickers D17. , Athar M. Oxidative stress in the pathogenesis of skin disease Journal of Investigative Dermatology. 2006;126:2565–75.
Dröge W. Free adicals in the physiological control of cell function. Physiological Reviews. 2002;82:47–95.18.
Rossi R, Colombo R, Milzani A. Biomarkers of oxidative damage in human disease. Clinical Chemistry. 2006;52(4):601-23.19.
Turrens JF. Superoxide dismutase and catalase. In Comprehensive Toxicology. McQueen Ch, editors. 220. nd Edition. New York; 2010: p.219-27.
Jaeschke H. Antioxidant defence mechanisms. In Comprehensive Toxicology. McQueen Ch, editors. New York. 221. nd Edition: 2010: p.319-37.
Fitzpatrick J, Bhargava A, Bedwani R, Gagnon M. Evaluation of blood catalase estimation for diagnosis of malignancy. Journal 22. of Surgical Oncology. 2006;1:37-41.
Pagano G, Korkina I, Brunk U, Chessa I, Degan P, del Principe D. Congenital disorders sharing oxidative stress and cancer 23. proneness as phenotypic hallmarks: prospects for joint research in pharmacology. Medical Hypotheses.1998;51:253-66.
Villaume M, Daya L, Vincens P, Pennetier JL. Striking differences in cellular catalase activity between two DNA repair-deficient 24. diseases: xeroderma pigmentosum and trichothiodystrophy. Carcinogenesis 1992;13:321-8.
Reed M, Thomas R, Pavisic J, James S, Ulrich C and Nijhout H. A mathematical model of glutathione metabolism. Theoretical 25. Biology and Medical Modelling. 2008;5:8-16.