Ann Dermatol.  2010 Aug;22(3):279-283. 10.5021/ad.2010.22.3.279.

Erythrocyte Malondialdehyde and Glutathione Levels in Vitiligo Patients

• Shin JW
• Nam KM
• Choi HR
• Huh SY
• Kim SW
• Youn SW
• Huh CH
• Park KC

• KMID: 2265360
• DOI: http://doi.org/10.5021/ad.2010.22.3.279

Abstract

BACKGROUND
Vitiligo is an acquired and progressive hypomelanotic disease that manifests as circumscribed depigmented patches on the skin. Although the precise mechanism remains to be elucidated, an imbalance of the oxidant/antioxidant system has been proposed as an important etiologic mechanism.
OBJECTIVE
The objective of this study was to evaluate the oxidant/antioxidant status of vitiligo patients at the erythrocyte level.
METHODS
Fifty-three vitiligo patients and 65 phototype-, age-, and sex-matched healthy controls were included in this study. Blood samples were collected from all subjects, and all patients were instructed to answer a questionnaire.
RESULTS
Erythrocyte levels of malondialdehyde (MDA) and glutathione (GSH) were measured. All patients were told to answer a questionnaire regarding their habitual behavior, including frequency of smoking and type of diet. We observed significantly lower levels of GSH in vitiligo patients, but the levels of MDA did not differ between patients and controls. Vitiligo patients who smoked showed significantly lower GSH levels compared to non-smoking patients, but the levels of MDA were unchanged between the 2 groups.
CONCLUSION
From our results, we conclude that reduced erythrocytic or systemic GSH levels constitute a distinctive feature in vitiligo patients regardless of disease activity.

Keyword

Erythrocyte; Glutathione; Malondialdehyde; Smoking; Vitiligo

MeSH Terms

Diet
Erythrocytes
Glutathione
Humans
Malondialdehyde
Skin
Smoke
Smoking
Vitiligo
Surveys and Questionnaires
Glutathione
Malondialdehyde
Smoke

Reference

1. Ongenae K, Van Geel N, De Schepper S, Naeyaert JM. Effect of vitiligo on self-reported health-related quality of life. Br J Dermatol. 2005. 152:1165–1172.

2. Sampogna F, Raskovic D, Guerra L, Pedicelli C, Tabolli S, Leoni L, et al. Identification of categories at risk for high quality of life impairment in patients with vitiligo. Br J Dermatol. 2008. 159:351–359.

3. Dammak I, Boudaya S, Ben Abdallah F, Turki H, Attia H, Hentati B. Antioxidant enzymes and lipid peroxidation at the tissue level in patients with stable and active vitiligo. Int J Dermatol. 2009. 48:476–480.

4. Passi S, Grandinetti M, Maggio F, Stancato A, De Luca C. Epidermal oxidative stress in vitiligo. Pigment Cell Res. 1998. 11:81–85.

5. Schallreuter KU, Wood JM, Berger J. Low catalase levels in the epidermis of patients with vitiligo. J Invest Dermatol. 1991. 97:1081–1085.

6. Yildirim M, Baysal V, Inaloz HS, Can M. The role of oxidants and antioxidants in generalized vitiligo at tissue level. J Eur Acad Dermatol Venereol. 2004. 18:683–686.

7. Cross CE, Halliwell B, Borish ET, Pryor WA, Ames BN, Saul RL, et al. Oxygen radicals and human disease. Ann Intern Med. 1987. 107:526–545.

8. Cucchi ML, Frattini P, Santagostino G, Orecchia G. Higher plasma catecholamine and metabolite levels in the early phase of nonsegmental vitiligo. Pigment Cell Res. 2000. 13:28–32.

9. Cucchi ML, Frattini P, Santagostino G, Preda S, Orecchia G. Catecholamines increase in the urine of non-segmental vitiligo especially during its active phase. Pigment Cell Res. 2003. 16:111–116.

10. Morrone A, Picardo M, de Luca C, Terminali O, Passi S, Ippolito F. Catecholamines and vitiligo. Pigment Cell Res. 1992. 5:65–69.

11. Park ES, Kim SY, Na JI, Ryu HS, Youn SW, Kim DS, et al. Glutathione prevented dopamine-induced apoptosis of melanocytes and its signaling. J Dermatol Sci. 2007. 47:141–149.

12. Picardo M, Passi S, Morrone A, Grandinetti M, Di Carlo A, Ippolito F. Antioxidant status in the blood of patients with active vitiligo. Pigment Cell Res. 1994. 7:110–115.

13. Casiano CA, Pacheco FJ. Pollard KM, editor. Cell death and autoimmunity. Autoantibodies and autoimmunity: molecular mechanisms in health and disease. 2006. 1st ed. Weinheim: Wiley-VCH;103–137.

14. Huang CL, Nordlund JJ, Boissy R. Vitiligo: a manifestation of apoptosis? Am J Clin Dermatol. 2002. 3:301–308.

15. Namazi MR. Neurogenic dysregulation, oxidative stress, autoimmunity, and melanocytorrhagy in vitiligo: can they be interconnected? Pigment Cell Res. 2007. 20:360–363.

16. Simon HU, Haj-Yehia A, Levi-Schaffer F. Role of reactive oxygen species (ROS) in apoptosis induction. Apoptosis. 2000. 5:415–418.

17. Kose K, Yazici C, Cambay N, Ascioglu O, Dogan P. Lipid peroxidation and erythrocyte antioxidant enzymes in patients with Behcet's disease. Tohoku J Exp Med. 2002. 197:9–16.

18. Yildirim M, Baysal V, Inaloz HS, Kesici D, Delibas N. The role of oxidants and antioxidants in generalized vitiligo. J Dermatol. 2003. 30:104–108.

19. Deakin SP, James RW. Genetic and environmental factors modulating serum concentrations and activities of the antioxidant enzyme paraoxonase-1. Clin Sci (Lond). 2004. 107:435–447.

20. Solak ZA, Kabaroglu C, Cok G, Parildar Z, Bayindir U, Ozmen D, et al. Effect of different levels of cigarette smoking on lipid peroxidation, glutathione enzymes and paraoxonase 1 activity in healthy people. Clin Exp Med. 2005. 5:99–105.