Sule Menziletoglu Yildiz, Sedefgul Yuzbasioglu Ariyurek, Murat Tahiroglu, Kiymet Aksoy among British was reported to be 24%, while easily modified. After the appropriate infrastructure among Iranian subjects it was 44%. It seems that has been established, the cost of the chemical the incidence of the silent mutation is higher in the substance required for the procedure may greatly population of the Mediterranean basin than among decrease, particularly when large numbers of populations of continental Europe [27]. samples need to be processed in a short period of Similar studies were performed by Kurdi-Haidar time and with a minimum of handling. et al. in 20 unrelated individuals with Gd-Med In conclusion, studying the polymorphisms of mutation from Saudi Arabia, Iraq, Iran, Jordan, the G6PD gene may facilitate the identification of Lebanon, and Israel. Except for one subject, all of the genetic basis of G6PD deficiency in different the cases were shown to have the C-to-T change at regions and in various ethnic groups. Furthermore, nucleotide 1311. Kurdi-Haidar et al. concluded that DNA polymorphisms have been shown to be very the silent mutation is an independent poly- supportive in the study of the human genome by morphism in the Middle East, and that the mutation providing markers for gene mapping as well as leading to Gd-Med deficiency probably arose on linkage analysis [30]. Although the G6PD gene holds a chromosome that already carried the silent a substantial number of polymorphic sites, whether mutation [11]. these genetic variants including the nucleotide Inconsistent with the above-mentioned reports, C1311T polymorphism could help us to understand the rate of 1311 polymorphism among our study the differences in disease severity in G6PD-deficient group was found to be low, with a percentage of individuals from distinct populations needs to be 4.7%. The most reasonable explanation for this may further clarified by additional investigations. be the extremely diverse ethnic background of the Adana population, which may be due in part to the Acknowledgments high level of immigration into this region. The G6PD This work was supported by grants from DPT- deficiency is mainly found in malaria-endemic areas, 2005K120320-E and Çukurova University, Grant No. and accordingly, it was hypothesized that G6PD TF2007BAP21. deficiency had arisen as a protective factor against lethal malaria [28]. Consistent with this data, the number of G6PD-deficient cases was reported to R e f e r e n c e s be significantly elevated in Adana, which has been 1. Beutler E, Westwood B, Kuhl W. Definition of the reported as one of the malaria-endemic regions in mutations of G6PD Wayne, G6PD Viangchan, G6PD Jammu, Turkey [8]. By using the microarray technique, and G6PD 'LeJeune'. Acta Haematol 1991; 86: 179-82. Menziletoglu Yildiz et al. revealed in a recent study 2. Lehninger AL, Nelson DL, Cox MM. Lehninger principles that the frequency of the Gd-Med mutation was of biochemistry. 5nd ed. W.H. Freeman Press, New York found to be substantially high in subjects with 3. B20e0u5tl;e3r50E-,85V.ulliamy TJ. Hematologically important G6PD deficiency in Adana [29]. However, the reason mutations: glucose-6-phosphate dehydrogenase. Blood why the number of subjects with 1311 poly- Cells Mol Dis 2002; 28: 93-103. morphism was observed to be significantly lower 4. Provan Drew. Molecular hematology. In: The molecular than expected and also below that reported by the basis of anemia. Luzzatto L, Karadimitris A. 3nd ed, John other Mediterranean countries may be the very Wiley & Sons Press 2010; 140-64. heterogeneous population residing in this area. It 5. Chalvam R, Colah RB, Mohanty D, Ghosh K, Mukherjee is also most likely that many variants of G6PD dMeBh.yMdroolgeecnualasre hdeetfeicrioegnecyneaimtyoonfggtlhuecotrsibea-6ls- pinhoWsepshteartne deficiency may exist in this area due to this highly India. Blood Cells Mol Dis 2009; 43: 156-7. divergent ethnicity. 6. Beutler E. G6PD: population genetics and clinical The PCR-based assays have been widely utilized manifestations. Blood Rev 1996; 10: 45-52. to detect the G6PD mutations and 1311 poly- 7. Altay C, Gümrük F. Red cell glucose-6-phosphate morphism. To our knowledge, this study represents dehydrogenase deficiency in Turkey. Turk J Hematol 2008; the first report of 1311 polymorphism in the 25: 1-7. Cukurova Region with the microarray technique. 8. YStüurdeigeisr oGnTr,edAckeslolygluKc,osAer-p6a-pchioAsp,hUantelüdkeuhrytdrIo,gTeunlaisAe:. The Nanogen® microarray system enabled us to evaluation of reference values. Ann Clin Biochem 1994; design a new probe to detect the 1311 poly- 31: 50-5. morphism in G6PD-deficient cases, and the results 9. Abdel Fattah M, Abdel Ghany E, Adel A, Mosallam D, obtained from the newly designed microarray probe Kamal S. Glucose-6-phosphate dehydrogenase and red were confirmed by the RFLP. We suggest that the cell pyruvate kinase deficiency in neonatal jaundice cases microarray technique can be safely utilized not only in egypt. Pediatr Hematol Oncol 2010; 7: 262-71. for analysis of mutations and gene expression, but 10. dBeefuictlieernEc,yDaunpdaarcnSti.mGal ulacroiasel-d6r-upghdoespvehlaotpemdeenhty.dAromgeJnTarospe also for detecting the single nucleotide poly- Med Hyg 2007; 77: 779-89. morphisms. Furthermore, it seems that it can also 11. Kurdi-Haidar B, Mason PJ, Berrebi A, et al. Origin and be used to develop new applications as it can be spread of the glucose-6-phosphate dehydrogenase variant 590 Arch Med Sci 4, August / 2011