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E. Peiretti, S. Dessì, D. Intilla, C. Mulas, C. Abete, M. Vinci, F. Orrù, I. Zucca, M. Fossarello; Pterygium and Glucose-6-Phosphate Dehydrogenase Deficiency. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5289.
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Recently, we have demonstrated that glucose-6-phosphate dehydrogenase (G6PD) deficient subjects are more prone to develop pterygia as compared to their G6PD normal counterpart. This lesion is considered to result from abnormal proliferation of conjunctival fibroblasts perhaps triggered by UV induced DNA damage, via the formation of reactive oxygen species (ROS). On the basis of this observation, we hypothesize that G6PD deficient subjects may be more exposed to DNA damage and pterygial formation due to their relative impaired capability to produce reduced molecular species [nicotinamide adenine dinucleotide phosphate hydrogenase (NADPH) and glutathione(GSH)] able to neutralize ROS. The aim of the present study was to explore possible molecular mechanisms to explain this hypothesis.
To test this hypothesis we used fibroblasts isolated from pterygial lesions of G6PD deficient and normal patients as well as fibroblasts from normal conjunctiva obtained at surgery from G6PD deficient and normal subjects undergoing cataract removal. In these cells we measured the amount of NADPH formation and the level of reduced GSH as well as the expression of G6PD mRNA by RT-PCR.
We found that, when growth-stimulated, G6PD-deficient fibroblast cell cultures from both pterygial lesions and normal conjunctiva had a slightly increased growth rate, as compared to non-deficient fibroblasts. Interestingly, growth-stimulated G6PD-deficient fibroblasts showed increased expression levels of G6PD mRNA. On the other hand, as expected, basal levels of NADPH and GSH were reduced in G6PD-deficient fibroblasts as compared to controls.
Although preliminary, these results support the hypothesis that G6PD-deficient fibroblasts may be more prone to oxidative DNA damage as compared to non-deficient cells, thus favoring the initiation of the pterygial lesion. In addition, we propose that the observed up-regulation of G6PD mRNA in G6PD-deficient fibroblasts could further contribute to pterygial progression by providing increased amounts of pentose phosphates for nucleic acid synthesis.
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