It is rather interesting to note that the incidence of glucose-6-phosphate dehydrogenase deficiency seems to be relatively high in places where Plasmodium falciparum malaria has been a life-threatening factor for centuries, as in the Mediterranean but rare elsewhere. This distribution is typical of other main genetically controlled traits, namely sickle cell anaemia, thalassaemia, haemoglobin E (HbE) and persistent foetal haemoglobin (HbF). Apparently, there is a positive biological selective pressure for the emergence of these mutations. 4. 7. 9.The answer lies in the fact that the malarial parasites which show a surprisingly high susceptibility to oxidative stress require glutathione and the products of the glucose-6-phosphate dehydrogenase oxidative shunt for optimal growth. Not unlike the sickle cell trait which utilises an independent mechanism of protection against malaria, glucose-6-phosphate dehydrogenase deficiency creates an inhospitable environment for the malarial parasites and discourage lodging of the protozoa in the red blood cells. 1. 6. 7. 9.
Several attempts have been made to associate other conditions with glucose-6-phosphate dehydrogenase deficiency based on the study of genetic locations. Many other genes are located on the sex X-chromosome besides the glucose-6-phosphate dehydrogenase gene. By examining genes located close to the Xq28 region, a possible linkage with the expression of glucose-6-phosphate dehydrogenase enzyme can be postulated. For example, the proximity of genes for red and green pigments to Xq28 has lead to the suggestion of a linkage between glucose-6-phosphate dehydrogenase deficiency and congenital colour blindness by Yucel. A study was carried out in Turkey to test the hypothesis. It was found that that none of the colour blind subjects were glucose-6-phosphate dehydrogenase deficient and vice versa. Based on the results obtained Yucel concluded that there was a linkage disequilibrium between congenital colour blindness and glucose-6-phosphate dehydrogenase deficiency, which may be due to crossing over of the closely situated genes during meiosis. 8.Nevertheless, this does not preclude conclusively the possibility of a linkage between glucose-6-phosphate dehydrogenase deficiency and other clinically significant conditions.
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Prepared on 01 Jan 2008 by teekoonhien |
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