Effects of G-6-PD deficiency, experimentally induced or genetically transmitted, on the sorbitol pathway activity. in vitro and in vivo studies
Vaca, G.; Ramírez, M.G.; Vargas, M.; Mendoza, R.; Chávez-Anaya, E.; Medina, M.D.; Alvarez, A.; Medina, C.; Sáenz, G.; Chávez, M.
Archives of Medical Research 23(1): 25-32
1992
ISSN/ISBN: 0188-4409 PMID: 1308788 Document Number: 388863
Aldose reductase catalyzes the NADPH-linked reduction of hexoses to their respective sugar-alcohols, which are involved in the pathogenesis of "sugar-cataracts". In the lenses, the reaction catalyzed by G-6-PD is the source of NADPH supply blocking sugar-alcohol formation and consequently prevents or delays the onset of "sugar-cataracts". We have investigated the effect of G-6-PD deficiency, either experimentally induced or genetically transmitted, on the sorbitol accumulation in whole cells incubated in high glucose media and on the "sugar-cataracts" formation in a galactosemic rat model. We also screened 31 Negro male adults with diabetes mellitus for red cell G-6-PD deficiency. G-6-PD deficiency produced a significant inhibition on sorbitol accumulation in rat lenses and human red cells incubated in 50 mM glucose. In the galactosemic rat model G-6-PD deficiency experimentally induced with acetaminophen delayed the development of cataracts. Finally, two diabetic individuals were G-6-PD deficient and did not show cataracts whereas cataracts were identified in six other diabetic patients.