GLUTATHIONE STATUS IN DIABETES-INDUCED EMBRYOPATHIES

The mechanism involved in diabetes-induced embryotoxicity is still unc lear. Mitochondrial alterations probably produced by oxidative stress have been described in embryos developing in a diabetic environment. F urthermore, oxygen radicals-scavenging enzymes can reduce the embryoto xic effects induced by diabetic conditions. In this work we tried to t est if glutathione (GSH), a tripeptide implicated in cellular protecti on against reactive oxygen species, is involved in diabetes-related em bryotoxicity. Rat embryos were explanted on day Il on gestation from n ormal and from streptozotocin-diabetic mothers. The embryos were exami ned morphologically, then protein, DNA and GSH were determined both in embryos and in their visceral yolk sacs. The embryos explanted from d iabetic mothers showed signs of developmental retardation and 16% were morphologically abnormal. GSH content was reduced in these embryos in comparison to control, but the GSH/protein in the visceral yolk sacs of conceptuses explanted from diabetic mothers was higher than in cont rol visceral yolk sacs. Our hypothesis is that the reduction of embryo nic GSH is a consequence of the alteration in GSH transport across the yolk sac endodermal cells damaged by diabetic conditions. The observe d reduction in embryonic GSH could reduce the protection against the o xidative stress condition described in diabetic pathology.