title: Vitamin E decreases the occurrence of malformations in the offspring of diabetic rats.
abstract: An association between excess oxygen radical activity and disturbed embryogenesis in diabetic pregnancy has been suggested. In the present study, the protective capacity of vitamin E with different treatment regimens was investigated in early and late pregnancy of streptozotocin-induced diabetic rats. Daily gavaging of 0.2 g/kg or 0.8 g/kg of vitamin E exerted moderate protective effects. In contrast, treatment with a diet enriched with 2% (wt/wt) of vitamin E, yielding an approximate daily dosage of 2 g/kg of vitamin E, clearly restored both embryonic and fetal morphology. High-performance liquid chromatography measurement showed that maternal diabetes decreased embryonic content of vitamin E. When pregnant diabetic animals were supplemented with vitamin E, increased concentrations of the vitamin were found in maternal, embryonic, and fetal tissues. Thus, despite marked accumulation of vitamin E in maternal tissues, the compound apparently reached the conceptus. Thiobarbituric acid reactive substances (TBARS) were estimated as a measure of lipid peroxidation, and no changes were observed in maternal tissue, embryonic tissue, placenta, and fetal brain in the untreated diabetic group. In contrast, a fivefold increase of TBARS was found in fetal liver, a rise that was reduced with vitamin E treatment of the diabetic pregnant rats and completely normalized with 2% vitamin E in the diet. Congenital malformations caused by experimental diabetes can be prevented by antioxidants in vivo. These findings further corroborate the notion that an imbalance in the metabolism of free oxygen radicals is involved in the embryonic maldevelopment of diabetic pregnancy, and suggest a direction for prophylactic treatment in the future.
authors.affiliation: Department of Medical Cell Biology, Uppsala University, Sweden. martin.siman@medcellbiol.uu.se
authors.forename: C M
authors.initials: CM
authors.lastname: Simán
authors.forename: U J
authors.initials: UJ
authors.lastname: Eriksson
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis / Q000187:drug effects / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000188:drug therapy / Q000196:embryology*; D004622:Embryo, Mammalian / Q000002:abnormalities* / Q000187:drug effects / Q000502:physiology; D005314:Embryonic and Fetal Development / Q000187:drug effects* / Q000502:physiology; D005260:Female; D005865:Gestational Age; D015227:Lipid Peroxidation / Q000187:drug effects; D008431:Maternal-Fetal Exchange / Q000187:drug effects; D009929:Organ Size / Q000187:drug effects; D010920:Placenta / Q000187:drug effects / Q000502:physiology; D011247:Pregnancy; D011256:Pregnancy Outcome; D011254:Pregnancy in Diabetics / Q000188:drug therapy / Q000196:embryology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism; D014810:Vitamin E / Q000097:blood / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D001786:Blood Glucose; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E