2013, Number 2
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Revista Habanera de Ciencias Médicas 2013; 12 (2)
Diabetic embryopathy in rats and effect of a nutritional supplement of vitamin e during gestation
Fernández RT, Clapés HS, Suárez RG, Perera CA, Rodríguez SVM, Purón GCA, Herrera ÁM, Antiguas PÁ, Castro MT
Language: Spanish
References: 31
Page: 176-186
PDF size: 128.43 Kb.
ABSTRACT
Introduction: experimental models have obtained good results with the
supplementation of antioxidants in the prevention of the diabetic embryopathy.
However, not always the effect is beneficial and the mechanism of these results is
unclear. T
Objective: was to evaluate the effect of nutritional supplementation with vitamin E
during gestation on offspring of diabetic rats.
Materials and Methods: we used wistar rats with diabetes induced by
streptozotocin and health rats like controls. During gestation, one group of diabetic
rats and one group of controls received vitamin E 150mg/kg/day, and the others
group the vehicle. Euthanasia was practiced at 11,5 day of pregnancy and we study
the morphology of the products, DNA, proteins and oxidative stress markers in
embryos. The statistic analyze was performed with non parametric tests and the
significant differences were considered with p ‹ 0, 05.
Results: in diabetic rats with vitamin E the embryos were higher and decreased the
number of resorptions, the developmental impairment and the content of oxidative
damage markers to lipids and proteins in the embryos.
Conclusions: nutritional supplementation with vitamin E during gestation in
diabetic rats decreased the loss of the conception products, increased the growth
and development of the embryos with decreased oxidative damage to biomolecules
that will be suggest a beneficial antioxidant effect of the vitamin.
REFERENCES
Chappell JH, Dan W, Loeken MR. Diabetes and apoptosis: neural crest cells and neural tube. Apoptosis. 2009; 14: 1472-83.
Morgan SC, Relaix F, Sandell LL, Loeken MR. Oxidative stress during diabetic pregnancy disrupts cardiac neural crest migration and causes outflow tract defects. Birth Defects Research (Part A). 2008; 453-63.
Mattos I, Rodrigues LT, Damasceno DC, Vieira M. Diabetes and pregnancy: an update of the problem. ARBS Annu Rev Biomed Sci. 2007; 9:1-11.
Eriksson UJ, Borg LA. Protection by free oxygen radical scavenging enzymes against glucosa- induced embryonic malformation in Vitro. Diabetología. 1991; 34: 325-31.
Wentzel P, Thunberg L, Eriksson UJ. Teratogenic effects of diabetic serum is prevented by supplementation of superoxide dismutase and N- acetylcysteine in rat embryo culture. Diabetologia. 1997; 40: 7-14.
Zaken V, Kohen R, Ornoy A. Vitamins C and E improve rat embryonic antioxidant defense mechanism in diabetic culture medium. Teratology. 2001; 64: 33-44.
Gäreskog M, Wentzel. N-Acetylcysteine and alpha-cyano-4-hydroxycinnamic acid alter protein kinase C (PKC)-delta and PKC-zeta and diminish dysmorphogenesis in rat embryos cultured with high glucose in vitro. J Endocrinol. 2007; 192 (1): 207- 14.
Viana M, Herrera E, Bonet B. Teratogenic effects of diabetes mellitus in the rat. Prevention with vitamin E. Diabetologia. 1996; 39: 1041-46.
Simán C M, Gittenberg-De A C, Wisse B, Eriksson U J. Malformations in offspring of diabetic rats: Morphometric analysis of neural crest-derived organs and effects of maternal vitamin E treatment. Teratology. 2000; 61: 355-67.
Viana M, Castro M, Barbas C, Herrera E, Bonet B. Effect of different doses of vitamin E on the incidence of malformations in pregnant diabetic rats. Annals of Nutrition & Metabolism. 2003; 47 (1): 6-10.
Cederberg J, Eriksson UJ. Antioxidative Treatment of Pregnant Diabetic Rats Diminishes Embryonic Dysmorphogenesis. Birth Defects Research (Part A). 2005; 73: 498-505.
Wentzel P, Eriksson UJA. Diabetes-Like Environment Increases Malformation Rate and Diminishes Prostaglandin E2 in Rat Embryos: Reversal by Administration of Vitamin E and Folic Acid. Birth Defects Research (Part A). 2005; 73: 506-511.
Cederberg J, Simán C M, Eriksson UJ. Combined treatment with vitamin E and vitamin C decreases oxidative stress and improves fetal outcome in experimental diabetic pregnancy. Pediatr Res. 2001: 49: 755-62.
Gäreskog M, Eriksson U J, Wentzel P. Combined supplementation of folic acid and vitamin E diminishes diabetes-induced embryotoxicity in rats. Birth Defects Research (Part A). 2006; 76: 483-90.
Pazdro Burges RJ. The role of vitamin E and oxidative stress in diabetes complications. Mechanisms of Ageing and Development. 2010; 131(4): 276-86.
Hajiani M, Razi F, Golestani A, Frouzandeh M, Owji AA, Khaghani S, et al. Timeand dose-dependent differential regulation of copper-zinc superoxide dismutase and manganese superoxide dismutase enzymatic activity and mRNA level by vitamin E in rat blood cells. Redox Report. 2012; 17 (3): 101-7.
Chen C. S, Wells P. G. Enhanced tumorigenesis in p53 knockout mice exposed in utero to high-dose Vitamin E. Carcinogenesis. 2006; 27 (7): 1358-68.
Sakamaki H, Akazawa S, Ishibashi M, Izumino K, Takino H, Yamasaki H, et al. Significance of glutathione- dependent antioxidant system in diabetes- induced embryonic malformations. Diabetes. 1999; 48: 1138-44.
Damasceno DC, Tadeu Volpato G, Paranhos Calderon IM, Cunha Rudge MV. Oxidative stress and diabetes in pregnant rats. Animal Reproduction Science. 2002; 72: 235-44.
American Association for Laboratory Animal Science. Laboratory mouse handbook. Crestwyn Hills Drive: Menphis; 2006.
Sivan E, Lee YK, Wu YK, Reece EA. Free radical scavenging enzymes in fetal dysmorphogenesis among offspring of diabetic rats. Teratology. 1997; 56: 343-49.
Eriksson UJ, Borg LA. Diabetes and embryonic malformation. Role of substrateinduced free oxygen radical production for dysmorphogenesis in culture rat embryos. Diabetes. 1993; 42: 411-19.
Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the foling phenol reagent. J Biol Chem. 1951; 193: 265-75.
Bunce M. PCR-SSP typing. En: Bidewell Jl, Navarrete C. Histocompatibility testing. England: Imperial College Press; 2000, p. 149-86.
Esterbauer H, Cheeseman KH. Determination of aldehydic lipid peroxidation products: malondialdehyde and 4-hydroxynonenal. Meth Enzymol. 1990; 186:407- 21.
Kalousavá M, Skrha J, Zima T. Advanced glycation end-products and advanced oxidation protein products in patients with Diabetes Mellitus. Physiol Res. 2002; 51:597-604.
González E. Diabetes mellitus experimental: etiología de las malformaciones congénitas en descendientes de ratas diabéticas. Rev Cubana Endocrinol. 2002; 13(1):53-63.
Gäreskog M, Cederberg J, Eriksson UJ, Wentzel P. Maternal diabetes in vivo and high glucose concentration in vitro increases apoptosis in rat embryos. Reprod Toxicol. 2007: 23(1):63-74.
Zangen SW, Ryu S, Ornoy A. Alterations in the Expression of Antioxidant Genes and the Levels of Transcription Factor NF-Kappa B in Relation to Diabetic Embryopathy in the Cohen Diabetic Rat Model. Birth Defects Research (Part A). 2006; 76A:107114.
Wu Y, Viana M, Thirumangalathu S, Loeken MR. AMP-activated protein kinase mediates effects of oxidative stress on embryo gene expression in a mouse model of diabetic embryopathy. Diabetología. 2012; 55:245-54.
Wang XD, Morgan SC, Loeken MR. Pax 3 stimulates p53 ubiquitination and degradation independent of transcription. PLoS ONE 2011; 6(12): e29379.