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bueno_a_me_botfm.pdf: 693767 bytes, checksum: 41a33fd1c28d4062c5457b2ea2de4450 (MD5) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / In vitro studies suggest that maternal hyperglycemia insult impairs the early embryogenesis in the preimplantation period. In this paper, we show that streptozotocin given at birth day of life or in adulthood of rats caused hyperglycemic state. Regardless of hyperglycemic intensities (mild or severe diabetes), the embryos of these dams presented development retardation and decreased development competence. Apoptosis was detected using terminal dUTP nick end labeling (TUNEL) assays, and the morulas from mild and severe diabetic rats have a higher incidence of apoptotic cells than control embryos. Tumor necrosis factor-alpha, a cytokine whose synthesis is up-regulated in the diabetic uterus, did not alter the incidence of TUNEL-positive nuclei. The glycemic intensity is related with the increased in the apoptosis indexes in morulas. On the other hand, dams with hyperglycemia, regardless of the glycemic intensity and of the tumor necrosis factor-alpha level presented preimplantation embryos with development retardation and increase of non-viable preimplantation embryos, suggesting that the presence of the hyperglycemia leads to a decreased competence development of preimplantation embryos
| Identifer | oai:union.ndltd.org:IBICT/oai:repositorio.unesp.br:11449/99239 |
| Date | 10 February 2012 |
| Creators | Bueno, Aline [UNESP] |
| Contributors | Universidade Estadual Paulista (UNESP), Damasceno, Débora Cristina [UNESP], Sinzato, Yuri Karen [UNESP] |
| Publisher | Universidade Estadual Paulista (UNESP) |
| Source Sets | IBICT Brazilian ETDs |
| Language | Portuguese |
| Detected Language | English |
| Type | info:eu-repo/semantics/publishedVersion, info:eu-repo/semantics/masterThesis |
| Format | 21 f. |
| Source | Aleph, reponame:Repositório Institucional da UNESP, instname:Universidade Estadual Paulista, instacron:UNESP |
| Rights | info:eu-repo/semantics/openAccess |
| Relation | -1, -1, -1 |
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