Estudio de los mecanismos de apoptosis y mitosis en el globo ocularModelo experimental del síndrome tóxico gestacional

  1. S. Pons-Vázquez
  2. V. Vila-Bou
  3. V. Zanon-Moreno
  4. F.J. Iborra
  5. R. Gallego-Pinazo
  6. P.M. Melo
  7. J.J. García-Medina
  8. M.D. Pinazo-Durán
Journal:
Archivos de la Sociedad Española de Oftalmologia

ISSN: 0365-6691

Year of publication: 2008

Volume: 83

Issue: 1

Pages: 37-43

Type: Article

DOI: 10.4321/S0365-66912008000100008 DIALNET GOOGLE SCHOLAR lock_openOpen access editor

More publications in: Archivos de la Sociedad Española de Oftalmologia

Abstract

Objective: To improve knowledge of the mechanisms of cellular differentiation and proliferation during retinal development, by studying cellular and molecular damage in a rat model of prenatal ethanol exposure. Methods: Female, juvenile Wistar rats (200g body weight) and their offspring were divided into two groups, which were fed a liquid diet: 1) ethanol-exposed group (5% ethanol weight/vol as 35% of daily total calories) and 2) isocaloric control group (maltose/dextrin as 35% of daily total calories). Eyeballs were obtained at 21 days of gestation, embedded in paraffin, and immunodetection procedures performed on apoptotic (TUNEL) and mitotic profiles, which were observed and photographed using a confocal microscope. Results: Analysis of the microphotographs revealed a statistically significant increase of apoptotic profiles and a decrease in mitotic profiles in the ethanol exposed group compared to controls (p<0.05). Ganglion cells and photoreceptors showed more changes than other retinal cell phenotypes. These findings suggest that abnormalities in the differentiation and proliferation processes of the retina were caused by the alcohol exposure. Conclusions: Alcohol abuse during pregnancy alters development of the visual system by inducing developmental changes in the mitotic and apoptotic processes of the retina. These latter changes may be the result of changes in the expression of regulatory genes as well as the result of alteration in signalling pathways for both differentiation-proliferation and apoptotic events.

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