April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa
Author Affiliations & Notes
  • M. Miranda
    Physiology, Universidad CEU-Cardenal Herrera, Moncada, Valencia, Spain
  • V. Sanchez-Vallejo
    Physiology, Universidad CEU-Cardenal Herrera, Moncada, Valencia, Spain
  • R. Alvárez-Nólting
    Physiology, Universidad CEU-Cardenal Herrera, Moncada, Valencia, Spain
  • P. A. Ekstrom
    Ophthalmology, Clinical Sci Lund, Lund University, Lund, Sweden
  • T. Van Veen
    Wallenberg Retina Ctr, Lund University Hospital, Lund, Sweden
  • Footnotes
    Commercial Relationships  M. Miranda, None; V. Sanchez-Vallejo, None; R. Alvárez-Nólting, None; P.A. Ekstrom, None; T. Van Veen, None.
  • Footnotes
    Support  Partially supported by Copernicus-Santander Program and Foundation Fighting Blindness (USA).
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3318. doi:
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      M. Miranda, V. Sanchez-Vallejo, R. Alvárez-Nólting, P. A. Ekstrom, T. Van Veen; The Effect of the Administration of Buthionine Sulfoximine in a Model of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3318.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : We have administered Buthionine sulfoximine (BSO) an inhibitor of gamma-glutamylcysteine synthetase to wild type and rd1 mice, an animal model of retinitis pigmentosa, to study its influence over retina development and retinal pathology.

Methods: : Two groups of wild type and rd1 mice received an intraperitoneal (ip) injection of BSO (1,5 g/kg body weight) once daily for eight consecutive days starting from postpartum day 3. In addition, another two group of wild type and rd1 pups received ip injections of BSO and the combination of antioxidants orally. Malondialdehyde (MDA) and glutathione (GSH) concentratioms as well as glutahione peroxidase (GPx) and glutathione reductase (GSSG-R) activities were measured and TUNEL, as well, as GSH inmunostaining were performanced.

Results: : BSO treatment decreased GSH in wild type and rd1 retinas as well as the ratio GSH/GSSG, the administration of antioxidants to BSO treated animals produced an small but non significant increase in both parameters.When BSO was administered daily antioxidants failed to increase retinal glutathione concentration or to decrease the number in TUNEL positive cells. In all groups BSO induced cataracts.

Conclusions: : The administration of BSO to control and rd1 mice depleted retina from GSH and the administration of our mixture of antioxidants could not increase it. Moreover when administered BSO and antioxidants at the same time, antioxidants failed to prevent photoreceptor apoptosis.

Keywords: antioxidants • retinal degenerations: cell biology • retina 

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