Cantó Catalá, AntolínAlmansa Frías, María InmaculadaHernández Rabaza, VicenteLópez Pedrajas, Rosa MaríaMartínez González, JavierMiranda Sanz, MaríaOlivar Rivas, TeresaUCH. Departamento de Ciencias BiomédicasProducción Científica UCH 20222023-04-012023-04-012022-09-29Cantó, A., Martínez-González, J., Almansa, I., López-Pedrajas, R., Hernández-Rabaza, V., Olivar, T. & Miranda, M. (2022). Time-course changes in oxidative stress and inflammation in the retinas of rds mice: a retinitis pigmentosa model. Antioxidants, vol. 11, i. 10 (29 sep.), art. 1950. DOI: https://doi.org/10.3390/antiox111019502076-3921 (Electrónico)http://hdl.handle.net/10637/14191Este artículo se encuentra disponible en la siguiente URL: https://www.mdpi.com/2076-3921/11/10/1950Este artículo de investigación pertenece al número especial "Retinal Diseases Associated with Oxidative Stress: Advances in Pathophysiology and Therapeutic Approaches".(1) Background: Retinitis pigmentosa (RP) is characterized by progressive photoreceptor death. A Prph2Rd2 or an rds mouse is an RP model that closely reflects human RP. The objective of this study was to investigate the relationship of rod and cone death with oxidative stress and inflammation in rds mice. (2) Methods: The retinas of control and rds mice on postnatal days (PN) 11, 17, 21, 28, 35, and 42 were used. Oxidative damage to macromolecules, glutathione (GSH and GSSG), GSH synthesis enzymes, glial fibrillar acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba1), and cluster of differentiation 68 (CD68) was studied. (3) Results: The time sequence of oxidative stress and inflammation changes in rds mice occurs as follows: (i) At PN11, there is a small increase in photoreceptor death and in the microglial cells; (ii) at PN17, damage to the macromolecules is observed; (iii) at PN21, the maximum photoreceptor death rate is detected and there is an increase in GSH-GSSG and GFAP; (iv) at PN21, the microglial cells are activated; and(v) at PN28, there is a decrease in GSH synthesis enzymes. (4) Conclusions: These findings contribute to the understanding of RP physiopathology and help us to understand whether oxidative stress and inflammation are therapeutic targets. These findings contribute to our understanding that, in RP, oxidative stress and inflammation evolution and their relationship are time-dependent. In this sense, it is important to highlight that both processes are potential therapeutic targets in this disease.application/pdfenopen accessRetina - Diseases - Treatment.Retinitis pigmentaria - Tratamiento.Estrés oxidativo - Tratamiento.Glutatión - Uso terapéutico.Retina - Enfermedades - Tratamiento.Oxidative stress - Treatment.Retinitis pigmentosa - Treatment.Hemodialysis.Exercise - Computer simulation.Glutathione - Therapeutic use.Artículohttps://doi.org/10.3390/antiox11101950https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es