Oxidative stress in retinal degeneration promoted by constant LED light
- Autores
- Benedetto, Maria Mercedes; Contin, Maria Ana
- Año de publicación
- 2019
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Light pollution by artificial light, might accelerate retinal diseases and circadian asynchrony. The excess of light exposure is a growing problem in societies, so studies on the consequences of long-term exposure to low levels of light are needed to determine the effects on vision. The possibility to understand the molecular mechanisms of light damage will contribute to the knowledge about visual disorders related to defects in the phototransduction. Several animal models have been used to study retinal degeneration (RD) by light; however, some important aspects remain to be established. Previously, we demonstrated that cool white treatment of 200 lux light-emitting diode (LED) induces retinal transformation with rods and cones cell death and significant changes in opsin expression in the inner nuclear layer (INL) and ganglion cell layer (GCL). Therefore, to further develop describing the molecular pathways of RD, we have examined here the oxidative stress and the fatty acid composition in rat retinas maintained at constant light. We demonstrated the existence of oxidative reactions after 5 days in outer nuclear layer (ONL), corresponding to classical photoreceptors; catalase (CAT) enzyme activity did not show significant differences in all times studied and the fatty acid study showed that docosahexaenoic acid decreased after 4 days. Remarkably, the docosahexaenoic acid diminution showed a correlation with the rise in stearic acid indicating a possible association between them. We assumed that the reduction in docosahexaenoic acid may be affected by the oxidative stress in photoreceptors outer segment which in turn affects the stearic acid composition with consequences in the membrane properties. All these miss-regulation affects the photoreceptor survival through unknown mechanisms involved. We consider that oxidative stress might be one of the pathways implicated in RD promoted by light.
Fil: Benedetto, Maria Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; Argentina
Fil: Contin, Maria Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; Argentina - Materia
-
ELECTRORETINOGRAM
FATTY ACID
LED LIGHT
OXIDATIVE STRESS
RETINAL LIGHT DAMAGE - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/128873
Ver los metadatos del registro completo
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Oxidative stress in retinal degeneration promoted by constant LED lightBenedetto, Maria MercedesContin, Maria AnaELECTRORETINOGRAMFATTY ACIDLED LIGHTOXIDATIVE STRESSRETINAL LIGHT DAMAGEhttps://purl.org/becyt/ford/1.4https://purl.org/becyt/ford/1Light pollution by artificial light, might accelerate retinal diseases and circadian asynchrony. The excess of light exposure is a growing problem in societies, so studies on the consequences of long-term exposure to low levels of light are needed to determine the effects on vision. The possibility to understand the molecular mechanisms of light damage will contribute to the knowledge about visual disorders related to defects in the phototransduction. Several animal models have been used to study retinal degeneration (RD) by light; however, some important aspects remain to be established. Previously, we demonstrated that cool white treatment of 200 lux light-emitting diode (LED) induces retinal transformation with rods and cones cell death and significant changes in opsin expression in the inner nuclear layer (INL) and ganglion cell layer (GCL). Therefore, to further develop describing the molecular pathways of RD, we have examined here the oxidative stress and the fatty acid composition in rat retinas maintained at constant light. We demonstrated the existence of oxidative reactions after 5 days in outer nuclear layer (ONL), corresponding to classical photoreceptors; catalase (CAT) enzyme activity did not show significant differences in all times studied and the fatty acid study showed that docosahexaenoic acid decreased after 4 days. Remarkably, the docosahexaenoic acid diminution showed a correlation with the rise in stearic acid indicating a possible association between them. We assumed that the reduction in docosahexaenoic acid may be affected by the oxidative stress in photoreceptors outer segment which in turn affects the stearic acid composition with consequences in the membrane properties. All these miss-regulation affects the photoreceptor survival through unknown mechanisms involved. We consider that oxidative stress might be one of the pathways implicated in RD promoted by light.Fil: Benedetto, Maria Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; ArgentinaFil: Contin, Maria Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; ArgentinaFrontiers Media S.A.2019-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/128873Benedetto, Maria Mercedes; Contin, Maria Ana; Oxidative stress in retinal degeneration promoted by constant LED light; Frontiers Media S.A.; Frontiers in Cellular Neuroscience; 13; 139; 1-2019; 1-111662-5102CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fncel.2019.00139/full?&utm_source=Email_to_authors_&utm_medium=Email&utm_content=T1_11.5e1_author&utm_campaign=Email_publication&field=&journalName=Frontiers_in_Cellular_Neuroscience&id=441593info:eu-repo/semantics/altIdentifier/doi/10.3389/fncel.2019.00139info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:08:56Zoai:ri.conicet.gov.ar:11336/128873instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-10 13:08:56.868CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Oxidative stress in retinal degeneration promoted by constant LED light |
title |
Oxidative stress in retinal degeneration promoted by constant LED light |
spellingShingle |
Oxidative stress in retinal degeneration promoted by constant LED light Benedetto, Maria Mercedes ELECTRORETINOGRAM FATTY ACID LED LIGHT OXIDATIVE STRESS RETINAL LIGHT DAMAGE |
title_short |
Oxidative stress in retinal degeneration promoted by constant LED light |
title_full |
Oxidative stress in retinal degeneration promoted by constant LED light |
title_fullStr |
Oxidative stress in retinal degeneration promoted by constant LED light |
title_full_unstemmed |
Oxidative stress in retinal degeneration promoted by constant LED light |
title_sort |
Oxidative stress in retinal degeneration promoted by constant LED light |
dc.creator.none.fl_str_mv |
Benedetto, Maria Mercedes Contin, Maria Ana |
author |
Benedetto, Maria Mercedes |
author_facet |
Benedetto, Maria Mercedes Contin, Maria Ana |
author_role |
author |
author2 |
Contin, Maria Ana |
author2_role |
author |
dc.subject.none.fl_str_mv |
ELECTRORETINOGRAM FATTY ACID LED LIGHT OXIDATIVE STRESS RETINAL LIGHT DAMAGE |
topic |
ELECTRORETINOGRAM FATTY ACID LED LIGHT OXIDATIVE STRESS RETINAL LIGHT DAMAGE |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.4 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Light pollution by artificial light, might accelerate retinal diseases and circadian asynchrony. The excess of light exposure is a growing problem in societies, so studies on the consequences of long-term exposure to low levels of light are needed to determine the effects on vision. The possibility to understand the molecular mechanisms of light damage will contribute to the knowledge about visual disorders related to defects in the phototransduction. Several animal models have been used to study retinal degeneration (RD) by light; however, some important aspects remain to be established. Previously, we demonstrated that cool white treatment of 200 lux light-emitting diode (LED) induces retinal transformation with rods and cones cell death and significant changes in opsin expression in the inner nuclear layer (INL) and ganglion cell layer (GCL). Therefore, to further develop describing the molecular pathways of RD, we have examined here the oxidative stress and the fatty acid composition in rat retinas maintained at constant light. We demonstrated the existence of oxidative reactions after 5 days in outer nuclear layer (ONL), corresponding to classical photoreceptors; catalase (CAT) enzyme activity did not show significant differences in all times studied and the fatty acid study showed that docosahexaenoic acid decreased after 4 days. Remarkably, the docosahexaenoic acid diminution showed a correlation with the rise in stearic acid indicating a possible association between them. We assumed that the reduction in docosahexaenoic acid may be affected by the oxidative stress in photoreceptors outer segment which in turn affects the stearic acid composition with consequences in the membrane properties. All these miss-regulation affects the photoreceptor survival through unknown mechanisms involved. We consider that oxidative stress might be one of the pathways implicated in RD promoted by light. Fil: Benedetto, Maria Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; Argentina Fil: Contin, Maria Ana. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigaciones en Química Biológica de Córdoba. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Centro de Investigaciones en Química Biológica de Córdoba; Argentina |
description |
Light pollution by artificial light, might accelerate retinal diseases and circadian asynchrony. The excess of light exposure is a growing problem in societies, so studies on the consequences of long-term exposure to low levels of light are needed to determine the effects on vision. The possibility to understand the molecular mechanisms of light damage will contribute to the knowledge about visual disorders related to defects in the phototransduction. Several animal models have been used to study retinal degeneration (RD) by light; however, some important aspects remain to be established. Previously, we demonstrated that cool white treatment of 200 lux light-emitting diode (LED) induces retinal transformation with rods and cones cell death and significant changes in opsin expression in the inner nuclear layer (INL) and ganglion cell layer (GCL). Therefore, to further develop describing the molecular pathways of RD, we have examined here the oxidative stress and the fatty acid composition in rat retinas maintained at constant light. We demonstrated the existence of oxidative reactions after 5 days in outer nuclear layer (ONL), corresponding to classical photoreceptors; catalase (CAT) enzyme activity did not show significant differences in all times studied and the fatty acid study showed that docosahexaenoic acid decreased after 4 days. Remarkably, the docosahexaenoic acid diminution showed a correlation with the rise in stearic acid indicating a possible association between them. We assumed that the reduction in docosahexaenoic acid may be affected by the oxidative stress in photoreceptors outer segment which in turn affects the stearic acid composition with consequences in the membrane properties. All these miss-regulation affects the photoreceptor survival through unknown mechanisms involved. We consider that oxidative stress might be one of the pathways implicated in RD promoted by light. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-01 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/128873 Benedetto, Maria Mercedes; Contin, Maria Ana; Oxidative stress in retinal degeneration promoted by constant LED light; Frontiers Media S.A.; Frontiers in Cellular Neuroscience; 13; 139; 1-2019; 1-11 1662-5102 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/128873 |
identifier_str_mv |
Benedetto, Maria Mercedes; Contin, Maria Ana; Oxidative stress in retinal degeneration promoted by constant LED light; Frontiers Media S.A.; Frontiers in Cellular Neuroscience; 13; 139; 1-2019; 1-11 1662-5102 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fncel.2019.00139/full?&utm_source=Email_to_authors_&utm_medium=Email&utm_content=T1_11.5e1_author&utm_campaign=Email_publication&field=&journalName=Frontiers_in_Cellular_Neuroscience&id=441593 info:eu-repo/semantics/altIdentifier/doi/10.3389/fncel.2019.00139 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Frontiers Media S.A. |
publisher.none.fl_str_mv |
Frontiers Media S.A. |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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