Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit

Autores
Valle, María Ivone; Campelo, Adrián Esteban; Massheimer, Virginia Laura
Año de publicación
2022
Idioma
inglés
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
Obesity and diabetes prompt oxidative stress and an inflammatory environment that alter the homeostasis of several tissues, including uterine tissue. Estrogens are the main regulators of the endometrial function through the interaction with estrogen receptors. In this work we studied the effect of estradiol (E2) and estrone (E1) on the uterine oxidative stress induced by hyperglycemia; inflammation or obesity. To that end uterine slices isolated from female bilaterally ovariectomized (OVX) obese (Ob) and non-obese (nOb) Wistar rats were in vitro incubated with E2 or E1 in the presence of high glucose (25mM) or the pro-inflammatory agent LPS (5µg/mL). Oxidative-non oxidative stress was determined measuring the release to the incubation medium of the reactive oxygen species (ROS) hydrogen peroxide (H2O2, fluorescence assay) or nitric oxide (NO, Griess technique) respectively. Short interval treatment (10-20 min) with E2 or E1 (0.1-10 nM) increased NO production (2.20 ±0.22; 4.3 ± 0.64; 3.2 ±0.45 nmolNO/mg prot E2; E1; control, p< 0.01); effect detected either in young and adult OVX rats (3-14 month old age). The stimulatory action of both estrogens on NO synthesis was also evidenced in Ob rats (38; 33% a/c E2; E1 p< 0.05). H2O2 measurements showed that diabetic rats exhibited a 0.6 fold increase in ROS production respect to control group. Similar results were obtained in Ob rats (2656 ±632 vs 1595±287 nmol H2O2/mg prot, Ob vs nOb, p< 0.02). When uterine slices were exposed to E2 in the presence of LPS, a markedly reduction in ROS synthesis induced by LPS was observed (50 vs 12 % a/c, LPS vs LPS+E2, p< 0.05). Indeed, the steroid completely blunted the enhancement of H2O2 production induced by high glucose. Interestingly, E1 elicited similar action than E2. The results presented suggest that estrogens counteracted uterine oxidative stress induced by diabetes or obesity. A point to highlight is that the forgotten estrone exhibits comparable action than estradiol.
Fil: Valle, María Ivone. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Campelo, Adrián Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Massheimer, Virginia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Reunión conjunta SAIC - SAI & FAIC - SAFIS 2022
Mar del Plata
Argentina
Sociedad argentina de investigación clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
Materia
UTERUS
OXIDATIVE STRESS
OBESITY
DIABETES
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/246296
Acceder
id CONICETDig_2ef8fae56ed87a06b3063de97db5fc91
oai_identifier_str oai:ri.conicet.gov.ar:11336/246296
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesitValle, María IvoneCampelo, Adrián EstebanMassheimer, Virginia LauraUTERUSOXIDATIVE STRESSOBESITYDIABETEShttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Obesity and diabetes prompt oxidative stress and an inflammatory environment that alter the homeostasis of several tissues, including uterine tissue. Estrogens are the main regulators of the endometrial function through the interaction with estrogen receptors. In this work we studied the effect of estradiol (E2) and estrone (E1) on the uterine oxidative stress induced by hyperglycemia; inflammation or obesity. To that end uterine slices isolated from female bilaterally ovariectomized (OVX) obese (Ob) and non-obese (nOb) Wistar rats were in vitro incubated with E2 or E1 in the presence of high glucose (25mM) or the pro-inflammatory agent LPS (5µg/mL). Oxidative-non oxidative stress was determined measuring the release to the incubation medium of the reactive oxygen species (ROS) hydrogen peroxide (H2O2, fluorescence assay) or nitric oxide (NO, Griess technique) respectively. Short interval treatment (10-20 min) with E2 or E1 (0.1-10 nM) increased NO production (2.20 ±0.22; 4.3 ± 0.64; 3.2 ±0.45 nmolNO/mg prot E2; E1; control, p< 0.01); effect detected either in young and adult OVX rats (3-14 month old age). The stimulatory action of both estrogens on NO synthesis was also evidenced in Ob rats (38; 33% a/c E2; E1 p< 0.05). H2O2 measurements showed that diabetic rats exhibited a 0.6 fold increase in ROS production respect to control group. Similar results were obtained in Ob rats (2656 ±632 vs 1595±287 nmol H2O2/mg prot, Ob vs nOb, p< 0.02). When uterine slices were exposed to E2 in the presence of LPS, a markedly reduction in ROS synthesis induced by LPS was observed (50 vs 12 % a/c, LPS vs LPS+E2, p< 0.05). Indeed, the steroid completely blunted the enhancement of H2O2 production induced by high glucose. Interestingly, E1 elicited similar action than E2. The results presented suggest that estrogens counteracted uterine oxidative stress induced by diabetes or obesity. A point to highlight is that the forgotten estrone exhibits comparable action than estradiol.Fil: Valle, María Ivone. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Campelo, Adrián Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Massheimer, Virginia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaReunión conjunta SAIC - SAI & FAIC - SAFIS 2022Mar del PlataArgentinaSociedad argentina de investigación clínicaSociedad Argentina de InmunologíaSociedad Argentina de FisiologíaFundación Revista MedicinaMalchiodi, Emilio Luis2022info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/246296Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit; Reunión conjunta SAIC - SAI & FAIC - SAFIS 2022; Mar del Plata; Argentina; 2022; 119-1191669-9106CONICET DigitalCONICETenghttps://www.saic.org.ar/reuniones-anuales-previasinfo:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:13:32Zoai:ri.conicet.gov.ar:11336/246296instacron: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:34982025-10-22 12:13:32.546CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
title Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
spellingShingle Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
Valle, María Ivone
UTERUS
OXIDATIVE STRESS
OBESITY
DIABETES
title_short Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
title_full Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
title_fullStr Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
title_full_unstemmed Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
title_sort Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit
dc.creator.none.fl_str_mv Valle, María Ivone
Campelo, Adrián Esteban
Massheimer, Virginia Laura
author Valle, María Ivone
author_facet Valle, María Ivone
Campelo, Adrián Esteban
Massheimer, Virginia Laura
author_role author
author2 Campelo, Adrián Esteban
Massheimer, Virginia Laura
author2_role author
author
dc.contributor.none.fl_str_mv Malchiodi, Emilio Luis
dc.subject.none.fl_str_mv UTERUS
OXIDATIVE STRESS
OBESITY
DIABETES
topic UTERUS
OXIDATIVE STRESS
OBESITY
DIABETES
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Obesity and diabetes prompt oxidative stress and an inflammatory environment that alter the homeostasis of several tissues, including uterine tissue. Estrogens are the main regulators of the endometrial function through the interaction with estrogen receptors. In this work we studied the effect of estradiol (E2) and estrone (E1) on the uterine oxidative stress induced by hyperglycemia; inflammation or obesity. To that end uterine slices isolated from female bilaterally ovariectomized (OVX) obese (Ob) and non-obese (nOb) Wistar rats were in vitro incubated with E2 or E1 in the presence of high glucose (25mM) or the pro-inflammatory agent LPS (5µg/mL). Oxidative-non oxidative stress was determined measuring the release to the incubation medium of the reactive oxygen species (ROS) hydrogen peroxide (H2O2, fluorescence assay) or nitric oxide (NO, Griess technique) respectively. Short interval treatment (10-20 min) with E2 or E1 (0.1-10 nM) increased NO production (2.20 ±0.22; 4.3 ± 0.64; 3.2 ±0.45 nmolNO/mg prot E2; E1; control, p< 0.01); effect detected either in young and adult OVX rats (3-14 month old age). The stimulatory action of both estrogens on NO synthesis was also evidenced in Ob rats (38; 33% a/c E2; E1 p< 0.05). H2O2 measurements showed that diabetic rats exhibited a 0.6 fold increase in ROS production respect to control group. Similar results were obtained in Ob rats (2656 ±632 vs 1595±287 nmol H2O2/mg prot, Ob vs nOb, p< 0.02). When uterine slices were exposed to E2 in the presence of LPS, a markedly reduction in ROS synthesis induced by LPS was observed (50 vs 12 % a/c, LPS vs LPS+E2, p< 0.05). Indeed, the steroid completely blunted the enhancement of H2O2 production induced by high glucose. Interestingly, E1 elicited similar action than E2. The results presented suggest that estrogens counteracted uterine oxidative stress induced by diabetes or obesity. A point to highlight is that the forgotten estrone exhibits comparable action than estradiol.
Fil: Valle, María Ivone. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Campelo, Adrián Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Massheimer, Virginia Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Reunión conjunta SAIC - SAI & FAIC - SAFIS 2022
Mar del Plata
Argentina
Sociedad argentina de investigación clínica
Sociedad Argentina de Inmunología
Sociedad Argentina de Fisiología
description Obesity and diabetes prompt oxidative stress and an inflammatory environment that alter the homeostasis of several tissues, including uterine tissue. Estrogens are the main regulators of the endometrial function through the interaction with estrogen receptors. In this work we studied the effect of estradiol (E2) and estrone (E1) on the uterine oxidative stress induced by hyperglycemia; inflammation or obesity. To that end uterine slices isolated from female bilaterally ovariectomized (OVX) obese (Ob) and non-obese (nOb) Wistar rats were in vitro incubated with E2 or E1 in the presence of high glucose (25mM) or the pro-inflammatory agent LPS (5µg/mL). Oxidative-non oxidative stress was determined measuring the release to the incubation medium of the reactive oxygen species (ROS) hydrogen peroxide (H2O2, fluorescence assay) or nitric oxide (NO, Griess technique) respectively. Short interval treatment (10-20 min) with E2 or E1 (0.1-10 nM) increased NO production (2.20 ±0.22; 4.3 ± 0.64; 3.2 ±0.45 nmolNO/mg prot E2; E1; control, p< 0.01); effect detected either in young and adult OVX rats (3-14 month old age). The stimulatory action of both estrogens on NO synthesis was also evidenced in Ob rats (38; 33% a/c E2; E1 p< 0.05). H2O2 measurements showed that diabetic rats exhibited a 0.6 fold increase in ROS production respect to control group. Similar results were obtained in Ob rats (2656 ±632 vs 1595±287 nmol H2O2/mg prot, Ob vs nOb, p< 0.02). When uterine slices were exposed to E2 in the presence of LPS, a markedly reduction in ROS synthesis induced by LPS was observed (50 vs 12 % a/c, LPS vs LPS+E2, p< 0.05). Indeed, the steroid completely blunted the enhancement of H2O2 production induced by high glucose. Interestingly, E1 elicited similar action than E2. The results presented suggest that estrogens counteracted uterine oxidative stress induced by diabetes or obesity. A point to highlight is that the forgotten estrone exhibits comparable action than estradiol.
publishDate 2022
dc.date.none.fl_str_mv 2022
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
Congreso
Journal
http://purl.org/coar/resource_type/c_5794
info:ar-repo/semantics/documentoDeConferencia
status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/246296
Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit; Reunión conjunta SAIC - SAI & FAIC - SAFIS 2022; Mar del Plata; Argentina; 2022; 119-119
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/246296
identifier_str_mv Estrogens protect uterine against oxidative stress induced by hyperglycemia and obesit; Reunión conjunta SAIC - SAI & FAIC - SAFIS 2022; Mar del Plata; Argentina; 2022; 119-119
1669-9106
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.saic.org.ar/reuniones-anuales-previas
info:eu-repo/semantics/altIdentifier/url/https://www.medicinabuenosaires.com/
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
application/pdf
application/pdf
dc.coverage.none.fl_str_mv Nacional
dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
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instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv 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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