Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells

Autores
Astiz, Mariana; Hurtado de Catalfo, Graciela E.; Tacconi de Alaniz, María Josefa; Marra, Carlos Alberto
Año de publicación
2009
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The mechanism involved in the inhibition of testosterone (Te) biosynthesis after a sub-chronic exposure to low doses of dimethoate (D) was studied in rat interstitial cells (IC). Expression of COX-2 in IC isolated from D-treated rats increased by 44% over C data, while transcription of StAR decreased by approx. 50% and the expression of this protein was diminished by approximately 40%. PGE₂ and PGF2α were increased by 61 and 78%, respectively. Te concentration decreased by 49% in IC homogenates. Concomitantly, plasma concentration of LH and FSH both increased. Araquidonate (ARA) and C₂₂ fatty acyl chains in phospholipids from IC mitochondrial fraction decreased by approx. 30% after D treatment. Protein carbonyls, lipoperoxides and nitrite content increased while α-tocopherol and the antioxidant capacity of the soluble cellular fraction decreased significantly. Stimulation with h-CG 10 nM overnight failed to overcome the inhibition caused by D on both Te biosynthesis and 3β- and 17β-hydroxysteroid dehydrogenases. Decreased Te biosynthesis may be attributed to (1) inhibition of StAR protein activity due to the stimulation of COX-2 and the overproduction of PGF2α, (2) decreased stimulatory effect of ARA on StAR with a subsequent reduction in the availability of CHO for the androgenic pathway, and/or (3) indirect inhibition of steroidogenic enzymes by a lower transcriptional rate caused by elevated PGF2α. Rofecoxib administration prevents the deleterious effect(s) exerted by D.
Facultad de Ciencias Médicas
Instituto de Investigaciones Bioquímicas de La Plata
Materia
Medicina
Arachidonic acid
COX-2
Dimethoate
Oxidative stress
Prostaglandins
Rat interstitial cells
StAR
h-CG
Rofecoxib
TROLOX
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/131025
Acceder
id SEDICI_23b317d31f10cdbbe7685072fc4e2503
oai_identifier_str oai:sedici.unlp.edu.ar:10915/131025
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial CellsAstiz, MarianaHurtado de Catalfo, Graciela E.Tacconi de Alaniz, María JosefaMarra, Carlos AlbertoMedicinaArachidonic acidCOX-2DimethoateOxidative stressProstaglandinsRat interstitial cellsStARh-CGRofecoxibTROLOXThe mechanism involved in the inhibition of testosterone (Te) biosynthesis after a sub-chronic exposure to low doses of dimethoate (D) was studied in rat interstitial cells (IC). Expression of COX-2 in IC isolated from D-treated rats increased by 44% over C data, while transcription of StAR decreased by approx. 50% and the expression of this protein was diminished by approximately 40%. PGE₂ and PGF<sub>2α</sub> were increased by 61 and 78%, respectively. Te concentration decreased by 49% in IC homogenates. Concomitantly, plasma concentration of LH and FSH both increased. Araquidonate (ARA) and C₂₂ fatty acyl chains in phospholipids from IC mitochondrial fraction decreased by approx. 30% after D treatment. Protein carbonyls, lipoperoxides and nitrite content increased while α-tocopherol and the antioxidant capacity of the soluble cellular fraction decreased significantly. Stimulation with h-CG 10 nM overnight failed to overcome the inhibition caused by D on both Te biosynthesis and 3β- and 17β-hydroxysteroid dehydrogenases. Decreased Te biosynthesis may be attributed to (1) inhibition of StAR protein activity due to the stimulation of COX-2 and the overproduction of PGF<sub>2α</sub>, (2) decreased stimulatory effect of ARA on StAR with a subsequent reduction in the availability of CHO for the androgenic pathway, and/or (3) indirect inhibition of steroidogenic enzymes by a lower transcriptional rate caused by elevated PGF<sub>2α</sub>. Rofecoxib administration prevents the deleterious effect(s) exerted by D.Facultad de Ciencias MédicasInstituto de Investigaciones Bioquímicas de La Plata2009-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf703-718http://sedici.unlp.edu.ar/handle/10915/131025enginfo:eu-repo/semantics/altIdentifier/issn/1558-9307info:eu-repo/semantics/altIdentifier/issn/0024-4201info:eu-repo/semantics/altIdentifier/doi/10.1007/s11745-009-3323-5info:eu-repo/semantics/altIdentifier/pmid/19579042info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:31:43Zoai:sedici.unlp.edu.ar:10915/131025Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:31:43.263SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
title Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
spellingShingle Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
Astiz, Mariana
Medicina
Arachidonic acid
COX-2
Dimethoate
Oxidative stress
Prostaglandins
Rat interstitial cells
StAR
h-CG
Rofecoxib
TROLOX
title_short Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
title_full Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
title_fullStr Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
title_full_unstemmed Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
title_sort Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
dc.creator.none.fl_str_mv Astiz, Mariana
Hurtado de Catalfo, Graciela E.
Tacconi de Alaniz, María Josefa
Marra, Carlos Alberto
author Astiz, Mariana
author_facet Astiz, Mariana
Hurtado de Catalfo, Graciela E.
Tacconi de Alaniz, María Josefa
Marra, Carlos Alberto
author_role author
author2 Hurtado de Catalfo, Graciela E.
Tacconi de Alaniz, María Josefa
Marra, Carlos Alberto
author2_role author
author
author
dc.subject.none.fl_str_mv Medicina
Arachidonic acid
COX-2
Dimethoate
Oxidative stress
Prostaglandins
Rat interstitial cells
StAR
h-CG
Rofecoxib
TROLOX
topic Medicina
Arachidonic acid
COX-2
Dimethoate
Oxidative stress
Prostaglandins
Rat interstitial cells
StAR
h-CG
Rofecoxib
TROLOX
dc.description.none.fl_txt_mv The mechanism involved in the inhibition of testosterone (Te) biosynthesis after a sub-chronic exposure to low doses of dimethoate (D) was studied in rat interstitial cells (IC). Expression of COX-2 in IC isolated from D-treated rats increased by 44% over C data, while transcription of StAR decreased by approx. 50% and the expression of this protein was diminished by approximately 40%. PGE₂ and PGF<sub>2α</sub> were increased by 61 and 78%, respectively. Te concentration decreased by 49% in IC homogenates. Concomitantly, plasma concentration of LH and FSH both increased. Araquidonate (ARA) and C₂₂ fatty acyl chains in phospholipids from IC mitochondrial fraction decreased by approx. 30% after D treatment. Protein carbonyls, lipoperoxides and nitrite content increased while α-tocopherol and the antioxidant capacity of the soluble cellular fraction decreased significantly. Stimulation with h-CG 10 nM overnight failed to overcome the inhibition caused by D on both Te biosynthesis and 3β- and 17β-hydroxysteroid dehydrogenases. Decreased Te biosynthesis may be attributed to (1) inhibition of StAR protein activity due to the stimulation of COX-2 and the overproduction of PGF<sub>2α</sub>, (2) decreased stimulatory effect of ARA on StAR with a subsequent reduction in the availability of CHO for the androgenic pathway, and/or (3) indirect inhibition of steroidogenic enzymes by a lower transcriptional rate caused by elevated PGF<sub>2α</sub>. Rofecoxib administration prevents the deleterious effect(s) exerted by D.
Facultad de Ciencias Médicas
Instituto de Investigaciones Bioquímicas de La Plata
description The mechanism involved in the inhibition of testosterone (Te) biosynthesis after a sub-chronic exposure to low doses of dimethoate (D) was studied in rat interstitial cells (IC). Expression of COX-2 in IC isolated from D-treated rats increased by 44% over C data, while transcription of StAR decreased by approx. 50% and the expression of this protein was diminished by approximately 40%. PGE₂ and PGF<sub>2α</sub> were increased by 61 and 78%, respectively. Te concentration decreased by 49% in IC homogenates. Concomitantly, plasma concentration of LH and FSH both increased. Araquidonate (ARA) and C₂₂ fatty acyl chains in phospholipids from IC mitochondrial fraction decreased by approx. 30% after D treatment. Protein carbonyls, lipoperoxides and nitrite content increased while α-tocopherol and the antioxidant capacity of the soluble cellular fraction decreased significantly. Stimulation with h-CG 10 nM overnight failed to overcome the inhibition caused by D on both Te biosynthesis and 3β- and 17β-hydroxysteroid dehydrogenases. Decreased Te biosynthesis may be attributed to (1) inhibition of StAR protein activity due to the stimulation of COX-2 and the overproduction of PGF<sub>2α</sub>, (2) decreased stimulatory effect of ARA on StAR with a subsequent reduction in the availability of CHO for the androgenic pathway, and/or (3) indirect inhibition of steroidogenic enzymes by a lower transcriptional rate caused by elevated PGF<sub>2α</sub>. Rofecoxib administration prevents the deleterious effect(s) exerted by D.
publishDate 2009
dc.date.none.fl_str_mv 2009-08
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
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://sedici.unlp.edu.ar/handle/10915/131025
url http://sedici.unlp.edu.ar/handle/10915/131025
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/1558-9307
info:eu-repo/semantics/altIdentifier/issn/0024-4201
info:eu-repo/semantics/altIdentifier/doi/10.1007/s11745-009-3323-5
info:eu-repo/semantics/altIdentifier/pmid/19579042
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
703-718
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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score 13.070432

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