Involvement of lipids in dimethoate-induced inhibition of testosterone biosynthesis in rat interstitial cells

Mariana Astiz; Graciela E. Hurtado De Catalfo; María J.T. De Alaniz; Carlos Alberto Marra

doi:10.1007/s11745-009-3323-5

Involvement of lipids in dimethoate-induced inhibition of testosterone biosynthesis in rat interstitial cells

Mariana Astiz, Graciela E. Hurtado De Catalfo, María J.T. De Alaniz, Carlos Alberto Marra

Institute of Neurobiology

Universidad Nacional de La Plata

19 Citations (Scopus)

Abstract

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_2α 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_2α, (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_2α. Rofecoxib administration prevents the deleterious effect(s) exerted by D.

Original language	English
Journal	Lipids
Volume	44
Issue number	8
Pages (from-to)	703-718
Number of pages	16
ISSN	0024-4201
DOIs	https://doi.org/10.1007/s11745-009-3323-5
Publication status	Published - 08.2009

Funding

Acknowledgments This study was supported by a grant from Consejo Nacional de Investigaciones Científicas y Técnicas (CONI-CET), Argentina. We would like to thank Mrs. Agustina Zardis de Cobeñas, Eva Illara de Bozzolo, and Norma Cristalli for their excellent technical assistance.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being
SDG 8 Decent Work and Economic Growth
SDG 10 Reduced Inequalities

Research Areas and Centers

Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

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10.1007/s11745-009-3323-5

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title = "Involvement of lipids in dimethoate-induced inhibition of testosterone biosynthesis in rat interstitial cells",

abstract = "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.",

author = "Mariana Astiz and \{Hurtado De Catalfo\}, \{Graciela E.\} and \{De Alaniz\}, \{Mar{\'i}a J.T.\} and Marra, \{Carlos Alberto\}",

note = "Funding Information: Acknowledgments This study was supported by a grant from Consejo Nacional de Investigaciones Cient{\'i}ficas y T{\'e}cnicas (CONI-CET), Argentina. We would like to thank Mrs. Agustina Zardis de Cobe{\~n}as, Eva Illara de Bozzolo, and Norma Cristalli for their excellent technical assistance. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.",

year = "2009",

month = aug,

doi = "10.1007/s11745-009-3323-5",

language = "English",

volume = "44",

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journal = "Lipids",

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T1 - Involvement of lipids in dimethoate-induced inhibition of testosterone biosynthesis in rat interstitial cells

AU - Astiz, Mariana

AU - Hurtado De Catalfo, Graciela E.

AU - De Alaniz, María J.T.

AU - Marra, Carlos Alberto

N1 - Funding Information: Acknowledgments This study was supported by a grant from Consejo Nacional de Investigaciones Científicas y Técnicas (CONI-CET), Argentina. We would like to thank Mrs. Agustina Zardis de Cobeñas, Eva Illara de Bozzolo, and Norma Cristalli for their excellent technical assistance. Copyright: Copyright 2009 Elsevier B.V., All rights reserved.

PY - 2009/8

Y1 - 2009/8

N2 - 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.

AB - 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.

UR - https://www.scopus.com/pages/publications/68349092771

U2 - 10.1007/s11745-009-3323-5

DO - 10.1007/s11745-009-3323-5

M3 - Journal articles

C2 - 19579042

AN - SCOPUS:68349092771

SN - 0024-4201

VL - 44

SP - 703

EP - 718

JO - Lipids

JF - Lipids

IS - 8

ER -

Involvement of lipids in dimethoate-induced inhibition of testosterone biosynthesis in rat interstitial cells

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