Exogenous arachidonate restores the dimethoate-induced inhibition of steroidogenesis in rat interstitial cells

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

doi:10.1007/s11745-012-3669-y

Exogenous arachidonate restores the dimethoate-induced inhibition of steroidogenesis in rat interstitial cells

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

^*Corresponding author for this work

Institute of Neurobiology

Universidad Nacional de La Plata

12 Citations (Scopus)

Abstract

The present work studies the potential restorative effect of polyunsaturated fatty acids (PUFA, 5 μM/24 h) on the dimethoate (DMT)-induced inhibition of testosterone biosynthesis in Leydig cells isolated from rat testes. Various fatty acids (FA) from the n-6 (18:2, 20:3, 20:4, 22:4 and 22:5) and n-3 (18.3, 20:5, 22:5, 22:6) series were assayed in Leydig cells, alone (as delipidated BSA complexes) and in combination with DMT (1 ppm). The n-6 FA stimulated lipid peroxidation (LPO) and inhibited the activities of steroidogenic enzymes (3β- and 17β-hydroxysteroid dehydrogenases). The n-3 FA exerted an anti-oxidant effect, decreasing the production of thiobarbituricacid reactive substances (TBARS) and inhibiting phospholipase A₂ activity. The biosynthesis of testosterone in DMT-treated cultures was completely normalized by ARA (20:4n-6) and partially restored by the addition of 20:3n-6, increasing ARA content inside the mitochondria. The other FA assayed failed to restore androgenesis. COX-2 protein and prostaglandin F2α and E2 production were stimulated by 20:3n-6, ARA, 18:3n-3 and 20:5 n-3. COX-2 protein decreased upon addition of 22:5n-3 and 22:6n-3. StAR protein was increased by ARA and partially increased by 20:3n-6, likely due to its metabolic conversion into ARA. Both FA increased the mitochondrial cholesterol pool available for testosterone biosynthesis. The rate of androgenesis is likely the result of various regulatory factors acting concomitantly on the physiology of Leydig cells.

Original language	English
Journal	Lipids
Volume	47
Issue number	6
Pages (from-to)	557-569
Number of pages	13
ISSN	0024-4201
DOIs	https://doi.org/10.1007/s11745-012-3669-y
Publication status	Published - 06.2012

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.

Research Areas and Centers

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

UN SDGs

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

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10.1007/s11745-012-3669-y

Cite this

@article{5595e25730d64bd3af4230f0e5450ac9,

title = "Exogenous arachidonate restores the dimethoate-induced inhibition of steroidogenesis in rat interstitial cells",

abstract = "The present work studies the potential restorative effect of polyunsaturated fatty acids (PUFA, 5 μM/24 h) on the dimethoate (DMT)-induced inhibition of testosterone biosynthesis in Leydig cells isolated from rat testes. Various fatty acids (FA) from the n-6 (18:2, 20:3, 20:4, 22:4 and 22:5) and n-3 (18.3, 20:5, 22:5, 22:6) series were assayed in Leydig cells, alone (as delipidated BSA complexes) and in combination with DMT (1 ppm). The n-6 FA stimulated lipid peroxidation (LPO) and inhibited the activities of steroidogenic enzymes (3β- and 17β-hydroxysteroid dehydrogenases). The n-3 FA exerted an anti-oxidant effect, decreasing the production of thiobarbituricacid reactive substances (TBARS) and inhibiting phospholipase A2 activity. The biosynthesis of testosterone in DMT-treated cultures was completely normalized by ARA (20:4n-6) and partially restored by the addition of 20:3n-6, increasing ARA content inside the mitochondria. The other FA assayed failed to restore androgenesis. COX-2 protein and prostaglandin F2α and E2 production were stimulated by 20:3n-6, ARA, 18:3n-3 and 20:5 n-3. COX-2 protein decreased upon addition of 22:5n-3 and 22:6n-3. StAR protein was increased by ARA and partially increased by 20:3n-6, likely due to its metabolic conversion into ARA. Both FA increased the mitochondrial cholesterol pool available for testosterone biosynthesis. The rate of androgenesis is likely the result of various regulatory factors acting concomitantly on the physiology of Leydig cells.",

author = "Mariana Astiz and \{De Catalfo\}, \{Graciela Hurtado\} 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 2020 Elsevier B.V., All rights reserved.",

year = "2012",

month = jun,

doi = "10.1007/s11745-012-3669-y",

language = "English",

volume = "47",

pages = "557--569",

journal = "Lipids",

issn = "0024-4201",

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T1 - Exogenous arachidonate restores the dimethoate-induced inhibition of steroidogenesis in rat interstitial cells

AU - Astiz, Mariana

AU - De Catalfo, Graciela Hurtado

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 2020 Elsevier B.V., All rights reserved.

PY - 2012/6

Y1 - 2012/6

N2 - The present work studies the potential restorative effect of polyunsaturated fatty acids (PUFA, 5 μM/24 h) on the dimethoate (DMT)-induced inhibition of testosterone biosynthesis in Leydig cells isolated from rat testes. Various fatty acids (FA) from the n-6 (18:2, 20:3, 20:4, 22:4 and 22:5) and n-3 (18.3, 20:5, 22:5, 22:6) series were assayed in Leydig cells, alone (as delipidated BSA complexes) and in combination with DMT (1 ppm). The n-6 FA stimulated lipid peroxidation (LPO) and inhibited the activities of steroidogenic enzymes (3β- and 17β-hydroxysteroid dehydrogenases). The n-3 FA exerted an anti-oxidant effect, decreasing the production of thiobarbituricacid reactive substances (TBARS) and inhibiting phospholipase A2 activity. The biosynthesis of testosterone in DMT-treated cultures was completely normalized by ARA (20:4n-6) and partially restored by the addition of 20:3n-6, increasing ARA content inside the mitochondria. The other FA assayed failed to restore androgenesis. COX-2 protein and prostaglandin F2α and E2 production were stimulated by 20:3n-6, ARA, 18:3n-3 and 20:5 n-3. COX-2 protein decreased upon addition of 22:5n-3 and 22:6n-3. StAR protein was increased by ARA and partially increased by 20:3n-6, likely due to its metabolic conversion into ARA. Both FA increased the mitochondrial cholesterol pool available for testosterone biosynthesis. The rate of androgenesis is likely the result of various regulatory factors acting concomitantly on the physiology of Leydig cells.

AB - The present work studies the potential restorative effect of polyunsaturated fatty acids (PUFA, 5 μM/24 h) on the dimethoate (DMT)-induced inhibition of testosterone biosynthesis in Leydig cells isolated from rat testes. Various fatty acids (FA) from the n-6 (18:2, 20:3, 20:4, 22:4 and 22:5) and n-3 (18.3, 20:5, 22:5, 22:6) series were assayed in Leydig cells, alone (as delipidated BSA complexes) and in combination with DMT (1 ppm). The n-6 FA stimulated lipid peroxidation (LPO) and inhibited the activities of steroidogenic enzymes (3β- and 17β-hydroxysteroid dehydrogenases). The n-3 FA exerted an anti-oxidant effect, decreasing the production of thiobarbituricacid reactive substances (TBARS) and inhibiting phospholipase A2 activity. The biosynthesis of testosterone in DMT-treated cultures was completely normalized by ARA (20:4n-6) and partially restored by the addition of 20:3n-6, increasing ARA content inside the mitochondria. The other FA assayed failed to restore androgenesis. COX-2 protein and prostaglandin F2α and E2 production were stimulated by 20:3n-6, ARA, 18:3n-3 and 20:5 n-3. COX-2 protein decreased upon addition of 22:5n-3 and 22:6n-3. StAR protein was increased by ARA and partially increased by 20:3n-6, likely due to its metabolic conversion into ARA. Both FA increased the mitochondrial cholesterol pool available for testosterone biosynthesis. The rate of androgenesis is likely the result of various regulatory factors acting concomitantly on the physiology of Leydig cells.

UR - https://www.scopus.com/pages/publications/84863448329

U2 - 10.1007/s11745-012-3669-y

DO - 10.1007/s11745-012-3669-y

M3 - Journal articles

C2 - 22476691

AN - SCOPUS:84863448329

SN - 0024-4201

VL - 47

SP - 557

EP - 569

JO - Lipids

JF - Lipids

IS - 6

ER -

Exogenous arachidonate restores the dimethoate-induced inhibition of steroidogenesis in rat interstitial cells

Abstract

Funding

Research Areas and Centers

UN SDGs

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