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

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Lipids

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.

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Abbreviations

C:

Control group

CM:

Cytoplasmic membrane

D:

Dimethoate

FSH:

Follicle-stimulating hormone

LH:

Luteinizing hormone

LPO:

Lipid peroxidation

MDA:

Malonedialdehyde

N:

Nucleus

OS:

Oxidative stress

RNS:

Reactive nitrogen species

PS:

Protein synthesis

R:

Rofecoxib

ROS:

Reactive oxygenated species

StAR:

Steroidogenic acute regulatory protein

T:

TROLOX®

TBARS:

Thiobarbituric acid-reactive substances

Te:

Testosterone

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Acknowledgments

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

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  1. Instituto de Investigaciones Bioquímicas de La Plata (INIBIOLP), CCT La Plata, CONICET-UNLP, Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Calles 60 y 120, 1900, La Plata, Argentina

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

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  1. Mariana Astiz
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  2. Graciela E. Hurtado de Catalfo
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  3. María J. T. de Alaniz
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  4. Carlos Alberto Marra
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Correspondence to Carlos Alberto Marra.

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Astiz, M., Hurtado de Catalfo, G.E., de Alaniz, M.J.T. et al. Involvement of Lipids in Dimethoate-Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells. Lipids 44, 703–718 (2009). https://doi.org/10.1007/s11745-009-3323-5

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