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Involvement of Lipids in Dimethoate‐Induced Inhibition of Testosterone Biosynthesis in Rat Interstitial Cells
Author(s) -
Astiz Mariana,
Hurtado de Catalfo Graciela E.,
Alaniz María J. T.,
Marra Carlos Alberto
Publication year - 2009
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-009-3323-5
Subject(s) - lipidology , clinical chemistry , biosynthesis , dimethoate , testosterone (patch) , chemistry , biochemistry , medicine , endocrinology , biology , enzyme , ecology , pesticide
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%. PGE 2 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 C 22 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.