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

被引：21
作者：
Astiz, Mariana [1 ]
Hurtado de Catalfo, Graciela E. [1 ]
de Alaniz, Maria J. T. [1 ]
Alberto Marra, Carlos [1 ]
机构：
[1] Natl Univ La Plata, INIBIOLP, CCT La Plata,Fac Ciencias Med, CONICET,Catedra Bioquim & Biol Mol, RA-1900 La Plata, Argentina
来源：
LIPIDS | 2009年 / 44卷 / 08期
关键词：
Arachidonic acid; COX-2; Dimethoate; Oxidative stress; Prostaglandins; Rat interstitial cells; StAR; h-CG; Rofecoxib; TROLOX; ACUTE REGULATORY PROTEIN; POLYCHLORINATED BIPHENYL AROCLOR-1254; ACTIVITY ENHANCES STEROIDOGENESIS; ARACHIDONIC-ACID RELEASE; MALE REPRODUCTIVE-SYSTEM; UNSATURATED FATTY-ACIDS; LEYDIG TUMOR-CELLS; ANTIOXIDANT SYSTEM; OXIDATIVE STRESS; GENE-EXPRESSION;
D O I：
10.1007/s11745-009-3323-5
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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(2 alpha) 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 alpha-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 3 beta- and 17 beta-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(2 alpha), (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(2 alpha). Rofecoxib administration prevents the deleterious effect(s) exerted by D.
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页码：703 / 718
页数：16
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