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The role of arachidonic acid on LH-stimulated steroidogenesis and steroidogenic acute regulatory protein accumulation in MA-10 mouse leydig tumor cells

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Abstract

Metabolic pathways leading to the production of arachidonic acid (AA) and its metabolites have been reported to have modulatory effects on steroidogenesis in a number of cell types. To examine the importance of the arachidonic acid pathway in steroid production and steroidogenic acute regulatory (StAR) protein expression, luteinizing hormones (LH) or N 6-2-o-dibutyryl-adenosine-3∶5-cyclic monophosphate-(Bt2cAMP) stimulated MA-10 mouse Leydig tumor cells were treated with various concentrations of quinacrine (an inhibitor of arachidonic acid production). Incubation of the cells with quinacrine resulted in dose-dependent decreases in steroid production and StAR protein. Twenty micromolars quinacrine inhibited 92 and 91% of LH-induced progesterone and StAR protein, respectively, and 98 and 90% of Bt2cAMP-induced progesterone and StAR protein. Reversal of this inhibition was obtained by incubation of quinacrine-treated cells with various levels of AA, which resulted in a dose-dependent increase in both steroid and StAR protein levels. Two hundred micromolars of AA rescued 57 and 60% of the LH-induced steroid production and StAR protein, respectively, and 52 and 89% of Bt2cAMP-induced steroid production and StAR protein. These results suggest that the effect of AA on LH- and cAMP-stimulated steroidogenesis is associated with the modulation of StAR protein expression.

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Authors and Affiliations

  1. Department of Cell Biology and Biochemistry, Texas Tech University Health Sciences Center, 79430, Lubbock, TX

    Xingjia Wang, Lance P. Walsh &  Douglas M. Stocco

Authors
  1. Xingjia Wang
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  2. Lance P. Walsh
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  3. Douglas M. Stocco
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Correspondence to Douglas M. Stocco.

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Wang, X., Walsh, L.P. & Stocco, D.M. The role of arachidonic acid on LH-stimulated steroidogenesis and steroidogenic acute regulatory protein accumulation in MA-10 mouse leydig tumor cells. Endocr 10, 7–12 (1999). https://doi.org/10.1385/ENDO:10:1:7

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  • DOI: https://doi.org/10.1385/ENDO:10:1:7

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