Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2008) 16 P27


Modulation of adrenocortical aldosterone and cortisol synthesis by in vitro oxidized low density lipoprotein

Steffi Kopprasch1, Ishrath Ansurudeen1, Juergen Graessler1, Stefan R Bornstein1 & Jens Pietzsch1,2

1Department of Internal Medicine 3, CG Carus Medical School, Dresden, Germany; 2Department of Radiopharmaceutical Biology, Institute of Radiopharmacy, Dresden-Rossendorf, Germany.

Objectives: Oxidative stress is of critical importance in the pathogenesis of endocrinopathies. Since cholesterol serves as a major source of steroid hormone synthesis we investigated the effect of hypochlorite-modified low density lipoprotein (LDL) on aldosterone and cortisol release from human adrenocortical NCI-H295R cells.

Methods: Native LDL obtained from healthy volunteers was oxidized to varying degrees by sodium hypochlorite. The resulting modified LDL was biochemically characterized by gas chromatography–mass spectrometry (GC–MS) analysis. Human NCI-H295R cells were cultured in DMEM/F12. Aldosterone release in supernatants was measured by RIA and cortisol secretion was determined by competitive luminometric assay.

Results: Incubation of LDL with sodium hypochlorite resulted in increasing concentrations of the apolipoprotein B-100 oxidation markers HAVA, HACA, and 3-chlorotyrosine in dependence on the degree of oxidation. Incubation of adrenocortical cells with 10–100 μg/ml native or oxidized LDL for 24 h stimulated hormone release dose-dependently up to 3-fold. Subsequent stimulation of NCI-H295R cells with the physiological stimulus angiotensin II induced an additional hormone secretion up to 2.9-fold in LDL-pretreated samples. Compared to native LDL, oxidized LDL induced a smaller stimulation of hormone secretion that decreased with increasing degree of oxidation.

Conclusion: Oxidation of LDL may contribute to endocrine dysfunction by decreasing adrenocortical aldosterone and cortisol release.

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