Dehydroepiandrosterone Treatment Alters Lipid/Phospholipid Profiles of Rat Brain and Liver Mitochondria

Abstract

Stimulation of mitochondrial function following treatment with dehydroepiandrosterone (DHEA) has been demonstrated. Since the activity of several electron transport chain components is dependent on specific lipid/phospholipid components, we examined the effects of DHEA treatment (0.1-2.0 mg/kg body weight for 7 consecutive days) on lipid/phospholipids profiles of rat brain and liver mitochondria. In the brain mitochondria, contents of both total phospholipids (TPL) and cholesterol (CHL) increased. The major effect on phospholipids profile was increase in the contents of lysophospholipids (Lyso) and sphingomyelin (SPM) component followed by phosphatidylinositol (PI) and phosphatidylserine (PS). The contents of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and diphosphatidylglycerol (DPG) were not affected. At the higher dose (2.0 mg) the observed effects declined. The TPL and CHL contents of liver mitochondria were generally unchanged by DHEA treatment. Under this condition the content of PI and PS increased. The contents of other phospholipid components were not changed. Our results suggest that the observed changes may complement the function of electron transport chain components.

The total and mitochondrial lipidome of Artemia franciscana encysted embryos

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MicroRNA-17 induces epithelial-mesenchymal transition consistent with the cancer stem cell phenotype by regulating CYP7B1 expression in colon cancer

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Polymorphisms in AKR1C4 and HSD3B2 and differences in serum DHEAS and progesterone are associated with paranoid ideation during mania or hypomania in bipolar disorder

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