Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Volume 56, Issue 3, Pages 263-267Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e3181eb3063
Keywords
7 beta-hydroxycholesterol; oxidative stress; apoptosis; dimethyl sulfoxide
Funding
- Swedish Research Council
- Swedish Heart Lung Foundation
- oLL Research Foundation
- Gamla Tjanarinnor Foundation
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Dimethyl sulfoxide (DMSO) is a widely used vehicle for water-insoluble substances and exerts a wide range of pharmacologic effects including anti-inflammatory and free radical scavenging properties. Additionally, in an animal model, DMSO inhibited cholesterol- induced atherosclerosis. Despite such profound pharmacologic effects, mechanisms at the cellular level are not well understood. Atherogenic oxysterols, especially 7-oxysterols, are potent inducers of oxidative stress, cell apoptosis, and are elevated in human atherosclerotic lesions. In this study, we first investigated the effect of DMSO on 7 beta-hydroxycholesterol-induced apoptosis of U937 cells and then focused on its influences on production of reactive oxygen species, lysosomal, and mitochondrial membrane permeability. Our results revealed that DMSO protected U937 cells against 7 beta-hydroxycholesterol- induced cell death by preventing lysosomal and mitochondrial membrane permeabilization and reactive oxygen species production. Our results also emphasize the necessity for appropriate solvent control groups in experimental models in which DMSO has been used to examine drug effect or identify pathways.
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