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To determine whether arsenic inhibits transcriptional activation of the liver X receptor (LXR)/retinoid X receptor (RXR) heterodimers, thereby impairing cholesterol efflux from macrophages and potentially contributing to a proatherogenic phenotype.

Inhibition of Liver X Receptor/Retinoid X Receptor–Mediated Transcription Contributes to the Proatherogenic Effects of Arsenic in Macrophages In Vitro