In cultured hepatoma cells ethanol affects PPARα transcriptional activity by inhibiting the ability of the receptor to bind its PPRE consensus sequences. This effect is dependent on the ability of the cell to metabolize ethanol to acetaldehyde as it was abolished by the ADH inhibitor 4-methylpirazole and enhanced by the ALDH inhibitor cyanamide. Moreover, administration of acetaldehyde alone to cultured cells inhibited PPARα binding to DNA, strongly suggesting that acetaldehyde is responsible for the effects of ethanol [28].
