Bisphenol A (BPA), is one of the most abundant endocrine disruptors in the environment, considered as a weak xenoestrogen. BPA has recently become of additional public health concern because of increasing evidence of deleterious effects on metabolism. Dietary intake seems the most important exposure route for BPA, followed by rapid biotransformation in the gut and liver and elimination in the urine. Although hepatocytes can represent a significant target for the effects of BPA, little is known on the direct effects and mechanisms of action of BPA on lipid homeostasis in these cells. In this work, the effects of BPA (0.3-300 ng/ml, 24 h) were investigated in rat FaO hepatoma. BPA significantly increased intracellular triglyceride (TAG) content and lipid accumulation in lipid droplets. The effects of BPA were associated with decreased mRNA levels of the transcription factors Peroxisome Proliferator-Activated Receptor isoforms a and b as well as of their downstream genes acyl-CoA oxidase and carnitine palmitoyl transferase involved in lipid oxidation. BPA also decreased transcription of ApolipoproteinB and the extracellular TAG content. FaO cells did not express Estrogen Receptors (ERa and ERb). All the effects of BPA were prevented by cell pretreatment with Wortmannin, indicating the involvement of PI-3 kinase. The results demonstrate a direct action of BPA on lipid homeostasis apparently through interference with the pathways involved in lipid oxidation and secretion.