Endocrine disruptors (EDs) can interfere with the action of endogenous hormones, thus affecting different physiological processes. Due to conservation of endocrine systems, common targets for the action of EDs can be envisaged in invertebrate and vertebrate systems. Data on the effects of EDs in invertebrate and mammalian cells are here summarized.

In the bivalve mollusk Mytilus, different EDs affected the response of hemocytes, the cells responsible for innate immunity, through modulation of kinase-mediated cell signaling (MAPKs and PKC) involved in mediating the effects of 17-b estradiol. Significant effects of estrogens and estrogenic EDs, alone and in mixtures, were observed also in the hepatopancreas, a tissue that plays a key role in bivalve metabolism. EDs affected lysosomal lipid metabolism, carbohydrate metabolism and the expression of different genes, including estrogen receptors-ERs.

The effects of selected EDs, Bisphenol A-BPA and its brominated derivative TBBPA were also investigated in rat FaO hepatoma cells. BPA induced lipid accumulation and downregulated the expression of Peroxisome Proliferator-Activated Receptors-PPARs and downstream genes involved in lipid oxidation and secretion. The effects were apparently not mediated by thyroid or estrogen nuclear receptors but involved activation of the PI-3K pathway. On the other hand, TBBPA per se did not induce lipid accumulation, but decreased lipid content and affected PPAR expression in fat-enriched FaO cells. The lipid lowering effect of TBBPA was similar to that induced by iodothyronines, in particular 3,5-L-diiodothyronine, supporting the thyroid hormonal activity of this compound. The results demonstrate that different EDs can selectively modulate conserved components of kinase mediated signaling, as well as of nuclear receptor signaling, in both invertebrate and vertebrate cells.