Pharmaceuticals are designed to target specific human metabolic and molecular pathways. When released into the environment they may affect the same or comparable pathways in vertebrates and invertebrates that possess similar targets. Unfortunately, little is known about possible counterparts of human pharmaceutical targets in aquatic organisms, and investigations need to be addressed to this issue. Pharmaceutical residues may act as endocrine-disrupting chemicals, and our work support the interaction of the antiepileptic drug carbamazepine with the cAMP-mediated signaling in the mussel, Mytilus galloprovincialis. In the same mollusc, the beta-adrenoceptor antagonist propranolol (PROP) affects cAMP levels, PKA activity and downstream transcriptional regulations. PROP also acts as a 5-HT1 receptor antagonist, which is the sole 5-HT receptor reported in bivalves. In vivo exposure of mussels at environmental PROP concentrations resulted in a tissue-specific modulation of cell signaling and a concerted regulation of ABCB1 gene expression. In mussel haemocytes exposed in vitro, PROP fully antagonized the effect of serotonin, a major neuromodulator in bivalves, that per se decreases cAMP levels and PKA activity and down-regulates ABCB1 expression. PROP bioconcentrates in fish blood, and interferes with glycogenolisis and lipolysis, and heart beating. Other pharmaceuticals have significant effects on cellular physiology in fish and molluscs, and are objects of recent investigations.