Effects on feeding rate and biomarker responses of marine mussels experimentally exposed to propranolol and acetaminophen

Environmental risk assessments of human pharmaceuticals and other 'emerging contaminants' should integrate both population-relevant endpoints and biomarkers of potential modes of action in a range of species. Adult Mytilus galloprovincialis were exposed to the beta-adrenergic receptor blocker propranolol or to the anti-inflammatory drug acetaminophen (paracetamol), both commonly used therapeutic drugs present in aquatic ecosystems. Mussels were exposed under semi-static conditions for 10 days to either acetaminophen (CAS number 103-90-2; mean measured concentrations 23 and 403 A mu g/L) or propranolol hydrochloride (CAS number 318-98-9; mean measured propranolol concentrations 11 and 147 A mu g/L) at 15 A +/- 1 A degrees C sea water. Feeding rate was assessed as an indicator of general toxicity. For propranolol, the 10-day no-observed effect concentration ((NOEC)-N-feeding rate) and lowest observed effect concentration ((LOEC)-L-feeding rate) were 11 and 147 A mu g/L, respectively. For acetaminophen, feeding rate was increased at both 23 and 403 A mu g/L, suggesting a 10-day (NOEC)-N-feeding rate of 403 A mu g/L. Primarily, phase I carboxylesterase (CbE), phase II glutathione S-transferase (GST) and the anti-oxidant catalase activities were evaluated in digestive gland. Gill GST and acetylcholinesterase (AChE) activities were also measured. Lipid peroxidation (LPO) levels were measured in both tissues to assess oxidative stress. Some enzymatic activities in liver were also reduced after propranolol exposure whilst acetaminophen enhanced them (CbE p < 0.05). Acetaminophen exposure significantly increased hepatic LPO levels and inhibited AChE activity in gill (10-day NOEC and LOEC of 23 and 403 A mu g/L, respectively), whereas propranolol (11 A mu g/L) enhanced gill GST.