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The presence of cocaine and its metabolites and by-products has been identified in different aquatic matrices, making crack cocaine the target of recent studies. The aim of this study was to evaluate the sublethal effects of crack on the brown mussel Perna perna. Mussels were exposed to three concentrations of crack cocaine (0.5, 5.0, and 50.0 μg L) for 168 h. Gills, digestive glands, and hemolymph were extracted and analyzed after three different exposure times using a suite of biomarkers (EROD, DBF, GST, GPX, LPO, DNA damage, ChE, and lysosomal membrane stability [LMS]). After 48 and 96 h of exposure, EROD, DBF, GST, GPX activities and DNA strand breaks in the gills increased significantly after 48 and 96 h of exposure. Alterations in LMS were also observed in the mussels exposed to all crack concentrations after 96 and 168 h. Our results demonstrated that crack cocaine is metabolized by CYP-like and GST activities in the gills. GPX was not able to prevent primary genetic damage, and cytotoxic effects in the hemocytes were also observed in a dose- and time-dependent response. Our study shows that the introduction of illicit drugs into coastal ecosystems must be considered a threat to marine organisms.

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Studies show that pharmaceuticals are being taken to the oceans causing contamination and toxicity to aquatic organisms. The present study evaluated the survival rate of microcrustaceans Artemia salina and the abnormal embryo larval development rate of sea urchin Echinometra lucunter, after exposure to the drug Losartan, an antihypertensive drug, and the drug Diclofenac, a non-steroidal antiinflammatory drug (NSAID), in addition to its mixture among its compounds. Acute toxicity tests were carried out using A. salina and chronic toxicity tests were carried out using embryos of E. lucunter. Organisms were exposed to isolated pharmaceuticals at different concentrations: 1.56 mg.L-1; 3.12 mg.L-1; 6.25 mg.L-1; 12.5 mg.L-1; 25 mg.L-1; 50 mg.L-1 and 100 mg.L-1, and their mixture at concentrations: 0.78 mg.L-1; 1.56 mg.L-1; 3.12 mg.L-1; 6.25mg.L-1; 12.5 mg.L-1; 25 mg.L-1 and 50 mg.L-1. The result obtained in the acute toxicity test did not show toxicity to A. salina. Chronic toxicity test with losartan did not show toxicity to sea urchin embryos, in contrast, the isolated diclofenac showed chronic toxicity at NOEC = 6.25 mg.L-1, LOEC = 12.5 mg.L-1 and IC50 = 62.15 mg.L-1. The result obtained with embryos exposed to the mixture of losartan and diclofenac, showed chronic toxicity at NOEC= 6.25 mg.L-1 and LOEC= 12.5 mg.L-1, not being possible to show the IC50. Our results suggest that the mixture of the two studied pharmaceuticals might decrease the toxicity, since diclofenac showed higher chronic toxicity to E. lucunter embryo larval development when it was isolated than when it was mixed with losartan. However, there is a need for further ecotoxicological studies that clarify the pathways of these pharmaceuticals in non-target organisms.

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