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Cannabis is the most used illicit drug worldwide and in some Countries a new regulatory policy makes it legal under some restrictions. This situation could lead to a substantial increase of the environmental levels of the cannabis active principle (Δ-9-tetrahydrocannabinol; Δ-9-THC) and its main metabolite, the 11-nor-9-carboxy-Δ9 -tetrahydrocannabinol (THC-COOH). Whilst previous studies highlighted the toxicity of Δ-9-THC, the adverse effects of THC-COOH to aquatic organisms is completely unknown, even if they could be higher because its environmental concentrations prevail on those of the parental compound. This study was aimed at assessing oxidative and genetic damage caused by 14-d exposures to three THC-COOH concentrations to the zebra mussel (Dreissena polymorpha), mimicking a current environmental situation (100 ng/L) and to two possible worst case scenarios (500 and 1,000 ng/L), due to the potential increase of THC-COOH in surface waters. We measured the variation in the activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities, as well as in levels of lipid peroxidation (LPO) and protein carbonyl content (PCC). Genetic injuries were investigated by the Single Cell Gel Electrophoresis (SCGE) assay, the DNA diffusion assay and the micronucleus test. A significant imbalance of antioxidant defense enzymes was noticed in response to the three tested concentrations, while oxidative damage was noted only at the higher one. Moreover, an increase of DNA fragmentation in zebra mussel hemocytes, but no fixed genetic damage, was found. Although our results showed that THC-COOH toxicity was lower than that of Δ-9-THC, the increase of cannabis use might increase its levels in freshwaters, enhancing its hazard to bivalves and likely to the whole aquatic community. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.