Avaliação do risco ambiental do fármaco diclofenaco em ambientes marinhos

• Ano de defesa: 2016
• Autor(a) principal: Fontes, Mayana Karoline [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo
• Palavras-chave em Português: Diclofenac; Perna perna; Environmental risk; Biomarkers; Santos; Diclofenaco; Risco ambiental; Biomarcadores
• Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=4772675; http://repositorio.unifesp.br/handle/11600/46645

Emerging contaminants are potentially toxic substances that are present in a wide variety of products such as drugs, pesticides and toiletries and personal care products. These substances are often detected in trace concentrations (ng.L-1 e µg.L-1), but not included in monitoring programs. Among these substances it highlights the drug Diclofenac that is an non-steroidal anti-inflammatory drugs (NSAIDs), most frequently detected in surface waters worldwide, and the majority of previous studies are in freshwater environments. In this context, this study conducted an ecotoxicological study and an environmental risk assessment for Diclofenac in Santos Bay, using a tiered approach (TIER) which involves determining the environmental concentration in the water column and adverse biological effects associated, considering a methodology prescribed by the framework of the European Union (EMEA CPMP/SWP/4447/00). At TIER 0 were carried out chemical analysis of water collected in the outfall of Santos. At TIER I was made the fertilization test. In TIER II, sublethal effects were analyzed. The organisms were exposed in three concentrations: 20 ng.L-1, 200 ng.L-1 and 2000 ng.L-1, for 96 hours and tissues of the gills and digestive glands were removed for evaluation of biomarkers (Cytotoxicity, EROD, DBF, GST, GPX, and DNA damage, Lipoperoxidation, AChE and COX). Diclofenac was quantified only on a point of the surface (20 ng.L-1). In the fertilization test, the EC50 obtained was 388.52 mg.L-1 and the IC50 assay embriolarval obtained was 18.92 mg.L-1. Negative effects on the stability of the lysosomal membrane were observed in all concentrations tested. The EROD activity was inhibited only in the concentration of 200 ng.L-1 and DBF has not changed significantly. The activities of GST and GPx enzymes were negatively affected by Diclofenac. There was damage to DNA in the tissue of the gland only at the highest concentration and lipid peroxidation was more intense in the tissue of the gills from the concentration of 200 ng.L-1, indicating oxidative stress. The AChE activity was induced in the tissue of the gills. Regarding COX, there was a significant inhibition of activity at concentrations of 20 ng.L-1 in the tissue of the gills. The risk assessment indicated low ecological risk in the Bay of Santos, when standard acute and crhonic ecotoxicological assays were employed. However, our results show that the environmental concentration of the drug, even though the order of 20 ng.L-1 is enough to cause cellular damage and physiological damage as of the lysosomal membrane destabilization, corroborating the biomarker data. Our results point to a environmental risk in the Santos bay caused by Diclofenac and suggest the need for improvement in the treatment of domestic wastewater to reduce this compound as well as regulations on environmental legislation.