Evaluation of the ecotoxicological effects of salinity and metformin in Gambusia holbrooki

• Autor(a) principal: Sousa, Maria de Jesus Rios
• Data de Publicação: 2021
• Tipo de documento: Dissertação
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• Texto Completo: http://hdl.handle.net/10773/33456
• topic: Climate change; Salinity; Metformin; Gambusia holbrooki; Oxidative stress; Energy reserves; Neurotoxicity

Aquatic ecosystems are threatened by factors related to climate change, leading to changes in the physical and chemical water properties. Between these changes, and as a consequence of global warming and extreme weather events, coastal systems are facing sudden fluctuations in salinity. Aquatic ecosystems are also threatened by organic and inorganic compounds that increase water pollution. Metformin is an antidiabetic drug commonly used by patients of diabetes type 2. It is also used as a treatment for polycystic ovary syndrome and as an anti-cancer drug. Metformin is not metabolized by the human body and has high watery mobility. Because wastewater treatment plants have low efficacy in removing these compounds, they may reach in the aquatic environment. The aim of this study was to evaluate the influence of different salinity levels (17, 24 means control, 31) on the effects of metformin (0-Control, 1.5, 15, 150 μ/L) in Gambusia holbrooki after acute exposure (96h). A chronic exposure was also performed to assess the effects of metformin (0-Control, 0.5, 1, 5, 10 μ/L) in G. holbrooki at salinity 17 for 28 days. For both assays, several biomarkers were quantified in the exposure organisms to assess: antioxidant capacity (superoxide dismutase-SOD, catalase-CAT, glutathione peroxidase-GPx, glutathione reductase-GRed) and biotransformation capacity (glutathione S-transferases-GSTs), cellular damage (levels of lipid peroxidation-TBARS), content of energy reserves (head and body protein levels- PROT, glycogen content- GLY) and neurotoxic effects (acetylcholinesterase-AChE). The results obtain from acute exposure showed interactions between salinity and metformin in SOD activity, body PROT levels and GLY content in G. holbrooki. The data obtain showed that an increase in salinity can modulate the response of the G. holbrooki to metformin. The results obtain from the chronic assay, showed that exposure of G. holbrooki to metformin led to a significant decrease in SOD activity at almost all concentrations tested. In addition, GPx and GSTs activity increased significantly at the concentration of metformin 10 and 5 μ/L, respectively. Therefore, metformin can lead to oxidative stress in G. holbrooki. Overall, the GLY content in G. holbrooki increased after exposure to metformin concentrations. No significant effects were observed in the remaining biomarkers measured. Although this work does not show a full oxidative stress scenario in G. holbrooki after exposure to metformin under different salinities, other studies have already shown that metformin alone can lead to oxidative damage in aquatic species. Therefore, additional ecotoxicological studies should be performed to find out if different metformin concentrations combined with salinity increase might impact non-target species.