RESUMO
The Villa Victoria dam is one of the most important storage reservoirs in Mexico since it distributes water to more than 20 million inhabitants in the Metropolitan Zone of Mexico City. In this dam, the common carp (Cyprinus carpio) is an important food resource for the inhabitants, so the aim of this work was to evaluate the oxidative damage (lipoperoxidation, oxidized proteins, antioxidant enzymes activity and gene expression), AChE, embryotoxicity and behavioral changes in C. carpio embryos and larvae exposed to water from Villa Victoria dam for 24, 48, 72 and 96 h. The embryotoxicity was evaluated trough the General Morphology Score (GMS) and the teratogenic index. Behavioral changes in basal locomotor activity and thigmotaxis were evaluated in a DanioVision, Noldus ™. An increase in lipid and protein oxidation as well as modification of CAT, SOD and GPx enzymatic activity was observed during the exposure times. The GMS indicated a low development in the embryos, the teratogenic index was less than 1, however teratogenic effects as yolk edema, fin malformation, head malformation and scoliosis were observed. In parallel, an increase in AChE activity and gene expression was observed reflecting changes in distance traveled of the basal locomotor activity and thigmotaxis at the sampling points. In conclusion, pollutants in water from Villa Victoria dam caused oxidative damage, changes in SOD, CAT, GPx and AChE activity as well as embryotoxicity and modifications in the behavior of C. carpio larvae. This study demonstrates the need to implement restoration programs for this reservoir since, contamination in the Villa Victoria dam could eventually endanger aquatic life and human health.
Assuntos
Acetilcolinesterase , Carpas , Embrião não Mamífero , Larva , Estresse Oxidativo , Poluentes Químicos da Água , Animais , Poluentes Químicos da Água/toxicidade , Estresse Oxidativo/efeitos dos fármacos , México , Acetilcolinesterase/metabolismo , Carpas/embriologia , Carpas/metabolismo , Larva/efeitos dos fármacos , Embrião não Mamífero/efeitos dos fármacos , Comportamento Animal/efeitos dos fármacosRESUMO
One of the most important causes of disease and premature death in the world is environmental pollution. The presence of pollutants in both water and air contributes to the deterioration of the health of human populations. The Mexico City Metropolitan Area is one of the most populous and affected by air pollution worldwide; in addition, in recent years there has been a growing demand for water, so urban reservoirs such as the Madin dam are vital to meet the demand. However, this reservoir is highly polluted due to the urban settlements around it. Therefore, the aim of the present study was to evaluate oxidative stress in clinically healthy subjects by means of the degree of lipoperoxidation, as well as the modification of serum enzyme levels, such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase associated with air and drinking water pollutants from three zones of the Mexico City Metropolitan Area, two of them related to Madin Dam. This descriptive cross-sectional study was conducted between March 2019 and September 2021 in 142 healthy participants (age range 18-65 years). Healthy subjects were confirmed by their medical history. The results showed that chronic exposure to air (SO2) and water pollutants (Al and Fe) was significantly associated with elevated levels of lipoperoxidation. There was evidence that contamination from the Madín dam can generate oxidative stress and affect the health status of people who receive water from this reservoir or who consume fish that inhabit it.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Hepatopatias , Poluentes da Água , Adolescente , Adulto , Idoso , Humanos , Pessoa de Meia-Idade , Adulto Jovem , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Estudos Transversais , Monitoramento Ambiental , México , Estresse Oxidativo , Projetos Piloto , ÁguaRESUMO
Several studies highlight the presence of aluminum and diclofenac in water bodies around the world and their ability to induce oxidative stress and a negative effect on biomolecules in several aquatic species. However, studies evaluating the toxic effect of mixtures of these contaminants are scarce. The objective of this work was to determine the genotoxic, cytotoxic and embryotoxic effect of the mixture of aluminum and diclofenac at environmentally relevant concentrations on Cyprinus carpio. Juveniles of Cyprinus carpio were exposed to 0.31 µg L-1 of diclofenac, 24.45 mg L-1 of aluminum, and a mixture of both contaminants at the same concentrations for 12, 24, 48, 72 and 96 h. After the exposure time the liver, gills and blood were extracted and the following biomarkers were evaluated: micronucleus frequency, comet assay, caspase activity and TUNEL test. On the other hand, Cyprinus carpio embryos were exposed to diclofenac (0.31 µg L-1), aluminum (0.06 mg L-1) and their mixture at the same concentrations and exposure time. Microscopic observation was performed to evaluate embryonic development at 12, 24, 48, 72 and 96 h. Diclofenac (0.31 µg L-1) induces significant increases in micronucleus frequency with respect to control (p < 0.05), in all tissues. Aluminum (24.45 mg L-1) significantly increases DNA damage index in liver and blood cells with respect to control (p < 0.05). All treatments increase caspases activity in all tissues with respect to control (p < 0.05). Diclofenac increases the percentage of TUNEL-positive cells in liver and blood; while aluminum and the mixture increases it significantly in gills and blood with respect to the control (p < 0.05). The mixture significantly delays embryonic development, while aluminum and the mixture significantly increase teratogenic index with respect to control (p < 0.05). In conclusion, exposure to environmental concentrations of aluminium, diclofenac and their mixture induces genotoxic damage, cell death by apoptosis and negative effects on the development of Cyprinus carpio and the toxic response is modified by the interaction of the xenobiotics.