RESUMEN
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.
Asunto(s)
Acetilcolinesterasa , Carpas , Embrión no Mamífero , Larva , Estrés Oxidativo , Contaminantes Químicos del Agua , Animales , Contaminantes Químicos del Agua/toxicidad , Estrés Oxidativo/efectos de los fármacos , México , Acetilcolinesterasa/metabolismo , Carpas/embriología , Carpas/metabolismo , Larva/efectos de los fármacos , Embrión no Mamífero/efectos de los fármacos , Conducta Animal/efectos de los fármacosRESUMEN
Current and thorough information on the ecotoxicological consequences of pharmaceuticals is accessible globally. However, there remains a substantial gap in knowledge concerning the potentially toxic effects of COVID-19 used drugs, individually and combined, on aquatic organisms. Given the factors above, our investigation assumes pivotal importance in elucidating whether or not paracetamol, dexamethasone, metformin, and their tertiary mixtures might prompt histological impairment, oxidative stress, and apoptosis in the liver of zebrafish. The findings indicated that all treatments, except paracetamol, augmented the antioxidant activity of superoxide dismutase (SOD) and catalase (CAD), along with elevating the levels of oxidative biomarkers such as lipid peroxidation (LPX), hydroperoxides (HPC), and protein carbonyl content (PCC). Paracetamol prompted a reduction in the activities SOD and CAT and exhibited the most pronounced toxic response when compared to the other treatments. The gene expression patterns paralleled those of oxidative stress, with all treatments demonstrating overexpression of bax, bcl2, and p53. The above suggested a probable apoptotic response in the liver of the fish. Nevertheless, our histological examinations revealed that none of the treatments induced an apoptotic or inflammatory response in the hepatocytes. Instead, the observed tissue alterations encompassed leukocyte infiltration, sinusoidal dilatation, pyknosis, fatty degeneration, diffuse congestion, and vacuolization. In summary, the hepatic toxicity elicited by COVID-19 drugs in zebrafish was less pronounced than anticipated. This attenuation could be attributed to metformin's antioxidant and hormetic effects.
Asunto(s)
Acetaminofén , Hígado , Metformina , Estrés Oxidativo , Pez Cebra , Animales , Hígado/efectos de los fármacos , Hígado/metabolismo , Estrés Oxidativo/efectos de los fármacos , Acetaminofén/toxicidad , Metformina/farmacología , Dexametasona/farmacología , COVID-19 , Apoptosis/efectos de los fármacos , Tratamiento Farmacológico de COVID-19 , Superóxido Dismutasa/metabolismo , Peroxidación de Lípido/efectos de los fármacos , Catalasa/metabolismo , Contaminantes Químicos del Agua/toxicidadRESUMEN
To mitigate the environmental impact of microplastics (MPs), the scientific community has innovated sustainable and biodegradable polymers as viable alternatives to traditional plastics. Chitosan, the deacetylated form of chitin, stands as one of the most thoroughly investigated biopolymers and has garnered significant interest due to its versatile applications in both medical and cosmetic fields. Nevertheless, there is still a knowledge gap regarding the impact that chitosan biopolymer films (CBPF) may generate in aquatic organisms. In light of the foregoing, this study aimed to assess and compare the potential effects of CBPF on the gastrointestinal tract, gills, brain, and liver of Danio rerio against those induced by MPs. The findings revealed that both CBPF and MPs induced changes in the levels of oxidative stress biomarkers across all organs. However, it is essential to note that our star plots illustrate a tendency for CBPF to activate antioxidant enzymes and for MPs to produce oxidative damage. Regarding gene expression, our findings indicate that MPs led to an up-regulation in the expression of genes associated with apoptotic response (p53, casp3, cas9, bax, and bcl2) in all fish organs. Meanwhile, CBPF produced the same effect in genes related to antioxidant response (nrf1 and nrf2). Overall, our histological observations substantiated these effects, revealing the presence of plastic particles and tissue alterations in the gills and gastrointestinal tract of fish subjected to MPs. From these results, it can be concluded that CBPF does not represent a risk to fish after long exposure.
Asunto(s)
Quitosano , Microplásticos , Estrés Oxidativo , Poliestirenos , Contaminantes Químicos del Agua , Pez Cebra , Animales , Microplásticos/toxicidad , Contaminantes Químicos del Agua/toxicidad , Quitosano/química , Estrés Oxidativo/efectos de los fármacos , Poliestirenos/toxicidad , Biopolímeros , EcotoxicologíaRESUMEN
Fluoxetine (FLX), a selective serotonin reuptake inhibitor (SSRI), is consistently introduced into the environment due to its ongoing consumption and inadequate removal by wastewater treatment plants. As a result, the scientific community has displayed a keen interest in investigating the potential toxicological effects associated with this medication. Nevertheless, there is a scarcity of available data regarding the impact of FLX on blood parameters. With this in mind, this study aimed to evaluate the potential toxicological consequences of FLX at environmentally significant concentrations (5, 16, and 40 ng/L) following a 96-hour acute exposure blood parameters in Danio rerio fish. Moreover, the investigation encompassed an assessment of oxidative stress parameters to determine whether the drug could induce disruptions in the REDOX status of the fish. The findings unveiled that FLX prompted the induction of oxidative stress in various organs of the fish, encompassing the liver, gut, brain, and gills. Notably, the gills and brain exhibited heightened susceptibility to the drug's effects compared to other organs. Furthermore, following acute exposure to FLX, there was an upregulation of antioxidant-related genes (sod, cat, gpx, nrf1, and nrf2), thereby providing additional evidence supporting the induction of oxidative stress in the organs of the fish. Lastly, FLX significantly impacted the customary values of various blood parameters, including glucose, blood urea nitrogen, alanine aminotransferase, alkaline phosphatase, red blood cell count, hemoglobin, and hematocrit. Thus, it can be inferred that FLX harmed the overall health status of the fish, resulting in the development of liver disease, anemia, and other associated illnesses.
Asunto(s)
Fluoxetina , Pez Cebra , Animales , Fluoxetina/toxicidad , Pez Cebra/fisiología , Inhibidores Selectivos de la Recaptación de Serotonina/toxicidad , Estrés Oxidativo , Antioxidantes/farmacologíaRESUMEN
The antidiabetic drug metformin (MET) and its metabolite guanylurea (GUA) have been frequently and ubiquitously detected in surface water. Consequently, there has been a consistent rise in studying the toxicity of MET and GUA in fish over the past decade. Nonetheless, it is noteworthy that no study has assessed the harmful effects both compounds might trigger on fish blood and organs after chronic exposure. Taking into consideration the data above, our research strived to accomplish two primary objectives: Firstly, to assess the effect of comparable concentrations of MET and GUA (1, 40, 100 µg/L) on the liver, gills, gut, and brain of Danio rerio after six months of flow-through exposure. Secondly, to compare the outcomes to identify which compound prompts more significant oxidative stress and apoptosis in organs and blood parameter alterations. Herein, findings indicate that both compounds induced oxidative damage and increased the expression of genes associated with apoptosis (bax, bcl2, p53, and casp3). Chronic exposure to MET and GUA also generated fluctuations in glucose, creatinine, phosphorus, liver enzymes, red and white blood count, hemoglobin, and hematocrit levels. The observed biochemical changes indicate that MET and GUA are responsible for inducing hepatic damage in fish, whereas hematological alterations suggest that both compounds cause anemia. Considering GUA altered to a more considerable extent the values of all endpoints compared to the control group, it is suggested transformation product GUA is more toxic than MET. Moreover, based on the above evidence, it can be inferred that a six-month exposure to MET and GUA can impair REDOX status and generate apoptosis in fish, adversely affecting their essential organs' functioning.
Asunto(s)
Metformina , Pez Cebra , Animales , Metformina/toxicidad , Evaluación del Impacto en la Salud , HipoglucemiantesRESUMEN
Sucralose (SUC) and acesulfame-k (ACE-K) are widely used artificial sweeteners worldwide; however, they are frequently detected in aquatic environments due to their low metabolism and inadequate removal during wastewater treatment. The harmful effects of these compounds on hydrobionts have yet to be fully understood, as data on their toxicity is limited and inconclusive. This research aimed to determine the impact of SUC (50, 75, 125 µg/L) and ACE-K (50, 75, 125 µg/L), individually and in combination, on fish's swimming behavior, acetylcholinesterase activity, and oxidative stress response after four months of exposure. Following exposure, adult Danio rerio displayed anxiety-like behavior, as evidenced by increased freezing time and decreased swimming activity. Additionally, analysis of fish brain tissue revealed a disruption of REDOX homeostasis, leading to oxidative stress, which may be responsible for the observed inhibition of AChE activity. The results indicated that ACE-K was more toxic than SUC, and the mixture of both compounds produced a more detrimental effect than when each compound was administered alone. These findings highlight the hazardous impacts of SUC and ACE-K on fish in environmentally relevant concentrations, suggesting that these compounds should be added to the priority pollutant list.
Asunto(s)
Acetilcolinesterasa , Estrés Oxidativo , Animales , Encéfalo , Pez CebraRESUMEN
In recent years and as a result of the Covid-19 pandemic, the consumption of dexamethasone (DXE) has increased. This favors that this corticosteroid is highly released in aquatic environments, generating deleterious effects in aquatic organisms. The information on the toxic effects of DXE in the environment is still limited. Thus, the objective of this work was to determine whether DXE at short-term exposure can cause alterations to embryonic development and alteration of oxidative stress-related gene expression patterns in Cyprinus carpio. For this purpose, common carp embryos (2 hpf) were exposed to realistic concentrations of DXE until 96 hpf. Alterations to embryonic development were evaluated at 12, 24, 48, 72 and 96 hpf. In addition, oxidative stress in carp embryos at 72 and 96 hpf was evaluated by cellular oxidation biomarkers (lipoperoxidation level, hydroperoxide and carbonyl protein content) and antioxidant enzymes activities (superoxide dismutase and catalase). Oxidative stress-related gene expression (sod, cat and gpx1) was also evaluated. Our results showed that DXE concentrations above 35 ng/L are capable of producing alterations to embryonic development in 50 % of the embryo population. Furthermore, DXE was able to induce alterations such as scoliosis, hypopigmentation, craniofacial malformations, pericardial edema and growth retardation, leading to the death of half of the population at 50 ng/L of DXE. Concerning oxidative stress, the results demonstrated that DXE induce oxidative damage on the embryos of C. carpio. In conclusion, DXE is capable of altering embryonic development and generating oxidative stress in common carp C. carpio.
Asunto(s)
COVID-19 , Carpas , Contaminantes Químicos del Agua , Animales , Humanos , Carpas/metabolismo , Bioacumulación , Pandemias , Peroxidación de Lípido , Contaminantes Químicos del Agua/toxicidad , Biomarcadores/metabolismo , Tratamiento Farmacológico de COVID-19 , Estrés Oxidativo , Antioxidantes/metabolismo , Desarrollo Embrionario , Expresión Génica , Dexametasona/toxicidadRESUMEN
The variety of activities carried out within hospitals results in their final discharges being considered hotspots for the emission of emerging pollutants. Hospital effluents contain different substances capable of altering the health of ecosystems and biota, furthermore, little research has been done to elucidate the adverse effects of these anthropogenic matrices. Taking this into account, herein we aimed to establish whether exposure to different proportions (2 %, 2.5 %, 3 %, and 3.5 %) of hospital effluent treated by hospital wastewater treatment plant (HWWTP) can induce oxidative stress, behavioral alterations, neurotoxicity, and disruption of gene expression in Danio rerio brain. Our results demonstrate that the hospital effluent under-study induces an anxiety-like state and alters swimming behavior, as fish exhibited increased freezing episodes, erratic movements and traveled less distance than the control group. In addition, after exposure we observed a meaningful rise in biomarkers related to oxidative damage, such as protein carbonyl content (PCC), lipoperoxidation level (LPX), hydroperoxide content (HPC), as well as an increase in enzyme antioxidant activities of catalase (CAT), and superoxide dismutase (SOD) upon short-term exposure. Moreover, we discovered an inhibition of acetylcholinesterase (AChE) activity in a hospital effluent proportion-dependent manner. Regarding gene expression, a significant disruption of genes related to antioxidant response (cat, sod, nrf2), apoptosis (casp6, bax, casp9), and detoxification (cyp1a1) was observed. In conclusion, our outcomes suggest that hospital effluents enhance the emergence of oxidative molecules, and promote a highly oxidative environment at the neuronal level that favors the inhibition of AChE activity, which consequently explains the anxiety-like behavior observed in D. rerio adults. Lastly, our research sheds light on possible toxicodynamic mechanism by which these anthropogenic matrices may trigger damage in D. rerio brain.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Animales , Pez Cebra/metabolismo , Antioxidantes/metabolismo , Carbonilación Proteica , Acetilcolinesterasa/metabolismo , Ecosistema , Estrés Oxidativo , Superóxido Dismutasa/metabolismo , Hospitales , Contaminantes Químicos del Agua/análisisRESUMEN
Hospital effluents represent a threat to the environment owing to the content of toxic substances capable of altering the structure and function of ecosystems. Despite the available information about the impact of hospital effluents on aquatic organisms, the molecular mechanism underlying this process has received little or no attention. The present study aimed to evaluate the oxidative stress and gene expression induced by different proportions (2 %, 2.5 %, 3 % and 3.5 %) of hospital effluent treated by hospital wastewater treatment plant (HWWTP) in liver, gut, and gills of Danio rerio at different exposure times. Significant increases in the levels of protein carbonylation content (PCC), hydroperoxides content (HPC), lipoperoxidation level (LPX) and superoxide dismutase (SOD) and catalase (CAT) activity were observed in most of the organs evaluated at the four proportions tested with respect to the control group (p < 0.05). It was found that at longer exposure times there is a lower response in SOD activity, suggesting catalytic depletion due to the oxidative environment at the intracellular level. The lack of complementarity between SOD and mRNA activity patterns indicates that the activity itself is subordinated to post-transcriptional processes. Upregulation of transcripts related to antioxidant processes (sod, cat, nrf2), detoxification (cyp1a1) and apoptosis (bax, casp6, and casp9) was observed in response to oxidative imbalance. On the other hand, the metataxonomic approach allowed the characterization of pathogenic bacterial genera such as Legionella, Pseudomonas, Clostridium XI, Parachlamydia and Mycobacterium present in the hospital effluent. Our findings indicate that although hospital effluent was treated by HWWTP, it caused oxidative stress damage and disrupted gene expression by decreasing the antioxidant response in Danio rerio.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Animales , Pez Cebra/metabolismo , Antioxidantes/metabolismo , Ecosistema , Estrés Oxidativo , Catalasa/metabolismo , Superóxido Dismutasa/metabolismo , Contaminantes Químicos del Agua/toxicidad , Hospitales , Expresión GénicaRESUMEN
Bisphenol A (BPA) is a micro-pollutant found in various environmental matrices at concentrations as low as ng/L. Recent studies have shown that this compound can cause oxidative damage and neurotoxic effects in aquatic organisms. However, there is a lack of research investigating the effects of BPA at environmentally relevant concentrations. Therefore, this study aimed to assess the neurotoxic effects of acute BPA exposure (96 h) at environmentally relevant concentrations (220, 1180, and 1500 ng/L) in adult zebrafish (Danio rerio). The Novel Tank trial was used to evaluate fish swimming behavior, and our results indicate that exposure to 1500 ng/L of BPA reduced the total distance traveled and increased freezing time. Furthermore, the evaluation of biomarkers in the zebrafish brain revealed that BPA exposure led to the production of reactive oxygen species and increased acetylcholinesterase activity. Gene expression analysis also indicated the overexpression of mbp, α1-tubulin, and manf in the zebrafish brain. Based on our findings, we concluded that environmentally relevant concentrations of BPA can cause anxiety-like behavior and neurotoxic effects in adult zebrafish.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Animales , Pez Cebra/metabolismo , Acetilcolinesterasa/genética , Acetilcolinesterasa/metabolismo , Compuestos de Bencidrilo/toxicidad , Compuestos de Bencidrilo/metabolismo , Estrés Oxidativo , Encéfalo/metabolismo , Expresión Génica , Contaminantes Químicos del Agua/toxicidad , Contaminantes Químicos del Agua/metabolismoRESUMEN
Gender-based violence (GBV) and cyber-aggression are growing problems in Mexico, but there is a dearth of information on their associated risks. We aimed to determine the prevalence of dating violence (DV) and cyber-aggression in a public campus and compared students' acceptability of abusive DV based on their sex and sexual orientation. We employed a cross-sectional design to survey 964 first-year medical students attending a public university. We analyzed who found "acceptable" abusive behaviors from a dating partner and carried out descriptive analyses of sample characteristics by sex. We included 633 women and 331 men. Homosexual and bisexual orientation was lower among women (1.5%, 4.8%) vs. men (16.9%, 7.2%). Of women and men, respectively, 64.2% and 35.8% reported having been in a dating relationship. Experiencing abusive behaviors in the year prior to the study was associated with students' level of "acceptability". A total of 43.5% of the students who experienced cyber-aggression did not report any mental health consequences, 32.6% did not seek professional help, and 17.4% reported feeling depressed. Students that accepted emotionally abusive DV behaviors displayed a fourfold risk of experiencing physical abuse. Women and sexual minorities are more at risk of experiencing GBV and DV. More male students reported being victims of cyber-aggression.
Asunto(s)
Víctimas de Crimen , Violencia de Pareja , Estudiantes de Medicina , Humanos , Masculino , Femenino , Universidades , México , Estudios Transversales , Víctimas de Crimen/psicología , Violencia de Pareja/psicologíaRESUMEN
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.
Asunto(s)
Contaminantes Atmosféricos , Contaminación del Aire , Hepatopatías , Contaminantes del Agua , Adolescente , Adulto , Anciano , Humanos , Persona de Mediana Edad , Adulto Joven , Contaminantes Atmosféricos/análisis , Contaminación del Aire/análisis , Estudios Transversales , Monitoreo del Ambiente , México , Estrés Oxidativo , Proyectos Piloto , AguaRESUMEN
Microplastics (MPs) alone may endanger the health and fitness of aquatic species through different mechanisms. However, the harmful effects of these when mixed with other emerging contaminants require additional research. Herein, we aimed to determine whether a mixture of MPs with metformin (MET) or guanylurea (GUA) might induce embryotoxicity and oxidative stress in Danio rerio. Upon exposure to mixtures, our results showed MPs reduced the mortality rate of MET and GUA in embryos. Moreover, the severity and the rate of malformations were also decreased in all mixtures with MPs. Concerning oxidative stress, our findings indicated MET, GUA, MPs, and the mixtures increased the levels of lipoperoxidation, hydroperoxide content, and protein carbonyl content in D. rerio larvae. However, the oxidative damage induced in all mixtures was lower than that produced by both drugs alone. Thus, it is likely that the accumulation of MPs avoided the entrance of MET and GUA into the embryos. Once the embryo hatched, MPs did only remain accumulated in the yolk sac of larvae and did not translocate to other organs. Our risk assessment analysis confirmed that MPs shrunk the damage produced by MET and GUA. In a nutshell, MPs mitigate the embryotoxic damage of metformin and guanylurea in D. rerio by blocking their entrance.
Asunto(s)
Metformina , Contaminantes Químicos del Agua , Animales , Microplásticos , Pez Cebra/metabolismo , Poliestirenos/toxicidad , Plásticos/toxicidad , Peróxido de Hidrógeno/metabolismo , Carbonilación Proteica , Contaminantes Químicos del Agua/metabolismo , LarvaRESUMEN
Metformin (MET) is among the most consumed drugs around the world, and thus, it is considered the uppermost drug in mass discharged into water settings. Nonetheless, data about the deleterious consequences of MET on water organisms are still scarce and require further investigation. Herein, we aimed to establish whether or not chronic exposure to MET (1, 20, and 40 µg/L) may alter the swimming behavior and induce neurotoxicity in Danio rerio adults. After 4 months of exposure, MET-exposed fish exhibited less swimming activity when compared to control fish. Moreover, compared with the control group, MET significantly inhibited the activity of AChE and induced oxidative damage in the brain of fish. Concerning gene expression, MET significantly upregulated the expression of Nrf1, Nrf2, BAX, p53, BACE1, APP, PSEN1, and downregulated CASP3 and CASP9. Although MET did not overexpress the CASP3 gene, we saw a meaningful rise in the activity of this enzyme in the blood of fish exposed to MET compared to the control group, which we then confirmed by a high number of apoptotic cells in the TUNEL assay. Our findings demonstrate that chronic exposure to MET may impair fish swimming behavior, making them more vulnerable to predators.
Asunto(s)
Metformina , Contaminantes Químicos del Agua , Secretasas de la Proteína Precursora del Amiloide/metabolismo , Animales , Ácido Aspártico Endopeptidasas/metabolismo , Conducta Animal , Caspasa 3/metabolismo , Metformina/toxicidad , Factor 2 Relacionado con NF-E2/metabolismo , Natación , Proteína p53 Supresora de Tumor/metabolismo , Agua/metabolismo , Contaminantes Químicos del Agua/metabolismo , Contaminantes Químicos del Agua/toxicidad , Pez Cebra/fisiología , Proteína X Asociada a bcl-2/metabolismoRESUMEN
This study assessed the effects of Bisphenol A in embryonic stages of zebrafish, applying an IBR multi-biomarker approach that included alterations in growth and oxidative status and relates it with the expression of Nrf1, Nrf2, Wnt3a, Wnt8a, COX-2, Qdpra, and DKK1 genes. For this purpose, we exposed zebrafish embryos to eight environmentally relevant concentrations of BPA (220, 380, 540, 700, 860, 1180, 1340, and 1500 ng L-1) until 96 h post-fertilization. Our results show that BPA induces several malformations in embryos (developmental delay, hypopigmentation, tail malformations, and on), leading to their death. The LC50, EC50 of malformations, and teratogenic index (TI) were 1234.60 ng L-1, 987.77 ng L-1, and 1.25, respectively; thus, this emerging contaminant is teratogenic. Regarding oxidative stress and gene expression, we demonstrated BPA altered oxidative status and the gene expression in embryos of Danio rerio.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Animales , Compuestos de Bencidrilo , Biomarcadores/metabolismo , Embrión no Mamífero , Desarrollo Embrionario , Fenoles , Contaminantes Químicos del Agua/metabolismo , Pez Cebra/metabolismoRESUMEN
Several studies have reported the presence of phenytoin (PHE) in wastewater treatment plant effluents, hospital effluents, surface water, and even drinking water. However, published studies on the toxic effects of PHE at environmentally relevant concentrations in aquatic organisms are scarce. The present study aimed to determine the effect of three environmentally relevant concentrations of PHE (25, 282, and 1500 ng L-1) on behavioral parameters using the novel tank test. Moreover, we also aimed to determine whether or not these concentrations of PHE may impair acetylcholinesterase (AChE) activity and oxidative status in the brain of Danio rerio adults. Behavioral responses suggested an anxiolytic effect in PHE-exposed organisms, mainly observed in organisms exposed to 1500 ng L-1, with a significant decrease in fish mobility and a significant increase in activity at the top of the tank. Besides the behavioral impairment, PHE-exposed fish also showed a significant increase in the levels of lipid peroxidation, hydroperoxides, and protein carbonyl content compared to the control group. Moreover, a significant increase in brain AChE levels was observed in fish exposed to 282 and 1500 ng L-1. The results obtained in the present study show that PHE triggers a harmful response in the brain of fish, which in turn generates fish have an anxiety-like behavior.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Acetilcolinesterasa/metabolismo , Animales , Biomarcadores/metabolismo , Estrés Oxidativo , Fenitoína/metabolismo , Fenitoína/toxicidad , Carbonilación Proteica , Contaminantes Químicos del Agua/metabolismo , Pez Cebra/metabolismoRESUMEN
Sucralose (SUC) is the most consumed artificial sweetener worldwide, not metabolized by the human body, and barely eliminated from water in wastewater treatment plants. Although different studies have reported high concentrations of this sweetener in aquatic environments, limited to no information is known about the toxic effects this drug may produce over water organisms. Moreover, most of the current studies have used non-environmentally relevant concentrations of SUC for these effects. Herein, we aimed to evaluate the harmful effects that environmentally relevant concentrations of SUC may induce in the early life stages of Danio rerio. According to our results, SUC altered the embryonic development of D. rerio, producing several malformations that led to their death. The major malformations were scoliosis, pericardial edema, yolk deformation, and tail malformation. However, embryos also got craniofacial malformations, eye absence, fin absence, dwarfism, delay of the hatching process, and hypopigmentation. SUC also generated an oxidative stress response in the embryos characterized by an increase in the levels of lipid peroxidation, hydroperoxides, and carbonyl proteins. To overcome this oxidative stress response, we observed a significant increase in the levels of antioxidant enzymes superoxide dismutase and catalase. Moreover, a significant boost in the expression of antioxidant defense-related genes, Nuclear respiratory factor 1a (Nrf1a) and Nuclear respiratory factor 2a (Nrf2a), was also observed at all concentrations. Concerning apoptosis-related genes, we observed the expression of Caspase 3 (CASP3) and Caspase 9 (CASP9) was increased in a concentration-dependent manner. Overall, we conclude environmentally relevant concentrations of SUC are harmful to the early life stages of fish as they produce malformations, oxidative stress, and increased gene expression of apoptosis-related genes on embryos.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Animales , Antioxidantes/metabolismo , Embrión no Mamífero , Desarrollo Embrionario , Estrés Oxidativo , Sacarosa/análogos & derivados , Edulcorantes/metabolismo , Agua/metabolismo , Contaminantes Químicos del Agua/metabolismo , Pez Cebra/metabolismoRESUMEN
Fluoxetine (FLX) exerts its therapeutic effect by inhibiting the presynaptic reuptake of the neurotransmitter serotonin. Nonetheless, at high concentrations of this drug, adverse effects occur in the brain of exposed organisms. Bearing this into account, the objective of this study was to evaluate the neurotoxic effects of the fluoxetine through the evaluation of behavior (Novel tank test), determination of oxidative stress, and determination of acetylcholinesterase (AChE) activity in adult zebrafish Danio rerio. For this purpose, Danio rerio adults were exposed to three environmentally relevant concentrations (5, 10, 16 ng L-1) of FLX for 96 h. Our results demonstrate fish presented a significant disruption in their behavior, as they remained long-lasting time frozen at the top of the tank. Since we observed a significant reduction of AChE activity in the brain of fish, we believe the above described anxiety-like state is the result of this enzyme impairment. Moreover, as FLX-exposed fish showed a significant increase in the levels of oxidative damage biomarkers, we suggest this AChE disruption is associated with the oxidative stress response fish exhibited. Based on our findings, we believe the environmentally relevant concentration of FLX alters the redox status of the brain, impairing this way the behavior of fish and making them more vulnerable to predation.
Asunto(s)
Contaminantes Químicos del Agua , Pez Cebra , Acetilcolinesterasa/metabolismo , Animales , Fluoxetina/toxicidad , Estrés Oxidativo , Contaminantes Químicos del Agua/toxicidad , Pez Cebra/metabolismoRESUMEN
Several studies have indicated that hospital effluents can produce genotoxic and mutagenic effects, cytotoxicity, hematological and histological alterations, embryotoxicity, and oxidative stress in diverse water organisms, but research on the neurotoxic effects hospital wastewater materials can generate in fish is still scarce. To fill the above-described knowledge gap, this study aimed to determine whether the exposure of adult zebrafish (Danio rerio) to several proportions (0.1%, 2.5%, 3.5%) of a hospital effluent can disrupt behavior or impair redox status and acetylcholinesterase content in the brain. After 96 h of exposure to the effluent, we observed a decrease in total distance traveled and an increase in frozen time compared to the control group. Moreover, we also observed a significant increase in the levels of reactive oxygen species in the brains of the fish, especially in hydroperoxide and protein carbonyl content, relative to the control group. Our results also demonstrated that hospital effluents significantly inhibited the activity of the AChE enzyme in the brains of the fish. Our Pearson correlation demonstrated that the response to acetylcholinesterase at the lowest proportions (0.1% and 2.5%) is positively related to the oxidative stress response and the behavioral changes observed. The cohort of our studies demonstrated that the exposure of adult zebrafish to a hospital effluent induced oxidative stress and decreased acetylcholinesterase activity in the brain of these freshwater organisms, which can lead to alterations in their behavior.
Asunto(s)
Acetilcolinesterasa , Conducta Animal , Estrés Oxidativo , Contaminantes Químicos del Agua , Pez Cebra , Acetilcolinesterasa/metabolismo , Animales , Conducta Animal/efectos de los fármacos , Encéfalo/efectos de los fármacos , Encéfalo/enzimología , Hospitales , Humanos , México , Estrés Oxidativo/efectos de los fármacos , Carbonilación Proteica/efectos de los fármacos , Natación , Contaminantes Químicos del Agua/toxicidad , Pez Cebra/metabolismoRESUMEN
Phenytoin (PHE) is an antiepileptic drug that has been widely used in clinical practice for about 80 years. It is mainly used in the treatment of tonic-clonic and partial seizures. The widespread consumption of this drug around the world has led to PHE being introduced into water bodies through municipal, hospital, and industrial effluent discharges. Since the toxic effects of this drug on aquatic species has been scarcely explored, the aim of this work was to investigate the influence of low (25-400 ngL-1) and high (500-1500 ngL-1) environmentally relevant concentrations of PHE on the development and oxidative status of zebrafish (Danio rerio) embryos. The toxicity of PHE was evaluated from 12 to 96 h after fertilization in D. rerio at concentrations between 25 and 1500 ngL-1. In both the control group and the 0.05% DMSO system, no malformations were observed, all embryos developed normally after 96 h. The severity and frequency of malformations increased with increasing PHE concentration compared to embryos in the control group. Malformations observed included developmental delay, hypopigmentation, miscellaneous (more than one malformation in the same embryo), modified chorda structure, tail malformation, and yolk deformation. Concerning the biomarkers of oxidative stress, an increase in the degree of lipid peroxidation, protein carbonylation, and hydroperoxide content was observed (p < 0.05) concerning the control. In addition, a significant increase (p < 0.05) in antioxidant enzymes (SOD, CAT, and GPx) was observed at low exposure concentrations (25-400 ngL-1), with a decrease in enzyme activity at high concentrations (500-1500 ngL-1). Our IBR analysis demonstrated that oxidative damage biomarkers got more influence at 500ngL-1 of PHE. The results demonstrated that PHE may affect the embryonic development of zebrafish and that oxidative stress may be involved in the generation of this embryotoxic process.