Eco-endocrinological dynamics: Unraveling dexamethasone's influence on the interrenal axis in juvenile carp Cyprinus carpio.

This study delves into the eco-endocrinological dynamics concerning the impact of dexamethasone (DXE) on the interrenal axis in juvenile carp, Cyprinus carpio. Through a comprehensive analysis, we investigated the effects of DXE exposure on oxidative stress, biochemical biomarkers, gene expression, and bioaccumulation within the interrenal axis. Results revealed a concentration-dependent escalation of cellular oxidation biomarkers, including 1) hydroperoxides content (HPC), 2) lipid peroxidation level (LPX), and 3) protein carbonyl content (PCC), indicative of heightened oxidative stress. Concurrently, the activity of critical antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT), significantly increased, underscoring the organism's response to oxidative insult. Notable alterations were observed in biochemical biomarkers, particularly Gamma-glutamyl-transpeptidase (GGT) and alkaline phosphatase (ALP) activity, with GGT displaying a significant decrease with increasing DXE concentrations. Gene expression analysis revealed a significant upregulation of stress and inflammation response genes, as well as those associated with sensitivity to superoxide ion presence and calcium signaling, in response to DXE exposure. Furthermore, DXE demonstrated a concentration-dependent presence in interrenal tissue, with consistent bioconcentration factors observed across all concentrations tested. These findings shed light on the physiological and molecular responses of juvenile carp to DXE exposure, emphasizing the potential ecological implications of DXE contamination in aquatic environments. Understanding these dynamics is crucial for assessing the environmental impact of glucocorticoid pollutants and developing effective management strategies to mitigate their adverse effects on aquatic ecosystems.

Ecotoxicological evaluation of chitosan biopolymer films particles in adult zebrafish (Danio rerio): A comparative study with polystyrene microplastics.

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.

Acute exposure to fluoxetine leads to oxidative stress and hematological disorder in Danio rerio adults.

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.

Short-term exposure to dexamethasone at environmentally relevant concentrations impairs embryonic development in Cyprinus carpio: Bioconcentration and alteration of oxidative stress-related gene expression patterns.

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.

Oxidative stress as regulator of neuronal impairment after exposure to hospital effluents in Danio rerio.

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.

Integrative approach to elucidate the embryological effects of caffeine in Cyprinus carpio: Bioconcentration and alteration of oxidative stress-related gene expression patterns.

Caffeine (CAF) is an alkaloid, which acts as a central nervous system (CNS) stimulant drug. In recent years, CAF has been recurrently detected in water bodies, generating deleterious effects in aquatic organisms. The information on the toxic effects of CAF in the environment is still limited. Thus, the objective of this work was to determine whether CAF at environmentally relevant concentrations (CAF concentrations were selected based on studies on the worldwide occurrence of this compound and on the toxicity of CAF in aquatic species) is capable of inducing 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 CAF until 96 hpf. Alterations to embryonic development and teratogenic effects 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 content 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 CAF concentrations above 500 ng/L are capable of producing teratogenic effects. Furthermore, CAF was able to induce alterations such cardiac malformations, somite alterations, pericardial edema and chorda malformations. Concerning oxidative stress, the results demonstrated that CAF induce oxidative damage on the embryos of C. carpio. Our outcomes also showed up-regulations in genes related to antioxidant activity sod, cat and gpx by CAF exposure. In conclusion CAF at environmentally relevant concentrations is able to alter the embryonic development of common carp by the oxidative stress pathway. Based on the above evidence, it can be inferred that acute exposure to CAF can lead to a toxic response that significantly harms fish's health, adversely affecting their essential organs' functioning.

Women with preeclampsia exposed to air pollution during pregnancy: Relationship between oxidative stress and neonatal disease - Pilot study.

Oxidative imbalance as a pathophysiological mechanism has been reported as an adverse outcome in pregnant women who develop preeclampsia and in their newborns. Furthermore, emerging evidence suggests the same mechanism by which air pollutants may exert their toxic effects. Therefore, the objective of the study was to evaluate the biomarkers of oxidative stress and their relationship with neonatal disease in premature newborns from mothers with preeclampsia exposed to air pollution during pregnancy. The data of air pollutants (PM2.5, PM10 and ozone) were collected at fixed monitoring stations. Oxidative and antioxidant status markers were obtained through special techniques in women with preeclampsia and in umbilical cord blood of their premature newborns. The oxidative stress markers were significantly higher in women with preeclampsia and their newborns who were exposed to higher levels of ambient air pollutants in the first and second trimester of pregnancy. Neonatal diseases are associated with preeclampsia in pregnancies, specifically intrauterine growth restriction (IUGR) and necrotizing enterocolitis (NEC). A significant correlation was identified in the levels of prooxidant agents and antioxidant enzyme activity in the presence of neonatal diseases associated with preeclampsia. There is increased oxidative damage in both the maternal and fetal circulation in women who develop preeclampsia exposed to air pollution during pregnancy. Therefore, these pregnancies complicated by preeclampsia have a greater adverse outcome as neonatal disease in the preterm infant.

Chronic exposure to realistic concentrations of metformin prompts a neurotoxic response in Danio rerio adults.

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.

Multi-biomarker approach and IBR index to evaluate the effects of bisphenol A on embryonic stages of zebrafish (Danio rerio).

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.

Multi-biomarker approach to evaluate the neurotoxic effects of environmentally relevant concentrations of phenytoin on adult zebrafish Danio rerio.

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.

Fluoxetine-induced neurotoxicity at environmentally relevant concentrations in adult zebrafish Danio rerio.

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.

Brain damage induced by contaminants released in a hospital from Mexico: Evaluation of swimming behavior, oxidative stress, and acetylcholinesterase in zebrafish (Danio rerio).

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.

Chronic exposure to environmentally relevant concentrations of guanylurea induces neurotoxicity of Danio rerio adults.

Recent studies have shown guanylurea (GUA) alters the growth and development of fish, induces oxidative stress, and disrupts the levels and expression of several genes, metabolites, and proteins related to the overall fitness of fish. Nonetheless, up to date, no study has assessed the potential neurotoxic effects that GUA may induce in non-target organisms. To fill the current knowledge gaps about the effects of this metabolite in the central nervous system of fish, we aimed to determine whether or not environmentally relevant concentrations of this metabolite may disrupt the behavior, redox status, AChE activity in Danio rerio adults. In addition, we also meant to assess if 25, 50, and 200 µg/L of GUA can alter the expression of several antioxidant defenses-, apoptosis-, AMPK pathway-, and neuronal communication-related genes in the brain of fish exposed for four months to GUA. Our results demonstrated that chronic exposure to GUA altered the swimming behavior of D. rerio, as fish remained more time frozen and traveled less distance in the tank compared to the control group. Moreover, this metabolite significantly increased the levels of oxidative damage biomarkers and inhibited the activity of acetylcholinesterase of fish in a concentration-dependent manner. Concerning gene expression, environmentally relevant concentrations of GUA downregulated the expression GRID2IP, PCDH17, and PCDH19, but upregulated Nrf1, Nrf2, p53, BAX, CASP3, PRKAA1, PRKAA2, and APP in fish after four months of exposure. Collectively, we can conclude that GUA may alter the homeostasis of several essential brain biomarkers, generating anxiety-like behavior in fish.

Low concentrations of ciprofloxacin alone and in combination with paracetamol induce oxidative stress, upregulation of apoptotic-related genes, histological alterations in the liver, and genotoxicity in Danio rerio.

Nowadays, there are countless articles about the harmful effects of paracetamol (PCM) in non-target organisms. Nonetheless, information regarding the toxicity of ciprofloxacin (CPX) and the CPX-PCM mixture is still limited. Herein, we aimed to evaluate the hepatotoxic and genotoxic effects that ciprofloxacin alone and in combination with paracetamol may induce in Danio rerio adults. For this purpose, we exposed several D. rerio adults to three environmentally relevant concentrations of PCM (0.125, 0.250, and 0.500 µg/L), CPX (0.250, 0.500, and 1 µg/L), and their mixture (0.125 + 0.250, 0.250 + 0.500, and 0.500 + 1 µg/L) for 96 h. The blood samples showed CPX alone and in combination with PCM damaged the liver function of fish by increasing the serum levels of liver enzymes alanine aminotransferase and alkaline phosphatase. Moreover, our histopathological study demonstrated liver of fish suffered several tissue alterations, such as congestion, hyperemia, infiltration, sinusoidal dilatation, macrovascular fatty degeneration, and pyknotic nuclei after exposure to CPX alone and in combination with PCM. Concerning oxidative stress biomarkers and the expression of genes, we demonstrated that CPX and its mixture, with PCM, increased the levels of antioxidant enzymes and oxidative damage biomarkers and altered the expression of Nrf1, Nrf2, BAX, and CASP3, 6, 8, and 9 in the liver of fish. Last but not least, we demonstrated CPX alone and with PCM induced DNA damage via comet assay and increased the frequency of micronuclei in a concentration-dependent manner in fish. Overall, our results let us point out CPX, even at low concentrations, induces hepatotoxic effects in fish and that its combination with PCM has a negative synergic effect in the liver of this organism.

Acute exposure to environmentally relevant concentrations of phenytoin damages early development and induces oxidative stress in zebrafish embryos.

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.

Teratogenic effects induced by paracetamol, ciprofloxacin, and their mixture on Danio rerio embryos: Oxidative stress implications.

Even though the toxic effects of paracetamol (PCM) and ciprofloxacin (CPX) have been deeply studied in the last decades, the impact of the PCM-CPX mixture may induce in aquatic organisms is poorly known. Thus, the objective of this work was to investigate the teratogenic effects and oxidative stress that PCM, CPX, and their mixture induce in Danio rerio embryos. Moreover, we aimed to determine whether the PCM-CPX mixture induces more severe effects on the embryos than the individual drugs. For this purpose, zebrafish embryos (4 hpf) were exposed to environmentally relevant concentrations of PCM, CPX, and their mixture until 96 hpf. In addition, at 72 hpf and 96 hpf, we also evaluated the oxidative stress biomarkers (superoxide dismutase, catalase, glutathione peroxidase, lipid peroxidation, and hydroperoxides and carbonyl content) in the embryos. Our results demonstrated that PCM, CPX, and their mixture reduced the survival rate of embryos by up to 75%. In addition, both drugs, induced morphological alterations in the embryos, causing their death. The most observed malformations were: scoliosis, craniofacial malformations, hypopigmentation, growth retardation, pericardial edema. Concerning oxidative stress, our integrated biomarkers response (IBR) analysis demonstrated that PCM, CPX, and their mixture induce oxidative damage on the embryos. In conclusion, PCM, CPX, and their mixture can alter zebrafish embryonic development via an oxidative stress response.

Effects of oxidative stress induced by environmental relevant concentrations of fluoxetine on the embryonic development on Danio rerio.

Fluoxetine (FLX) is a psychoactive drug that acts as an antidepressant. FLX is one of the world's best-selling prescription antidepressants. FLX is widely used for the treatment of various psychiatric disorders. For these reasons, this drug may eventually end up in the aquatic environment via municipal, industrial, and hospital discharges. Even though the occurrence of FLX in aquatic environments has been reported as ubiquitous, the toxic effects that this drug may induce, especially at environmentally relevant concentrations, on essential biological processes of aquatic organisms require more attention. In the light of this information, this work aimed to investigate the influence that fluoxetine oxidative stress-induced got over the embryonic development of Danio rerio. For this purpose, D. rerio embryos (4 h post fertilization) were exposed to environmentally relevant concentrations (5, 10, 15, 20, 25, 30, 35, and 40 ng L-1) of fluoxetine, until 96 h post fecundation. Along the exposure, survival, alterations to embryonic development, and teratogenic effects were evaluated using a stereomicroscope. Furthermore, oxidative stress biomarkers (superoxide dismutase, catalase, glutathione peroxidase, lipid peroxidation, hydroperoxide, and carbonyl content) were evaluated at 72 and 96 h post fecundation. LC50, EC50m, and teratogenic index were 30 ng L-1, 16 ng L-1, and 1.9, respectively. The main teratogenic effects induced by fluoxetine were pericardial edema, hatching retardation, spine alterations and craniofacial malformations. Concerning oxidative stress, our integrated biomarkers (IBR) analysis demonstrated that as the concentration increased, oxidative damage biomarkers got more influence over the embryos than antioxidant enzymes. Thus, fluoxetine induces an important oxidative stress response on the embryos of D. rerio. Collectively, our results allow us to concluded that FLX is a dangerous drug in the early life stages of D. rerio due to its high teratogenic potential and that FLX-oxidative stress induced may be involved in this toxic process.

Acute exposure to 17-α-ethinylestradiol disrupt the embryonic development and oxidative status of Danio rerio.

17-Alpha-ethinylestradiol (EE2) is an estrogen derived from estradiol (E2). This compound and is one of the most widely used drugs both in humans and animals. Numerous studies have reported the ability of EE2 to alter sex determination and delay sexual maturity, but there are toxic effects that need to be explored. In this work, we analyzed the effect of EE2 on embryonic development and oxidative stress biomarkers in Danio rerio. For this effect, zebrafish embryos in the blastula period (2.5 h post fecundation) were exposed to different concentrations of EE2 (36-106 ng L-1) until 96 hpf. Survival, alterations to embryonic development, and teratogenic effects were evaluated using a stereomicroscope. Furthermore, oxidative stress biomarkers: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) activities, lipid peroxidation (LPX), hydroperoxide content (HPX), and protein carbonyl content (POX) were evaluated at 72 and 96 hpf using spectrophotometric methods. LC50 and EC50 of malformations got values of 82 ng L-1 and 57.7 ng L-1, respectively. The main teratogenic effects found were: chorda malformation, body malformation, and developmental delay. These alterations occurred at 86, 96, and 106 ng L-1. Integrated biomarker index showed that the oxidative stress biomarkers that had the most influence on embryos were SOD, CAT, GPX, and LPX. Overall, our results allow us to conclude that low concentrations of EE2 may potentially alter the development and oxidative status in the early life stages of zebrafish. Therefore, this bio-active estrogen can be considered a hazardous substance for fish.

Effects of effluent from a hospital in Mexico on the embryonic development of zebrafish, Danio rerio.

Hospitals consume a large amount of water, so they also generate large amounts of wastewater, which contain a wide variety of contaminants. It is important to consider that hospital effluents are a mixture of pollutants that can interact with each other and have a negative impact on aquatic species of water bodies. The aim of this study was to evaluate the effects induced by a hospital effluent using Danio rerio embryos. In this study, Danio rerio embryos were exposed to different concentrations of the hospital effluent and a lethality test was evaluated and the malformations present in zebrafish embryos were evaluated. The lethal concentration of effluent 50% was 6.1% and the effective malformation concentration was of 2.5%. The teratogenic index was 2.45%. The main malformations identified were yolc sac malformation, pericardial edema, hatching abnormalities, hypopigmentation, tail deformation, chorda malformation, without fin, chorion deformation and craniofacial malformation. The risks that this type of water represents for the survival of living organisms, as well as the presence of malformations in them, are reference indicators for a future regulation focused on the adequate treatment of hospital effluents.