Synthetic estrogen 17α-ethinyl estradiol (EE2) is recognized for its ability to cause endocrine disruption in aquatic organisms and its high resistance to environmental degradation, being found in Brazilian waterbodies up to 100 ng L -1 . Thus, the aim of this study was to evaluate the exploratory behavior and the histological effects on zebrafish gonads, caused by environmentally relevant concentrations of EE2. Females were exposed to nominal concentrations of 25 ng L -1 and 100 ng L -1 EE2 for 21 days. After that, a behavioral and histological analysis of gonads was performed. The EE2 caused the reduction of the exploratory activity of the animals, when observed the behavior, and an acceleration of the maturation process of the oocytes evaluated in the histological analysis. Considering the results obtained after the exposure to EE2, we highlight the concern about the potential risks it may cause to the aquatic biota, alerting to the need to control and monitor these micropollutants present in Brazilian water resources.
Titanium dioxide nanoparticles (TiO2-NPs) are among the most used nanomaterials worldwide, but studies evaluating its genotoxicity and histopathological effects are scarce, dealing with short exposure times and low concentrations for human use. The aim was to evaluate TiO2-NPs genotoxicity and histological alterations in the intestine and liver of zebrafish after exposure to human consumption compatible concentrations. Fishes were acutely (96 hours) and chronically (30 days) exposed to 5.0, 20 and 40 mg L-1 of TiO2-NPs and later euthanized for organ and blood analysis through histological procedures and the micronucleus test, respectively. An increase in the thickness of intestinal villi was observed after acute and chronic exposure in the higher concentrations. The liver showed an increase in vacuolated hepatocytes after both exposures, besides an increase in hepatocytes with peripheral nucleus. Genotoxicity was only observed after chronic exposure, demonstrated by the increase in micronucleus and cell buddings. These findings indicate that TiO2-NPs cause histopathological damage even in acute exposures, as the intestine serves as a barrier for NPs and the liver is an organ that accumulates Ti. Genotoxicity was possibly mediated by reactive oxygen species through chronic inflammation, leading to tissue damage and carcinogenesis in longer exposures that represents human exposure time.
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