Juliana Machado Kayser

This study aimed to report the effects of chronic exposure of zebrafish exposed to environmentally relevant concentrations of 0.5, 2.4, and 5.0 mg L⁻¹ iron (Fe) and 0.2, 0.4, and 2.0 mg L⁻¹ aluminum (Al). We also evaluated the reversal and generational transposition (F1) of possible histopathological, behavioral, and genotoxic changes in the species. Locomotion changes that may have been caused by the increase in the number of apoptotic cells and in the telencephalic mitochondrial activity were observed especially after the 30 days exposure to Al and persisted after recovery (30 days). We also observed histopathological changes, such as an increase in the number of intestinal goblet cells, even after the recovery period in these animals. Our results also showed that the Fe concentrations used were insufficient to cause genotoxicity, behavioral and intestinal epithelium changes. The adult offspring (F1) of animals exposed to Al showed changes in locomotion and in the amount of goblet cells, demonstrating that even in low concentrations this pollutant can harm subsequent generations in the aquatic biota. Animals demonstrate, in general, greater tolerance to Fe which may be related to the physiological demand of this metal by the body. Even so, all concentrations of both metals that caused some change in the species represent Brazilian environmental occurrences or Brazilian legislation. It highlights the need for updating the guidelines and constant monitoring of aquatic environments, since even in the face of a hypothetical decontamination of the environment, some changes could persist and affect different trophic levels.

The PT-31 molecule, a potential antipsychotic, has demonstrated promising results when orally administrated to in vivo models. A recent study suggested the genotoxic and mutagenic potential of PT-31 after acute treatment by intraperitoneal route. This study aimed to evaluate PT-31 potential of inducing genotoxic or mutagenic damage after acute oral administration. For that, adult males and females Balb/C mice were treated acutely by oral administration with vehicle or PT-31 in three different doses (10, 20, and 40 mg kg-1). After 24 hours from PT-31 administration, animals were euthanized for performing the comet and micronucleus assays. None of the tested groups of PT-31 presented a significant increase in damage index and MN frequency. However, they presented the following tendency on damage index: females presented a tendency at 40 mg kg-1 and males at 20 mg kg-1. Regarding the MN assay, male mice at the highest dose of 40 mg kg-1 presented a tendency of increased MN frequency. Also, there was a significant increase in PCE/NCE ratio in male mice. Results suggest that the male mice group presented higher susceptibility to damage. The tendency of increased damage to DNA and MN frequency suggests that the molecule PT-31 may induce reparable damage to DNA, and these DNA strand repairs may have originated from the MN. However, significant genotoxic and mutagenic effects were not observed. This study reinforces the atypicality of the molecule as much as its safety by oral route administration.

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.