Snapshot of the pollution-driven metabolic and microbiota changes in Carassius gibelio from Bucharest leisure lakes.

In the last decades, increased intakes of contaminants and the habitats' destruction have produced drastic changes in the aquatic ecosystems. The environmental contaminants can accumulate in aquatic organisms, leading to the disturbance of the antioxidant/prooxidant balance in fish. In this context, we evaluated the level of organic, inorganic and microbiological pollutants in four leisure lakes (Chitila, Floreasca, Tei and Vacaresti) from Bucharest, the largest city of Romania, in order to compare their effects on hepatopancreas and gills metabolism and antioxidant defense mechanisms in Carassius gibelio, the most known and widespread freshwater fish in this country. The lowest level of oxidative stress was recorded in the case of fish collected from the Vacaresti lake, a protected wetland area where aquatic organisms live in wild environmental conditions. In contrast, significant oxidative changes were observed in the hepatopancreas and gills of fish from the Chitila, Floreasca and Tei lakes, such as reduced glutathione S-transferase activity and glutathione level, and increased degree of lipid peroxidation, being correlated with elevated levels of pesticides (such as 2,4'-methoxychlor) and Escherichia coli load in these organs. Although different patterns of pollutants' accumulation were observed, no important interindividual variations in cytosine methylation degree were determined. In conclusion, the presence and concentrations of metals, pesticides and antibiotics varied with the analyzed tissue and sampling site, and were correlated with changes in the cellular redox homeostasis, but without significantly affecting the epigenetic mechanisms.

Fe-N Co-Doped Titanium Dioxide Nanoparticles Induce Cell Death in Human Lung Fibroblasts in a p53-Independent Manner.

The advancement of nanotechnology in the last decade has developed an abundance of novel and intriguing TiO2-based nanomaterials that are widely used in many sectors, including industry (as a food additive and colorant in cosmetics, paints, plastics, and toothpaste) and biomedicine (photoelectrochemical biosensing, implant coatings, drug delivery, and new emerging antimicrobial agents). Therefore, the increased use of engineered nanomaterials in the industry has raised serious concern about human exposure and their unexpected cytotoxic effects. Since inhalation is considered the most relevant way of absorbing nanomaterials, different cell death mechanisms induced in MRC-5 lung fibroblasts, following the exposure to functionalized TiO2 NPs, were investigated. Long-term exposure to TiO2 nanoparticles co-doped with 1% of iron and nitrogen led to the alteration of p53 protein activity and the gene expression controlled by this suppressor (NF-kB and mdm2), DNA damage, cell cycle disruptions at the G2/M and S phases, and lysosomal membrane permeabilization and the subsequent release of cathepsin B, triggering the intrinsic pathway of apoptosis in a Bax- and p53-independent manner. Our results are of major significance, contributing to the understanding of the mechanisms underlying the interaction of these nanoparticles with in vitro biological systems, and also providing useful information for the development of new photocatalytic nanoparticles that are active in the visible spectrum, but with increased biocompatibility.