39 research outputs found
Quinoxyfen 1995-2019 is the story's end? Evaluation of its adverse effects on head size and nervous system genes involved in synaptic maturation
No full textIn 2013 quinoxyfen (QXY) was included in the list of priority hazard pollutants of the European Water Framework Directive due to its toxicity to aquatic organisms. The use of products formulated containing QXY was banned from all commercials starting from 27th June of 2019. QXY is an organic pollutant with potential persistence, bioaccumulation and this must not lower attention to this pollutant. To date the effects of this compound on development are not completely clear, thus this research tries to elucidate the adverse effects of QXY on zebrafish development. The study aims to understand the toxicological effects of QXY using the zebrafish as in vivo model and performing toxicological and molecular investigations. Considering the FET test results two sublethal concentrations, 0.4 mg/L and 0.8 mg/L were chosen for subsequent analysis. The expression of the gad1b, cyp19a1b, shank3a, nrxn1a and c-fos genes, involved in the development of the nervous system and the regulation of synaptic transmission, were evaluated. To confirm the potential neurotoxic effects of the treatment on the development of the central nervous system, both a transgenic Tg(neuroD:gfp ia50) line was used for confocal microscopy and Orange Acridine was used on wild type larvae to assess the presence of neuronal apoptosis. The results showed sub-lethal alterations, particularly affecting craniofacial and brain development highlighting as QXY may represent a possible endocrine disruptor able to induce severe cartilage defects, small head and tremor phenotype in zebrafish larvae and a strong modulation of the selected gene
Quinoxyfen 1995-2019 is the story's end? Evaluation of its adverse effects on head size and nervous system genes involved in synaptic maturation
No full text: In 2013 quinoxyfen (QXY) was included in the list of priority hazard pollutants of the European Water Framework Directive due to its toxicity to aquatic organisms. The use of products formulated containing QXY was banned from all commercials starting from 27th June of 2019. QXY is an organic pollutant with potential persistence, bioaccumulation and this must not lower attention to this pollutant. To date the effects of this compound on development are not completely clear, thus this research tries to elucidate the adverse effects of QXY on zebrafish development. The study aims to understand the toxicological effects of QXY using the zebrafish as in vivo model and performing toxicological and molecular investigations. Considering the FET test results two sublethal concentrations, 0.4 mg/L and 0.8 mg/L were chosen for subsequent analysis. The expression of the gad1b, cyp19a1b, shank3a, nrxn1a and c-fos genes, involved in the development of the nervous system and the regulation of synaptic transmission, were evaluated. To confirm the potential neurotoxic effects of the treatment on the development of the central nervous system, both a transgenic Tg(neuroD:gfp ia50) line was used for confocal microscopy and Orange Acridine was used on wild type larvae to assess the presence of neuronal apoptosis. The results showed sub-lethal alterations, particularly affecting craniofacial and brain development highlighting as QXY may represent a possible endocrine disruptor able to induce severe cartilage defects, small head and tremor phenotype in zebrafish larvae and a strong modulation of the selected genes
Quinoxyfen 1995-2019 is the story's end? Evaluation of its adverse effects on head size and nervous system genes involved in synaptic maturation
No full text
Valutazione tossicologica del glifosate associato ad una condizione ipossica nelle forme larvali di zebrafish
No full text
Oxysterols Profile in Zebrafish Embryos Exposed to Triclocarban and Propylparaben—A Preliminary Study
No full textOxysterols have long been considered as simple by-products of cholesterol metabolism, but they are now fully designed as bioactive lipids that exert their multiple effects through their binding to several receptors, representing endogenous mediators potentially involved in several metabolic diseases. There is also a growing concern that metabolic disorders may be linked with exposure to endocrine-disrupting chemicals (EDCs). To date, there are no studies aimed to link EDCs exposure to oxysterols perturbation—neither in vivo nor in vitro studies. The present research aimed to evaluate the differences in oxysterols levels following exposure to two metabolism disrupting chemicals (propylparaben (PP) and triclocarban (TCC)) in the zebrafish model using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Following exposure to PP and TCC, there were no significant changes in total and individual oxysterols compared with the control group; however, some interesting differences were noticed: 24-OH was detected only in treated zebrafish embryos, as well as the concentrations of 27-OH, which followed a different distribution, with an increase in TCC treated embryos and a reduction in zebrafish embryos exposed to PP at 24 h post-fertilization (hpf). The results of the present study prompt the hypothesis that EDCs can modulate the oxysterol profile in the zebrafish model and that these variations could be potentially involved in the toxicity mechanism of these emerging contaminants
