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Those results indicate that DZP exhibits sex-dependent effects on the behaviors of fish. Moreover, exposure to DZP for 21 days significantly disturbed almost all of the tested behavioral traits associated with courtship when both genders were put together. Sex-dependent responses in brain GABA and AChE levels due to DZP exposure were also identified. Significant relationships between the brain GABA/AChE levels and some behavioral parameters related to locomotor activity were detected in females, but not in males.Plasticizers are widespread environmental contaminants that have been described as obesogens in terrestrial vertebrates. However, its effects on fish lipids homeostasis are almost unknown. This work explores the use of PLHC-1 cells as an alternative model to assess the disruption of hepatic lipids by plastic additives and to gather information on the mode of action of these chemicals in fish. PLHC-1 lipid extracts were analyzed by flow injection coupled to high resolution mass spectrometry (FIA-ESI(+/-)-Orbitrap-Exactive) after 24 h exposure of the cells to the selected plasticizers dibutyl phthalate (DBP), di-(2-ethylhexyl) phthalate (DEHP), bisphenol A (BPA), bisphenol F (BPF), and chlorinated bisphenol A diglycidyl ether (BADGE·2HCl). The analysis of the culture medium and the intracellular concentration of the chemicals revealed the highest bioconcentration of BADGE·2HCl, DBP and DEHP, which was in agreement with the strongest alteration of the cells lipidome. BADGE·2HCl induced a significant depletion of triacylglycerides (TGs), while DEHP and DBP stimulated the accumulation of TGs. Exposure to BPF induced the generation of reactive oxygen species in PLHC-1 cells and a significant depletion of phosphatidylcholine (PC)- and phosphatidylethanolamine (PE)-plasmalogens, and TGs (cell depots of polyunsaturated fatty acids). Overall, this study evidences different modes of action of plastic additives in topminnow liver cells, describes differential lipidomic signatures, and highlights the higher lipotoxicity of BADGE·2HCl and BPF compared to BPA.Brominated diphenyl ethers (BDEs) are halogenated flame retardants. Several concerns related to persistence and toxicity of BDEs have been resulted in a growing need of BDEs replacement. DNA Repair inhibitor The use of halogen-free flame retardants (HFFR) has increased as a safer alternative, but little information is available on their toxic potential for environmental health and for developing organisms. Therefore, the aim of this study was to evaluate and compare the toxicity of three congeners of BDEs (BDE-47, BDE-99 and BDE-154) with an HFFR (aluminum diethylphosphinate, ALPI) on zebrafish (Danio rerio) by assessing endpoints of lethality, sub-lethality and teratogenicity at the earlier stages of development. The highest tested concentration of BDE-47 (12.1 mg/L) induced pericardium and yolk sac edemas that first appeared at 48 h post-fertilization (hpf) and then were mostly reabsorbed until 144 hpf. BDE-47 also showed a slight but non-significant tendency to affect swim bladder inflation. The rate of edemas increased in a concentration-dependent manner after exposure to BDE-99, but there were no significant differences. In addition, the congener BDE-99 also presented a slight and non-significant effect on swim bladder inflation, but only at the highest concentration tested. Regarding BDE-154 exposure, the rate of edemas and swim bladder inflation were not affected. Finally, in all ALPI exposure concentrations (0.003 up to 30 mg/L), no sub-lethal or teratogenic effects were observed on developing organisms until 96 hpf. Although further studies are needed, our results demonstrate that when comparing the developmental toxicity induced by flame retardants in zebrafish, the HFFR ALPI may be considered a more suitable alternative to BDE-47.Arsenic (As) a non-essential element is of particular concern with respect to harmful effects on plant metabolism. While extensive studies have been conducted on the physiological responses of plants to increase As concentrations, however, molecular differences elucidating species-specific changes remain largely unknown. In the present experiment, two oilseed Brassica napus (B. napus) cultivars, ZS758 and ZD622, were treated by elevated As concentration. Their responses to the As stress have been investigated through pulse amplitude modulated fluorometer and isobaric tags based proteomic (iTRAQ) analysis. The chlorophyll fluorescence attributes showed that As stress significantly decrease the photochemical efficiency of photosystem II (PSII) and photosystem I (PSI) as well as the comparatively closed stomata observed under scanning electron microscopy (SEM). In this study, 65 proteins displayed increased abundance and 52 down-regulated were found in the control vs As comparison in cultivar ZS758, while 44 up nce.Autophagy dysregulation plays a pivotal role in cadmium (Cd)-induced nephrotoxicity. Quercetin (Qu), a flavonoid antioxidant with autophagy-enhancing effect, has protective effect on Cd-induced toxicity, but whether it can prevent Cd-induced nephrotoxicity via restoration of autophagy remains unknown. Here, primary rat proximal tubular (rPT) cells were exposed to Cd and/or Qu in vitro to clarify this issue. Data first showed that Cd-impaired autophagic flux was markedly alleviated by Qu, including decreased levels of autophagy marker proteins and recovery of autophagosome-lysosome fusion targeted for lysosomes. Meanwhile, Cd-induced lysosomal alkalization due to v-ATPases inhibition was prominently recovered by Qu. Accordingly, Qu enhanced Cd-diminished lysosomal degradation capacity and lysosome-related gene transcription levels. Notably, Qu improved Cd-inhibited TFEB nuclear translocation and its gene transcription level. Furthermore, data showed that the restoration of Cd-impaired autophagy-lysosome pathway and resultant alleviation of cytotoxicity by Qu are TFEB-dependent using TFEB gene silencing and overexpression technologies. In summary, these data provide novel evidences that the protective action of Qu against Cd-induced autophagy inhibition is attributed to its restoration of lysosomal dysfunction, which is dependent on TFEB.
Homepage: https://www.selleckchem.com/products/zotatifin.html
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