ABSTRACT: Dynamic Alterations in DNA Methylation within Early Zebrafish Embryos Following Exposure to Tris(1,3-dichloro-2-propyl)phosphate or Folic Acid
Project description:Tris(1,3-dichloro-2-propyl)phosphate is widely used in consumer products as a flame retardant. Humans are often exposed to this compound. However, the molecular mechanisms of the compound`s adverse effects are still unclear. We address the molecular and cellular mechanisms underlying tris(1,3-dichloro-2-propyl)phosphate effects on HeLa cells. Here RNA-Seq analysis was performed to identify distinct classes of up- or down-regulated genes and their connections to different metabolic pathways.
Project description:Human cell cultures A549 and HepG2/C3 were exposed to 0-100 micromolar Tris(1,3-dichloro-2-propyl)phosphate (TDCIPP) in 0.5% DMSO or to 0.5% DMSO alone for 24 h. RNA was prepared and labeled with Cy3. Agilent SurePrint G3 Human GE v2 8x60k Microarrays, Agilent design ID 039494, were used to profile transcriptional responses to TDCIPP.
Project description:Alzheimer's disease is the most common form of dementia characterized on cognitive impairment. Autophagy-lysosome dysfunction is linked to AD pathology. Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is a widely used organophosphorus flame retardants with the potential to induce neuronal damage. We found that TDCIPP significantly increased expression of BACE1 and of Aβ42. TMT labeled proteomic study were used to reveal profile changes of N2a-APPswe cells after exposure by TDCIPP. Proteomic and bioinformatic analysis revealed that lysosomal proteins were dysregulated after TDCIPP treatment in N2a-APPswe cells. LC3, P62, CTSD, and LAMP1 were increased, while STAT1 was decreased after TDCIPP exposure and dysregulated proteins were validated by Western blotting. Our results, for the first time revealed that TDCIPP could be one of potential environment risk factors for AD development. Autophagy dysregulation may take an important role on TDCIPP induced Aβ42 production.
Project description:Mussels (Mytilus galloprovincialis) were exposed during 7 and 28 days in seawater (control), seawater + acetone (solvent control, SC), and 10 micrograms per Litre of tris(1,3-dichloro-2-propyl) phosphate (TDCPP). TDCPP was added from a stock solution prepared in acetone, the volume added being 100 µL per 30 L aquaria. The same volume of acetone was added to SC aquaria. Mussel density was 20 mussels per each 30 L aquaria at the beginning of the experiment and varied between 15 ‒ 20 mussels/30 L aquaria during the 28 days exposure period. Exposure conditions were the following: T = 15.6 ± 0.7 ºC, S = 35.5 ± 0.5 ppt, pH = 7.9 ± 0.1, O2 = 7.9 ± 0.6 mg L-1 and 10:14h light:dark photoperiod. Water was renewed twice per week and mussels were fed before every water renewal with a mixture of phytoplankton representing 1% of mussel tissue dry weight.
Project description:Complex Interplay Among Nuclear Receptors, Cytosine Methylation, and the Metabolome in Driving Tris(1,3-Dichloro-2-Propyl) Phosphate-Induced Epiboly Defects in Zebrafish
Project description:Progression of liver tumor was promoted by tris(1,3-dichloro-2-propyl)phosphate through the induction of inflammatory responses in krasV12 transgenic zebrafish
