Pyrite-embedded porous carbon nanocatalysts assembled in polyvinylidene difluoride membrane for organic pollutant oxidation.

FeS2-embedded in porous carbon (FeS2/C) was prepared by simultaneous sulfidation and carbonization of an iron-based metal-organic framework precursor, and subsequently immobilized in polyvinylidene fluoride membranes (FeS2/C@PVDF) for organics removal via peroxymonosulfate (PMS) activation. The composition, structure, and morphology of the FeS2/C@PVDF membrane were extensively characterized. Scanning electron microscopy images manifest that the FeS2/C nanoparticles with an average diameter of 40 nm are assembled on the external and internal membrane surface. The as-prepared FeS2/C@PVDF membrane exhibits excellent performances over a wide pH range of 1.53-9.50, exceeding carbon-free syn-FeS2@PVDF. The effective degradation could be improved by inner pyrite FeS2 cores and thus enhanced the electron transfer between carbon shell and PMS. Electron paramagnetic resonance and quenching experiments elucidated that radical (HO∙, SO4∙-) and nonradical (1O2) species were the predominant reactive oxidants. In addition, FeS2/C@PVDF exhibited high stability with low Fe leaching (0.377 mg/L) owing to the effective protection of the outer carbon skeleton. Plentiful porosity of PVDF membranes not only affords a controlled size and confined uniform distribution of the immobilized FeS2/C nanoparticles, but also enables a persistent exposure of active sites and enhanced mass transfer efficiency. Our findings demonstrate a promise for utilizing the novel FeS2/C@PVDF membrane as an efficient catalyst for the environmental cleanup.

Evaluation on the thyroid disrupting mechanism of malathion in Fischer rat thyroid follicular cell line FRTL-5.

Thyroid hormones are involved in many important physiological activities including regulation of energy metabolism, development of nervous system, maintenance of cerebral functions, and so on. Endocrine-disrupting chemicals (EDCs) that interfere with thyroid functions raise serious concerns due to their frequent misuse in areas where regulations are poorly implemented. In addition, chemicals that are originally regarded safe may now be considered as toxic with the development of life sciences. Malathion is an organophosphate insecticide that is widely applied and distributed in agricultural and residential settings. Due to the low acute toxicity and rapid degradation, malathion is not listed as a primary thyroid disrupting chemical. However, emerging evidences reported that malathion affected thyroperoxidase catalyzed iodide oxidation which in turn influenced thyroid hormone transportation, and enhanced parathyroid hyperplasia prevalence. Nevertheless, direct effect of malathion on thyroid hormone biosynthesis remains to be elucidated. This study investigated the effects of thyroid disruption of malathion in Fischer rat thyroid follicular cell line, FRTL-5. Transcriptional and translational analyses on thyroglobulin demonstrated that both mRNA and protein expression levels were significantly inhibited by malathion. Cellular cAMP level and TSH receptor expression were distinctly reduced by malathion (6.0 µg/ml). These results suggested that malathion directly disrupted the biosynthesis of thyroid hormone and the mechanism involved down-regulation of TSH receptor and cellular cAMP. This subsequently led to the suppression of TSH dependent signal transduction, TG transcription inhibition, and obstruction of thyroid hormone biosynthesis.

[The disruptive effect of N'N-methylene-bis on the function of FRTL-5 cells].

OBJECTIVE: To study the impact of N' N-methylene-bis on thyroglobulin produced by FRTL-5 cells, and to explore the potential of using FRTL-5 cells to screen environmental thyroid hormone disruptors in vitro. METHODS: The FRTL-5 cells were treated with 0.1, 1.0 and 10.0 microg/mL N'N-methylene-bis for 48 hours, respectively. The concentrations of thyroglobulin in the medium of the treated cells were detected by radioimmunoassay. The expression of thyroid peroxidases in the FRTL-5 cells was assessed by enzyme cytochemistry technique. The ultrastructure of the cells was also observed. RESULTS: The FRTL-5 cells treated with 0.1 and 1.0 microg/mL of N' N-methylene-bis produced less thyroglobulin than the controls (P < 0.05). No thyroglobulin was detected with the cells treated with 10.0 microg/mL of N' N-methylene-bis. No difference in the expression of thyroid peroxidases was found between the treated cells and the controls. The treated cells had expanded rough endoplasmic reticulum. CONCLUSION: N' N-methylene-bis disrupts the bio-function of thyroid by damaging the rough endoplasmic reticulum of thyroid follicular cells. FRTL-5 cells can be used for screening thyroid hormone disruptors in vitro.