MIL-100(Fe)/g-C3N4 composites with enhanced photocatalytic activity for UO22+ reduction under visible light.

As a clean energy source, nuclear energy can gradually replace traditional fossil energy sources, and is an important means to achieve the "double carbon goal". Uranium-containing wastewater is inevitable in the development of nuclear energy. The composites MIL/CNx of MOF material MIL-100(Fe) and carbon nitride (CN) were obtained by a simple solvo-thermal method using iron nitrate, homophthalic acid and CN. The material MIL-100(Fe) with high specific surface area was compounded with CN to increase the in-plane adsorption sites, which could adsorb 30% of uranium in solution during the dark reaction. The close interfacial contact of the two materials effectively inhibited the complexation of photo-generated electrons and holes and promotes electron migration. These two synergistic effects improved their overall photocatalytic reduction capacity, which could reduce 97% of UO22+ in solution in 20 min. The UO22+ removal efficiency of MIL/CN0.1 was 2.3 and 1.6 times higher than that of CN and MIL-100(Fe), respectively. In addition, MIL/CN0.1 was stable in reducing uranium during the five cycles of the experiment.

4-Hydroxynonenal promotes growth and angiogenesis of breast cancer cells through HIF-1α stabilization.

4-Hydroxynonenal (4-HNE) is a stable end product of lipid peroxidation, which has been shown to play an important role in cell signal transduction, while increasing cell growth and differentiation. 4-HNE could inhibit phosphatase and tensin homolog (PTEN) activity in hepatocytes and increased levels have been found in human invasive breast cancer. Here we report that 4-HNE increased the cell growth of breast cancer cells as revealed by colony formation assay. Moreover, vascular endothelial growth factor (VEGF) expression was elevated, while protein levels of hypoxia inducible factor 1 alpha (HIF-1α) were up-regulated. Sirtuin-3 (SIRT3), a major mitochondria NAD+-dependent deacetylase, is reported to destabilize HIF-1α. Here, 4-HNE could inhibit the deacetylase activity of SIRT3 by thiol-specific modification. We further demonstrated that the regulation by 4-HNE of levels of HIF-1α and VEGF depends on SIRT3. Consistent with this, 4-HNE could not increase the cell growth in SIRT3 knockdown breast cancer cells. Additionally, 4-HNE promoted angiogenesis and invasion of breast cancer cells in a SIRT3-dependent manner. In conclusion, we propose that 4-HNE promotes growth, invasion and angiogenesis of breast cancer cells through the SIRT3-HIF-1α-VEGF axis.