As(iii) removal through catalytic oxidation and Fe(iii) precipitation.

To remove arsenite (As(iii)) from wastewater effectively, the catalytic oxidation of As(iii) to arsenate (As(v)) and As(v) precipitation with iron ions (Fe(iii)) was investigated. The Pt/SiO2 catalyst functioned as a reaction site for As(iii) with oxygen in the atmosphere. The combination of the Pt/SiO2 catalyst and Fe(iii) precipitant improved the removal of As(iii) in the precipitate; Pt/SiO2 worked as both an As(iii) oxidation site and precipitation site with Fe(iii) precipitant.

Hyperactivation of 4E-binding protein 1 as a mediator of biguanide-induced cytotoxicity during glucose deprivation.

Biguanides, including metformin, buformin, and phenformin, are potential antitumorigenic agents and induce cell death during glucose deprivation, a cell condition that occurs in the tumor microenvironment. Here, we show that this selective killing of glucose-deprived cells is coupled with hyperactivation of eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), a negative regulator of translation initiation. We found, in fact, that the 4E-BP1 hyperactivation led to failure of the unfolded protein response (UPR), an endoplasmic reticulum-originated stress signaling pathway for cell survival. We also found that the 4E-BP1-mediated UPR inhibition occurred through a strong inhibition of the mTOR signaling pathway, a proven antitumor target. Importantly, the 4E-BP1 hyperactivation can be also seen in xenografted cancer cells through an in vivo biguanide treatment. Our findings indicate that antitumor action of biguanides can be mediated by 4E-BP1 hyperactivation, which results in UPR inhibition and selective cell killing when glucose is withdrawn.