Nitrate and nitrite reduction activity of activated sludge microcosm in a highly alkaline environment with solid cementitious material

Denitrification is a major biological process contributing to nitrate and nitrite reduction. However, this process remains poorly understood at alkaline pH although such conditions can be encountered in natural (e.g. soda lakes) or industrial environments (e.g. geological waste repositories with cementitious materials). To investigate the nitrate reduction (NR) rate for pH > 9.5 in a cementitious environment, several batch reactors were implemented, with cement leachate or with hardened cement paste (HCP). In the experiments carried out with cement leachate, NR dropped from 0.72 mM/h at pH 9.5 to 0.17 mM/h at pH > 11, while the concentration of nitrite increased. The NR was inhibited at pH close to 12, as was the nitrite reduction at pH above 11. In the reactor containing HCP, the NR rate was 0.75 mM/h at pH close to 10. Calcite precipitated on the HCP surface. Epifluorescence microscopy observations coupled with DNA labelling suggested the presence of microorganisms attached to the HCP surface. This was confirmed by biological growth coupled with NR activity after the transfer of the HCP into a new medium, considered to be sterile. The bacterial community analysis showed that the highly selective culture conditions led to the selection of two species: Halomonas sp. and a species known for its versatile metabolism and ability to form biofilms, i.e. Thauera sp

From hexafluorotitanate waste to TiO2 powder: Characterization and evaluation of the influence of synthesis parameters by the experimental design method

International audienc

Metal swap between Zn7metallothionein–3 and amyloid–β–Cu protects against amyloid–β toxicity

Aberrant interactions of copper and zinc ions with the amyloid–β peptide (Aβ) potentiate Alzheimer disease (AD) by participating in the aggregation process of Aβ and in the generation of reactive oxygen species (ROS). The ROS production and the neurotoxicity of Aβ are associated with copper binding. Metallothionein–3 (Zn7MT–3), an intra– and extracellularly occurring metalloprotein, is highly expressed in the brain and down–regulated in AD. This protein protects, by an unknown mechanism, cultured neurons from the toxicity of Aβ. Herein, we show that a metal swap between Zn7MT–3 and soluble and aggregated Aβ1–40–Cu(II) abolishes the ROS production and the related cellular toxicity. In this process, copper is reduced by the protein thiolates forming Cu(I)4Zn4MT–3 in which an air stable Cu(I)4–thiolate cluster and two disulfide bonds are present. The discovered protective effect of Zn7MT–3 from the copper–mediated Aβ1–40 toxicity may lead to new therapeutic strategies in treating AD