Nitrification inhibitors have been used for decades to improve nitrogen fertilizer utilization in farmland. However, their effect on ammonia-oxidizing Archaea (AOA) in soil is little explored. Here, we compared the impact of diverse inhibitors on nitrification activity of the soil archaeon Ca. Nitrososphaera viennensis EN76 and compared it to that of the ammonia-oxidizing bacterium (AOB) Nitrosospira multiformis. Allylthiourea, amidinothiourea, and dicyandiamide (DCD) inhibited ammonia oxidation in cultures of both N. multiformis and N. viennensis, but the effect on N. viennensis was markedly lower. In particular, the effective concentration 50 (EC50) of allylthiourea was 1000 times higher for the AOA culture. Among the tested nitrification inhibitors, DCD was the least potent against N. viennensis. Nitrapyrin had at the maximal soluble concentration only a very weak inhibitory effect on the AOB N. multiformis, but showed a moderate effect on the AOA. The antibiotic sulfathiazole inhibited the bacterium, but barely affected the archaeon. Only the NO-scavenger carboxy-PTIO had a strong inhibitory effect on the archaeon, but had little effect on the bacterium in the concentrations tested. Our results reflect the fundamental metabolic and cellular differences of AOA and AOB and will be useful for future applications of inhibitors aimed at distinguishing activities of AOA and AOB in soil environments.

A greenhouse pot experiment was conducted to select vegetables for iodine uptake. The residual effect of iodate fertilization on the growth of and iodine uptake by spinach plants were also investigated. Results showed that the concentrations of iodate in soil had significant effect on the biomass of edible parts of pakchoi and spinach (p<0.01), whereas the concentrations of iodate in soil had no significant effect on that of carrots, water spinach, celery, and onion. Iodine concentrations in edible parts of vegetables and the transfer factors (TF edible parts ) of soil-to-edible parts of vegetables significantly increased with increasing iodine concentrations in soil (p<0.001), and iodine concentrations in edible parts and TF edible parts of spinach were much higher than those of other vegetables at any treatment. Both transfer coefficients for edible parts (TC edible parts ) and for aerial parts (TC aerial parts ) of vegetables changed differently with increasing iodine concentrations in the soil, and TC edible parts and TC aerial parts of spinach were higher than those of other vegetables. Therefore, spinach (leafy vegetable) was considered as an efficient vegetable for iodine biofortification. Further experiment showed that there is considerable residual effect of soil fertilization with iodate.

BackgroundNotch1 is a potent regulator known to play an oncogenic role in many malignancies including T-cell acute lymphoblastic leukemia (T-ALL). Tumor hypoxia and increased hypoxia-inducible factor-1α (HIF-1α) activity can act as major stimuli for tumor aggressiveness and progression. Although hypoxia-mediated activation of the Notch1 pathway plays an important role in tumor cell survival and invasiveness, the interaction between HIF-1α and Notch1 has not yet been identified in T-ALL. This study was designed to investigate whether hypoxia activates Notch1 signalling through HIF-1α stabilization and to determine the contribution of hypoxia and HIF-1α to proliferation, invasion and chemoresistance in T-ALL.MethodsT-ALL cell lines (Jurkat, Sup-T1) transfected with HIF-1α or Notch1 small interference RNA (siRNA) were incubated in normoxic or hypoxic conditions. Their potential for proliferation and invasion was measured by WST-8 and transwell assays. Flow cytometry was used to detect apoptosis and assess cell cycle regulation. Expression and regulation of components of the HIF-1α and Notch1 pathways and of genes related to proliferation, invasion and apoptosis were assessed by quantitative real-time PCR or Western blot.ResultsHypoxia potentiated Notch1 signalling via stabilization and activation of the transcription factor HIF-1α. Hypoxia/HIF-1α-activated Notch1 signalling altered expression of cell cycle regulatory proteins and accelerated cell proliferation. Hypoxia-induced Notch1 activation increased the expression of matrix metalloproteinase-2 (MMP2) and MMP9, which increased invasiveness. Of greater clinical significance, knockdown of Notch1 prevented the protective effect of hypoxia/HIF-1α against dexamethasone-induced apoptosis. This sensitization correlated with losing the effect of hypoxia/HIF-1α on Bcl-2 and Bcl-xL expression.ConclusionsNotch1 signalling is required for hypoxia/HIF-1α-induced proliferation, invasion and chemoresistance in T-ALL. Pharmacological inhibitors of HIF-1α or Notch1 signalling may be attractive interventions for T-ALL treatment.