Microbial processes influencing methane emission from rice fields

Irrigated rice fields are an important source of atmospheric methane. In order to improve our understanding of the controlling processes, we measured in situ CH₄ emission and CH₄ oxidation in an Italian rice field in 1998 and 1999, and studied CH₄ production in soil and root samples. The CH₄ emission rates were correlated with diurnal temperature variations and showed pronounced seasonal and interannual variations. The contribution of CH₄ oxidation to total CH₄ flux, determined by specific inhibition with difluoromethane, decreased from 40% at the beginning to zero at the end of the season. The stable carbon isotopic composition of the emitted CH₄ also decreased. The CH₄‐oxidizing bacteria probably became limited by nitrogen as indicated by the seasonal decrease of NH₄⁺. Thus, CH₄ oxidation had little effect on CH₄ emission. Methane production on rice roots was relatively constant over the season. Methane production in soil slowly increased after flooding and was highest in the middle of the season. Pore water concentrations of CH₄ showed a similar seasonal pattern. In 1999, CH₄ production increased later in the season and reached lower rates than in 1998. An additional drainage in 1999 resulted in higher ferric iron concentrations, higher soil redox potentials and lower acetate concentrations. As a result, acetate‐utilizing methanogens were probably out‐competed by iron‐reducers so that a larger percentage of [2–¹⁴C]acetate was converted to ¹⁴CO₂ instead of ¹⁴CH₄. The residual CH₄ production was relatively low and was mainly due to H₂/CO₂‐dependent methanogenesis. Experiments with radioactive bicarbonate and with methyl fluoride as specific inhibitor showed that the theoretical ratio of 7:3 of methanogenesis from acetate vs. H₂/CO₂ was only reached later in the season when total CH₄ production was at the maximum. In conclusion, our results give a mechanistic explanation for the intraseasonal and interannual differences in CH₄ emission.     

Luminescent properties of 4‐aminobenzo‐15‐crown‐5 after preferential binding of ferric ions in aqueous solutions

We report a combined approach that introduces the use of 4‐aminobenzo‐15‐crown‐5 (4AB15C5) for the detection of ferric(III) ions by colorimetric, ultraviolet (UV)–visible light absorption, fluorescence, and live‐cell imaging techniques along with density functional theory (DFT) calculations. We have found that 4AB15C5 is sensitive and selective for binding ferric(III) ions in aqueous solutions. DFT calculations using the polarizable continuum model have been used to explain the strong binding of the ferric ion by 4AB15C5 in aqueous solutions. The detection limit in the fluorescence quenching measurements was found to be as low as 50 μM for the ferric ion with a determined Stern–Volmer constant of 1.52 × 10⁴ M^?1. Fluorescence intensity did not change for other ions tested, Fe²⁺, Co²⁺, Mn²⁺, Mg²⁺, Zn²⁺, Ca²⁺, NH₄⁺, Na⁺, and K⁺ ions. Live‐cell fluorescence imaging was also used to check the intracellular variations in ferric ion levels. Our spectroscopic data indicated that 4AB15C5 can bind ferric ions selectively in aqueous solutions.     

Effects of trace elements on the telomere lengths of hepatocytes L-02 and hepatoma cells SMMC-7721

The effects of selenium, zinc, iron, chromium, and lead on telomere lengths of human cells have not been investigated. This article adopted flow cytometry and fluorescence in situ hybridization to investigate the impact of different elements on cellular apoptosis and telomere lengths of human hepatocytes L-02 and hepatoma cells SMMC-7721. Results showed that these trace elements under the following dosages did not have remarkable effect on cellular apoptosis. However, sodium selenite at doses of 0.5 and 2.5 μmol/L significantly extended the telomere length of hepatocytes L-02; 0.5 μmol/L lead acetate remarkably shortened the telomere length of L-02 cells; 80 μmol/L zinc sulfate, 20 μmol/L ferric chloride, and 200 μmol/L chromic chloride only had slight impact on the telomere length, respectively. Regarding hepatoma cells SMMC-7721, sodium seleite at 0.5 and 2.5 μmol/L had little impact on the telomere length; 80 μmol/L zinc sulfate significantly accelerated the loss of telomere length, whereas 20 μmol/L ferric chloride, 200 μmol/L chromic chloride, and 0.5 μmol/L lead acetate remarkably extended the telomere lengths, respectively. The results revealed differential effects of each trace element on the life-span of human hepatocytes and hepatoma cell lines, which suggested further research on somatic hepatocytes and hepatoma in vivo.     

N-Sulfonyl hydroxamate derivatives as inhibitors of class II fructose-1,6-diphosphate aldolase

Dihydroxyacetone-phosphate and phosphonate derivatives were synthesized bearing a N-sulfonyl hydroxamate moiety. The phosphate derivatives represent competitive inhibitors for the class II-FBP aldolase catalyzed reaction, while the phosphonate isosteres are comparatively weaker inhibitors.     

FERRIC CHELATE REDUCTASE ACTIVITY AS AFFECTED BY THE IRON‐LIMITED GROWTH RATE IN FOUR SPECIES OF UNICELLULAR GREEN ALGAE (CHLOROPHYTA)1

Four species of green algae (Chlorella kessleri Fott et Nováková, Chlorococcum macrostigmatum Starr, Haematococcus lacustris[Girod‐Chantrans] Rostaf., Stichococcus bacillaris Näg.) were grown in iron‐limited chemostats and under phosphate limitation and iron (nutrient) sufficiency. For all four species, steady‐state culture density declined with decreasing degree of iron limitation (increasing iron‐limited growth rate), whereas chl per cell or biovolume increased. Plasma membrane ferric chelate reductase activity was enhanced by iron limitation in all species and suppressed by phosphate limitation and iron sufficiency. These results confirm previous work that C. kessleri uses a reductive mechanism of iron acquisition and also suggest that the other three species use the same mechanism. Although imposition of iron limitation led to enhanced activities of ferric chelate reductase in all species, the relationship between ferric chelate reductase activity and degree of iron limitation varied. Ferric chelate reductase activity in C. macrostigmatum and S. bacillaris was an inverse function of the degree of iron limitation, with the most rapidly growing iron‐limited cells exhibiting the highest ferric chelate reductase activity. In contrast, ferric chelate reductase activity was only weakly affected by the degree of iron limitation in C. kessleri and H. lacustris. Calculation of ferric reductase activity per unit chl allowed a clear differentiation between iron‐limited and iron‐sufficient cells. The possible extension of the ferric chelate reductase assay to investigate the absence or presence of iron limitation in natural waters may be feasible, but it is unlikely that the assay could be used to estimate the degree of iron limitation.     

Ferritinophagy drives uropathogenic Escherichia coli persistence in bladder epithelial cells

Autophagy is a cellular recycling pathway, which in many cases, protects host cells from infections by degrading pathogens. However, uropathogenic Escherichia coli (UPEC), the predominant cause of urinary tract infections (UTIs), persist within the urinary tract epithelium (urothelium) by forming reservoirs within autophagosomes. Iron is a critical nutrient for both host and pathogen, and regulation of iron availability is a key host defense against pathogens. Iron homeostasis depends on the shuttling of iron-bound ferritin to the lysosome for recycling, a process termed ferritinophagy (a form of selective autophagy). Here, we demonstrate for the first time that UPEC shuttles with ferritin-bound iron into the autophagosomal and lysosomal compartments within the urothelium. Iron overload in urothelial cells induces ferritinophagy in an NCOA4-dependent manner causing increased iron availability for UPEC, triggering bacterial overproliferation and host cell death. Addition of even moderate levels of iron is sufficient to increase and prolong bacterial burden. Furthermore, we show that lysosomal damage due to iron overload is the specific mechanism causing host cell death. Significantly, we demonstrate that host cell death and bacterial burden can be reversed by inhibition of autophagy or inhibition of iron-regulatory proteins, or chelation of iron. Together, our findings suggest that UPEC persist in host cells by taking advantage of ferritinophagy. Thus, modulation of iron levels in the bladder may provide a therapeutic avenue to controlling UPEC persistence, epithelial cell death, and recurrent UTIs.     

柠檬酸铁对过亚硝酸根硝化酪氨酸反应的影响

由一氧化氮和超氧阴离子迅速反应生成的过亚硝酸根(ONOO^-)是一种强细胞毒性物质. 使含酚基物质如酪氨酸等硝化,是过亚硝酸根损伤生物系统的重要途径之一. 研究了柠檬酸铁和草酸铁对过亚硝酸根硝化酪氨酸反应的影响.在生理pH条件下柠檬酸铁和草酸铁对硝化反应无影响. 在弱酸性条件下柠檬酸铁和草酸铁可催化硝化反应. 对pH影响铁配合物在硝化反应中的催化活性的原因进行了讨论.     

Effects of short-term drainage and aeration on the production of methane in submerged rice soil

Emission rates of CH₄ were measured in microcosms of submerged soil which were planted with rice. Drainage of the rice microcosms for 48 h resulted in drastically decreased CH₄ emission rates which only slowly recovered to the rates of the undrained controls. Drainage also resulted in drastically increased sulphate concentrations which only slowly decreased to nearly zero background values after the microcosms were submerged again. The mechanisms responsible for the decrease of CH₄ production by aeration were investigated in slurries of a loamy and a sandy Italian rice soil. Incubation of the soil slurries under anoxic conditions resulted first in the reduction of nitrate, sulphate and ferric iron before CH₄ production started. Incubation of the soil slurries for 48 h under air resulted in immediate and complete inhibition of CH₄ production. Although the soil slurries were then again incubated under anoxic conditions (N₂ atmosphere), the inhibition of CH₄ production persisted for more than 30 days. The redox potential of the soil increased after the aeration but returned within 15 days to the low values typical for CH₄ production. However, the concentrations of sulphate and of ferric iron increased dramatically after the aeration and stayed at elevated levels for the period during which CH₄ production was inhibited. These observations show that even brief exposure of the soil to O₂ allowed the production of sulphate and ferric iron from their reduced precursors. Elevated sulphate and ferric iron concentrations allowed sulphate-reducing and ferric iron-reducing bacteria to outcompete methanogenic bacteria on H₂ as common substrate. Indeed, concentrations of H₂ were decreased as long as sulphate and ferric iron were high so that the Gibbs free energy of CH₄ production from H₂/CO₂ was also increased (less exergonic). On the other hand, concentrations of acetate, the more important precursor for CH₄, were not much affected by the short aeration of the soil slurries, and the Gibbs free energy of CH₄ production from acetate was highly exergonic suggesting that acetotrophic methanogens were not outcompeted but were otherwise inhibited. Aeration also resulted in increased rates of CO₂ production and in a short-term increase of N₂O production. However, these increases were < 10% of the decreased production of CH₄ and did not represent a trade-off in terms of CO₂ equivalents. Hence, short-term drainage and aeration of submerged paddy fields may be a useful mitigation option for decreasing the emission of greenhouse gases.