排序方式: 共有27条查询结果,搜索用时 15 毫秒
1.
Iron deficiency in higher plants causes accumulation of salts of organic acids in the roots, the most characteristic being citrate. We show that citrate and malate accumulate in beans (Phaseolus vulgaris L. var Prélude), not because of a lack of the iron-containing enzyme aconitase (EC 4.2.1.3), but in close coupling to the extrusion of protons during rhizosphere acidification, one of the `Fe-efficiency' reactions of dicotyledonous plants. When proton excretion is induced in roots of control bean plants by addition of fusicoccin, only malate, not citrate, is accumulated. We propose that iron deficiency induces production of organic acids in the roots, which in beans leads to both proton excretion and an increased capacity to reduce ferric chelates via the induced electron transfer system in the root epidermis cells. 相似文献
2.
Amelia K. Kivaisi Huub J. M. Op den Camp Henk J. Lubberding Jaap J. Boon Godfried D. Vogels 《Applied microbiology and biotechnology》1990,33(1):93-98
Summary The supernatants of effluents from an artificial rumen reactor degrading barley straw have been shown to contain lignin-derived compounds by UV spectral characteristics and pyrolysis mass spectrometry (PYMS). Most of these compounds were shown to be released by the action of rumen microorganisms. The compounds were quantified by measuring absorbance at 280 nm using bamboo-milled wood lignin as a standard. The concentration of the compounds rose from 0.5 mg·ml–1 at solid and liquid retention times (SRT and HRT) of 60 and 12 h, respectively, and a loading rate (LR) of 25 g total solids (TS)·l–1 per day to 3.5 mg·ml–1 at a SRT of 144 h, an HRT of 20 days and an LR of 15 g TS·1–1 per day. The highest concentration was below the level known to be toxic to rumen microorganisms in vitro. No indications were found for anaerobic lignin degradation in the rumen reactor.
Offprint requests to: H. J. M. Op den Camp 相似文献
3.
The activities and kinetics of the enzymes G6PDH (glucose-6-phosphate dehydrogenase) and 6PGDH (6-phosphogluconate dehydrogenase) from the mesophilic cyanobacterium Synechococcus 6307 and the thermophilic cyanobacterium Synechococcus 6716 are studied in relation to temperature. In Synechococcus 6307 the apparent K
m's are for G6PDH: 80M (substrate) and 20M (NADP+); for 6PGDH: 90M (substrate) and 25M (NADP+). In Synechococcus 6716 the apparent K
m's are for G6PDH: 550M (substrate) and 30M (NADP+); for 6PGDH: 40M (substrate) and 10M (NADP+). None of the K
m's is influenced by the growth temperature and only the K
m's of G6PDH for G6P are influenced by the assay temperature in both organisms. The idea that, in general, thermophilic enzymes possess a lower affinity for their substrates and co-enzymes than mesophilic enzymes is challenged.Although ATP, ribulose-1,5-bisphosphate, NADPH and pH can all influence the activities of G6PDH and 6PGDH to a certain extent (without any difference between the mesophilic and the thermophilic strain), they cannot be responsible for the total deactivation of the enzyme activities observed in the light, thus blocking the pentose phosphate pathway.Abbreviations G6PDH
glucose-6-phosphate, dehydrogenase
- 6PGDH
6-phosphogluconate dehydrogenase
- G6P
glucose-6-phosphate
- 6PG
6-phosphogluconate
- RUDP
ribulose-1,5-bisphosphate
- Tricine
N-Tris (hydroxymethyl)-methylglycine 相似文献
4.
Werner A Havinga R Kuipers F Verkade HJ 《American journal of physiology. Gastrointestinal and liver physiology》2004,286(5):G822-G832
Essential fatty acid (EFA) deficiency during cholestasis is mainly due to malabsorption of dietary EFA (23). Theoretically, dietary phospholipids (PL) may have a higher bioavailability than dietary triglycerides (TG) during cholestasis. We developed murine models for EFA deficiency (EFAD) with and without extrahepatic cholestasis and compared the efficacy of oral supplementation of EFA as PL or as TG. EFAD was induced in mice by feeding a high-fat EFAD diet. After 3 wk on this diet, bile duct ligation was performed in a subgroup of mice to establish extrahepatic cholestasis. Cholestatic and noncholestatic EFAD mice continued on the EFAD diet (controls) or were supplemented for 3 wk with EFA-rich TG or EFA-rich PL. Fatty acid composition was determined in plasma, erythrocytes, liver, and brain. After 4 wk of EFAD diet, induction of EFAD was confirmed by a sixfold increased triene-to-tetraene ratio (T/T ratio) in erythrocytes of noncholestatic and cholestatic mice (P < 0.001). EFA-rich TG and EFA-rich PL were equally effective in preventing further increase of the erythrocyte T/T ratio, which was observed in cholestatic and noncholestatic nonsupplemented mice (12- and 16-fold the initial value, respectively). In cholestatic mice, EFA-rich PL was superior to EFA-rich TG in decreasing T/T ratios of liver TG and PL (each P < 0.05) and in increasing brain PL concentrations of the long-chain polyunsaturated fatty acids (LCPUFA) docosahexaenoic acid and arachidonic acid (each P < 0.05). We conclude that oral EFA supplementation in the form of PL is more effective than in the form of TG in increasing LCPUFA concentrations in liver and brain of cholestatic EFAD mice. 相似文献
5.
Corveleyn A Janssen H Martini A Somers R Cools J Marynen P 《Journal of cellular biochemistry》2005,94(6):1112-1125
6.
Ckless K Lampert A Reiss J Kasahara D Poynter ME Irvin CG Lundblad LK Norton R van der Vliet A Janssen-Heininger YM 《Journal of immunology (Baltimore, Md. : 1950)》2008,181(6):4255-4264
Pulmonary inflammation in asthma is orchestrated by the activity of NF-kappaB. NO and NO synthase (NOS) activity are important modulators of inflammation. The availability of the NOS substrate, l-arginine, is one of the mechanisms that controls the activity of NOS. Arginase also uses l-arginine as its substrate, and arginase-1 expression is highly induced in a murine model of asthma. Because we have previously described that arginase affects NOx content and interferes with the activation of NF-kappaB in lung epithelial cells, the goal of this study was to investigate the impact of arginase inhibition on the bioavailability of NO and the implications for NF-kappaB activation and inflammation in a mouse model of allergic airway disease. Administration of the arginase inhibitor BEC (S-(2-boronoethyl)-l-cysteine) decreased arginase activity and caused alterations in NO homeostasis, which were reflected by increases in S-nitrosylated and nitrated proteins in the lungs from inflamed mice. In contrast to our expectations, BEC enhanced perivascular and peribronchiolar lung inflammation, mucus metaplasia, NF-kappaB DNA binding, and mRNA expression of the NF-kappaB-driven chemokine genes CCL20 and KC, and lead to further increases in airways hyperresponsiveness. These results suggest that inhibition of arginase activity enhanced a variety of parameters relevant to allergic airways disease, possibly by altering NO homeostasis. 相似文献
7.
Anniek B. van der Waart Walter J. F. M. van der Velden Astrid G. S. van Halteren Marij J. L. G. Leenders Ton Feuth Nicole M. A. Blijlevens Robbert van der Voort Harry Dolstra 《PloS one》2012,7(12)
The C-type lectin-like receptor CD161 is a well-established marker for human IL17-producing T cells, which have been implicated to contribute to the development of graft-versus-host disease (GVHD) after allogeneic stem cell transplantation (allo-SCT). In this study, we analyzed CD161+ T cell recovery, their functional properties and association with GVHD occurrence in allo-SCT recipients. While CD161+CD4+ T cells steadily recovered, CD161hiCD8+ T cell numbers declined during tapering of Cyclosporine A (CsA), which can be explained by their initial growth advantage over CD161neg/lowCD8+ T cells due to ABCB1-mediated CsA efflux. Interestingly, occurrence of acute and chronic GVHD was significantly correlated with decreased levels of circulating CD161+CD4+ as well as CD161hiCD8+ T cells. In addition, these subsets from transplanted patients secreted high levels of IFNγ and IL17. Moreover, we found that CCR6 co-expression by CD161+ T cells mediated specific migration towards CCL20, which was expressed in GVHD biopsies. Finally, we demonstrated that CCR6+ T cells indeed were present in these CCL20+ GVHD-affected tissues. In conclusion, we showed that functional CD161+CCR6+ co-expressing T cells disappear from the circulation and home to GVHD-affected tissue sites. These findings support the hypothesis that CCR6+CD161-expressing T cells may be involved in the immune pathology of GVHD following their CCL20-dependent recruitment into affected tissues. 相似文献
8.
Huub J. Gijzen Henk J. Lubberding Martin J.T. Gerhardus Godfried D. Vogels 《FEMS microbiology letters》1988,53(1):35-43
Abstract The contribution of ciliates to rumen fermentation was estimated by determination of overall fibre degradation and cellulase activities (determined as carboxymethylcellulase activity) in faunated and defaunated 'artificial rumen' cultures. Experiments performed at loading rates of 22.5 and 35 g per liter per day of a grass-grain substrate revealed that fibre degradation was significantly lower in the absence of ciliates only at the high loading rate. This effect of defaunation was smaller at dilution rates below 1.7 fermenter volume turnovers per day. Bacterial numbers were higher in all experiments after removal of ciliates. Fractionation studies demonstrated that ciliates accounted for 19–28% of the total cellulase activity in faunated cultures fed on filter paper cellulose. 相似文献
9.
R. Valencia W. van der Zon H. Woelders H.J. Lubberding H.J. Gijzen 《Bioresource technology》2009,100(5):1754-1761
Seven bioreactor landfill simulators (mixed gravel, gravel in layers, and controls without gravel with two levels of compaction, i.e. normal and lower density) were used to investigate the effect of different hydraulic conditions on the waste stabilisation process. The simulators with mixed gravel showed a higher degree of waste stabilisation towards the end of the experiment due to higher moisture content, whereas the other simulators were prone to clogging thus reducing the overall treatment effectiveness. Moreover, reaching neutral pH levels seemed to be the “driving force” that enhanced physical, chemical and biological processes contributing to waste stabilisation in the simulators with mixed gravel. After one year of operation, the residues of the different simulators were very close to achieve a final storage quality status comparable to the waste acceptance criteria for inert waste of the European landfill directive. 相似文献
10.
Werner A Havinga R Bos T Bloks VW Kuipers F Verkade HJ 《American journal of physiology. Gastrointestinal and liver physiology》2005,288(6):G1150-G1158
Essential fatty acid (EFA) deficiency in mice decreases plasma triglyceride (TG) concentrations and increases hepatic TG content. We evaluated in vivo and in vitro whether decreased hepatic secretion of TG-rich very low-density lipoprotein (VLDL) contributes to this consequence of EFA deficiency. EFA deficiency was induced in mice by feeding an EFA-deficient (EFAD) diet for 8 wk. Hepatic VLDL secretion was quantified in fasted EFAD and EFA-sufficient (EFAS) mice using the Triton WR-1339 method. In cultured hepatocytes from EFAD and EFAS mice, VLDL secretion into medium was measured by quantifying [(3)H]-labeled glycerol incorporation into TG and phospholipids. Hepatic expression of genes involved in VLDL synthesis and clearance was measured, as were plasma activities of lipolytic enzymes. TG secretion rates were quantitatively similar in EFAD and EFAS mice in vivo and in primary hepatocytes from EFAD and EFAS mice in vitro. However, EFA deficiency increased the size of secreted VLDL particles, as determined by calculation of particle diameter, particle sizing by light scattering, and evaluation of the TG-to-apoB ratio. EFA deficiency did not inhibit hepatic lipase and lipoprotein lipase activities in plasma, but increased hepatic mRNA levels of apoAV and apoCII, both involved in control of lipolytic degradation of TG-rich lipoproteins. EFA deficiency does not affect hepatic TG secretion rate in mice, but increases the size of secreted VLDL particles. Present data suggest that hypotriglyceridemia during EFA deficiency is related to enhanced clearance of altered VLDL particles. 相似文献