Anaerobic degradation of m-cresol by Desulfobacterium cetonicum is initiated by formation of 3-hydroxybenzylsuccinate

The anaerobic bacterium Desulfobacterium cetonicum oxidized m-cresol completely with sulfate as electron acceptor. During growth, 3-hydroxybenzylsuccinate (identified by gas chromatography/mass spectroscopy and by comparison of high-performance liquid chromatography retention time and UV spectrum with a chemically synthesized reference compound) accumulated in the medium. This finding indicates that the methyl group of m-cresol is activated by addition to fumarate as in the case of anaerobic toluene metabolism. In cell-free extracts of D. cetonicum, the formation of 3-hydroxybenzylsuccinate from m-cresol and fumarate was detected at an activity of 0.5 nmol min^–1 (mg protein)^–1. This reaction depended strictly on anoxic assay conditions. Treatment with air resulted in a complete loss of activity; however, some activity could be recovered after restoring anoxic conditions. The activity was slightly membrane-associated. 3-Hydroxybenzylsuccinate was degraded via CoA thioesterification and further oxidation to 3-hydroxybenzoyl-CoA as subsequent steps in the degradation pathway. Received: 20 May 1999 / Accepted: 19 July 1999     

白色麝香霉挥发性有机化合物的抗菌活性和组成分析

采用核糖体RNA转录间隔区(internal transcribed spacer of ribosomal RNA,ITS r RNA)、RNA聚合酶II(RNA polymerase II,rpb2)和β-维管蛋白(beta-tubulin,tub1)基因系统发育分析法,鉴定了一株分离自浙江庆元的麝香霉ZJQY709,鉴定结果表明该菌为白色麝香霉Muscodor albus。生长速率法测定结果显示该菌株最适生长温度为22–28℃。二分格培养皿对峙培养法测定该菌挥发性有机化合物的抑菌活性,结果表明其挥发性有机化合物对灰葡萄孢菌和立枯丝核菌的生长抑制作用较强,而对尖孢镰刀菌和终极腐霉的抑制作用较弱。固相微萃取/气质联用法分析该菌产生的挥发性有机化合物,结果显示其挥发性有机化合物成分复杂,主要气体成分为2-甲基丙酸、乙酸-2-甲基丙酯和1-丁醇-2-甲基乙酸。     

Biological Screening of Polyphenol Derivatives for Anti-Proliferative,Anti-Apoptotic and Anti-Migrative Activities in Human Breast Cancer Cell Lines MCF-7

Breast cancer is known as the most common type of invasive cancer in women. It is well-known that phenolic compounds play an important role in the treatment of this disease. This study hypothesized that isoeugenol based two polyphenolic compounds 1 and 2 exerts its anti-proliferative effects through the induction of apoptosis and cell migration arrest on human breast cancer cell. Based on this hypothesis, the study aimed to investigate the anti-proliferative, anti-migrative effects of these compounds and their possible basic molecular mechanisms of action in MCF-7 cell lines. As a result, isoeugenol-based compounds 1 and 2 showed anti-proliferative, anti-apoptotic and anti-migrative effects in MCF-7 breast cancer cells. This result was supported by molecular analyzes and it was determined that there were changes in the expression of some gene regions involved in apoptosis and migration. Additionally, it was a remarkable result that cell viability inhibition did not occur in healthy breast tissue cells and no cytotoxic effect was observed. The existence of such a differentiation between cancer cells and healthy cells significantly increases the potential of these compounds to be used as chemotherapeutic drug active ingredients without side effects.     

Applying Life Cycle Tools and Process Engineering to Determine the Most Adequate Treatment Process Conditions. A Tool in Environmental Policy (12 pp)

Background The analysis of a wastewater treatment technology, under a expanded boundaries system which includes both the technology and the inputs required for its operation, quantifies the overall environmental impact that may result from the treatment of a wastewater stream. This is particularly useful for environmental policy makers being that a expanded boundaries system tends to provide a holistic view. The former view can be highly enriched with the use of process engineering tools, such as mathematical process modelling, process design, performance assessment and cost optimised models. Main Features The traditional approach used to assess waste treatment technologies is contrasted with a life cycle analysis (LCA) approach. The optimal design of a granular activated carbon adsorption (GAC) process is used as a model system to demonstrate the advantages of LCA approaches over traditional approaches. Further sections of the paper describe a mathematical framework for the assessment of technologies, design considerations applied in the cost optimised carbon adsorption model, the use of LCA techniques to perform an inventory of all emissions associated to the process system and, some of its environmental impacts. Results Economic and environmental considerations regarding the optimum process design are introduced as a basis for decision towards the selection and operating conditions of wastewater treatment technologies. Moreover, the use of LCA has revealed that the environmental burden associated with the wastewater treatment may produce a higher environmental impact than one that can be caused by untreated discharges. Conclusion The paper highlights the string advantages that environmental policy makers may have by combining LCA and process engineering tools. Furthermore, this approach can be incorporated into other existing treatment processes or for process designers.     

Differential expression of enzyme activities initiating anoxic metabolism of various aromatic compounds via benzoyl-CoA

The regulation of the expression of enzyme activities catalyzing initial reactions in the anoxic metabolism of various aromatic compounds was studied at the whole cell level in the denitrifying Pseudomonas strain K 172. The specific enzyme activities were determined after growth on six different aromatic substrates (phenol, 4-hydroxybenzoate, benzoate, p-cresol, phenylacetate, 4-hydroxyphenylacetate) all being proposed to be metabolized anaerobically via benzoyl-CoA. As a control cells were grown on acetate, or aerobically on benzoate. The expression of the following enzyme activities was determined.Phenol carboxylase, as studied by the isotope exchange between ¹⁴CO₂ and the carboxyl group of 4-hydroxybenzoate; 4-hydroxybenzoyl-CoA reductase (dehydroxylating); p-cresol methylhydroxylase; 4-hydroxybenzyl alcohol dehydrogenase; 4-hydroxybenzaldehyde dehydrogenase; coenzymeA ligases for the aromatic acids benzoate, 4-hydroxybenzoate, phenylacetate, and 4-hydroxyphenylacetate; phenylglyoxylate: acceptor oxidoreductase and 4-hydroxyphenylglyoxylate: acceptor oxidoreductase; aromatic alcohol and aldehyde dehydrogenases.The formation of most active enzymes is strictly regulated; they were only induced when required, the basic activities being almost zero. The observed whole cell regulation pattern supports the postulate that the enzyme activities play a role in anoxic aromatic metabolism and that the compounds are degraded via the following intermediates: Phenol 4-hydroxybenzoate 4-hydroxybenzoyl-CoA benzoyl-CoA; 4-hydroxybenzoate 4-hydroxybenzoyl-CoA benzoyl-CoA; benzoate benzoyl-CoA; p-cresol 4-hydroxybenzaldehyde 4-hydroxybenzoate 4-hydroxybenzoyl-CoA benzoyl-CoA; phenylacetate phenylacetyl-CoA phenylglyoxylate benzoyl-CoA plus CO₂; 4-hydroxyphenylacetate 4-hydroxyphenylacetyl-CoA 4-hydroxyphenylglyoxylate 4-hydroxybenzoyl-CoA plus CO₂ benzoyl-CoA.     

Iminophosphorane-organogold(III) complexes induce cell death through mitochondrial ROS production

Gold compounds are being investigated as potential antitumor drugs. Some gold(III) derivatives have been shown to induce cell death in solid tumors but their mechanism of action differs from that of cisplatin, since most of these compounds do not bind to DNA. We have explored cellular events triggered by three different iminophosphorane-organogold(III) compounds in leukemia cells (a neutral compound with two chloride ligands [Au{κ²-C,N-C₆H₄(PPh₂ = N(C₆H₅)-2}Cl₂] 1, and two cationic compounds with either a dithiocarbamate ligand [Au{κ²-C,N-C₆H₄(PPh₂ = N(C₆H₅)-2}(S₂CN-Me₂)]PF₆2, or a water-soluble phosphine and a chloride ligand [Au{κ²-C,N-C₆H₄(PPh₂ = N(C₆H₅)-2}(P{Cp(m-C₆H₄-SO₃Na)₂}₃) Cl]PF₆3). All three compounds showed higher toxicity against leukemia cells when compared to normal T-lymphocytes. Compounds 1 and 2 induced both necrosis and apoptosis, while 3 was mainly apoptotic. Necrotic cell death induced by 1 and 2 was Bax/Bak- and caspase-independent, while apoptosis induced by 3 was Bax/Bak-dependent. Reactive oxygen species (ROS) production at the mitochondrial level was a critical step in the antitumor effect of these compounds.     

海带中多糖类化合物的提取和应用

本课题从海带中提取多糖类化合物,并与丙烯酸接枝共聚、交联,制得了一系列耐盐性能良好的高吸水树脂,其对0.9%氯化钠水溶液(与体液中含盐浓度相当)吸收倍率在70～120倍,对重蒸馏水的吸收倍率为650～1075倍,本实验反应条件温和,重复性好,海带利用率高达72.5%.     

滨海湿地甲烷产生途径和产甲烷菌研究进展

滨海湿地在全球碳循环中起着重要的作用,其甲烷排放量占全球海洋甲烷排放的75%.本文综述了滨海湿地主要甲烷产生途径、产甲烷菌种类及其影响因子.滨海湿地SO₄^2-含量丰富,乙酸发酵和H₂/CO₂途径产甲烷受抑制,乙酸营养型和氢营养型产甲烷菌丰度较低;而利用甲胺类等“非竞争性”底物的C1甲基化合物歧化途径不受硫酸还原菌竞争底物的限制,兼性营养型产甲烷菌成为产甲烷优势菌.盐度与SO₄^2-含量和植被类型密切相关,影响竞争性电子和产甲烷底物的种类和含量,对甲烷产生途径和产甲烷菌群落结构有重要影响.目前,滨海湿地产甲烷菌群落结构、甲烷产生途径的关键控制因素尚需明确,其对甲烷排放的影响有待进一步研究.     

Isolation of a dimethylsulfide-utilizingHyphomicrobium species and its application in biofiltration of polluted air

The methylotrophic bacteriumHyphomicrobium VS was enriched and isolated, using activated sewage sludge as inoculum in mineral medium containing dimethylsulfide (DMS) at a low concentration to prevent toxicity. DMS concentrations above 1 mM proved to be growth inhibiting.Hyphomicrobium VS could use DMS, dimethylsulfoxide (DMSO), methanol, formaldehyde, formate, and methylated amines as carbon and energy source. Carbon was assimilated via the serine pathway. DMS-grown cells respired sulfide, thiosulfate, methanethiol, dimethyldisulfide and dimethyltrisulfide.To testHyphomicrobium VS for application in biofiltration of air polluted with volatile sulfur compounds two laboratory scale trickling biofilters with polyurethane and lava stone as carrier material were started up by inoculation with this bacterium. Both methanol- and DMS-grown cells could be used. Only a short adaptation period was needed. Short term experiments showed that high concentrations of DMS (1–2 µmol 1^–1) were removed very efficiently by the biofilters at space velocities up to 100 h^–1.Abbreviations VSC volatile sulfur compounds - DMS dimethylsulfide - DMDS dimethyldisulfide - DMTS dimethyltrisulfide - MT methanethiol - DMSO dimethylsulfoxide