滤后水中NOM经臭氧氧化产生的小分子醛、酮和酮酸

以富集、分离得到的滤后水中6种不同特性的天然有机物(NOM)为对象,测定了臭氧氧化NOM各组分后小分子醛、酮及酮酸的生成情况.NOM各组分臭氧氧化后甲醛和丙酮酸产量最大,特别是憎水中性物质(HON)的甲醛产率是其醛、酮总产率的70.58%,单位DOC丙酮酸的产率达103.2 μg/mg;憎水性NOM组分的小分子醛、酮、酮酸产率比亲水性组分的高,特别是憎水中性物质(HON)和憎水酸(HOA)的小分子醛、酮及酮酸类总产率最高,二者之和分别占NOM各组分的醛酮总产率及酮酸总产率的55.56%和60%; NOM碱性组分的醛、酮、酮酸产量最低.用小分子醛、酮、酮酸总量折算DOC占氧化后NOM的DOC的百分比作为衡量氧化后各组分可生物降解性的参考,则臭氧氧化后HON和HOA的可生物降解性比其他组分高得多.     

Energy-Based Land Use Predictors of Proximal Factors and Benthic Diatom Composition in Florida Freshwater Marshes

The Landscape Development Intensity index (LDI), which is based on non-renewable energy use and integrates diverse land use activities, was compared to other measures of LU (e.g., %agriculture, %urban) to determine its ability for predicting benthic diatom composition in freshwater marshes of peninsular Florida. In this study, 70 small, isolated herbaceous marshes located along a human disturbance gradient (generally agricultural) throughout peninsular Florida were sampled for benthic diatoms and soil and water physical/chemical parameters (i.e., TP, TKN, pH, specific conductance, etc.). Landscape measures of percent agriculture, percent urban, percent natural, and LDI index values were calculated for a 100 m buffer around each site. The strongest relationships using Mantel's r statistic, which ranges from −1 to 1, were found between benthic diatom composition, the combined soil and water variables, and LDI scores (r=0.51, P<0.0001). Although similar, soil and water variables alone (r=0.45, P<0.0001) or with percent agriculture or percent natural were not as strongly correlated (both Mantel's r=0.46, P<0.0001). Little urban land use was found in the areas surrounding the study wetlands. Diatom data were clustered using flexible beta into 2 groups, and stepwise discriminant analysis identified specific conductance, followed by LDI score, soil pH, water total phosphorus, and ammonia, as cluster-separating variables. The LDI explained slightly more of the variation in species composition than either percent agriculture or percent natural, perhaps because the LDI can combine disparate land uses into a single quantitative value. However, the ecological significance of the difference between land use metrics and diatom composition is controvertible, and additional tests including more varied land uses appear warranted.     

电解-水生植物-软隔离带复合技术治理重污染河流的中试研究

为了探索重污染河流的治理技术,2011年3月在无锡市新区鸿山镇徐塘桥河开展生态治理示范工程,通过电解技术、种植高等水生植物和构建软隔离带复合工程技术改善河流水质。实验结果表明,通过电解技术,可以迅速降低TP、氨氮（NH4＋-N）和COD;但较难减少TN。通过软隔离带可以有效隔离外源污染,在较短时间内改善河流TN、TP、COD的平均水平,但是难以提高河流的生态系统稳定性。电解能够有效的降解大分子有机物,为水生植物提供良好的生长环境,之后再种植水生植物,能够进一步降低的TN、TP。通过电解一水生植物一软隔离带复合技术不仅能够全面改善河流水质的平均水平,而且能够修复水生生态系统,提高生态系统稳定性。     

Direct toxicity of amyloid beta peptide on rat brain mitochondria: preventive role of Mangifera indica and Juglans regia

Role of mitochondrial dysfunction and oxidative stress has been well documented in various cognitive-related disorders such as Alzheimer's disease (AD). Evidence indicates that Aß formation impairs mitochondrial function and that mitochondrial dysfunction is an early event in the pathogenesis of AD. The present study was, therefore, designed to investigate the direct toxicity of Aß peptide on isolated mitochondria obtained from rat brain. Various mitochondrial toxicity/integrity parameters such as succinate dehydrogenase activity, reactive oxygen species (ROS) formation, mitochondrial membrane potential collapse (MMP), mitochondrial swelling, and cytochrome c release were measured following the addition of Aß peptide on isolated mitochondria and then, mitoprotective effect of aqueous extracts of Mangifera indica and Juglans regia against mitochondrial toxicity endpoints parameters induced by Aß peptide were assessed. Our results showed that exposure to Aß peptide (30 nM) in isolated brain mitochondria induced mitochondrial ROS formation, MMP collapse, mitochondrial swelling, and cytochrome c release which is the starting point of apoptosis signaling. All these mitochondrial toxic endpoints induced by Aß peptide inhibited by aqueous extracts of Mangifera indica (100–400 µg/ml) and Juglans regia (200–400 µg/ml). To our knowledge, this is one of the first apparent studies to claim directly targeting of brain mitochondria and induction of apoptosis by Aß peptide as a new hypothesis for etiology of AD and other related neurodegenerative diseases as well as mitopreventive role of common antioxidant nutritional products including walnut and mango.     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.     

Antimony induces oxidative stress and cell death in normal hepatocytes

Antimony (Sb) accumulates in the liver which is one of the target organs for metal-mediated toxicity. Although toxicity of Sb was previously investigated, the precise mechanism of Sb-induced hepatotoxicity remains to be determined. The aim of this study was to examine the role of oxidative stress, and mitochondria in the induction of cell death by Sb. Our results showed that liver cell lysis induced by Sb is mediated by reactive oxygen species (ROS) formation, lipid peroxidation and decline of mitochondrial membrane potential (MMP). Antimony-induced ROS formation, lipid peroxidation and reduction of MMP were significantly diminished by antioxidants and ROS scavengers such as dimethyl sulfoxide and mannitol; mitochondrial permeability transition (MPT) pore sealing agents such as carnitine and trifluoperazine; and adenosine triphosphate (ATP) generator, L-glutamine. Antimony-induced ROS formation, lipid peroxidation and fall in MMP were potentiated by glutathione (GSH) depletion via n-bromoheptane. MPT pore sealing agents and ATP generator inhibited hepatotoxicity, indicating Sb-activated cell death via mitochondrial pathway. Pretreatment of hepatocytes with antioxidants and ROS scavengers also blocked cell death induced by Sb, whereas GSH depletion enhances Sb-induced cell death, suggesting that oxidative stress may be directly involved in the reduction of MMP. These findings contribute to a better understanding of the mechanisms that mediate Sb-induced cell death in isolated rat hepatocytes.     

Prenatal diagnosis of NADH:ubiquinone oxidoreductase deficiency

NADH:ubiquinone oxidoreductase (complex I of the mitochondrial respiratory chain) deficiency is a severe disorder with an often early fatal outcome. Prenatal diagnosis for complex I defects currently relies mainly on biochemical assays of complex I in fetal tissues such as chorionic villi (CV), and is only in a minority of cases possible by means of mutational analysis of nuclear-encoded genes of complex I. We report on our experience to date with prenatal diagnosis in pregnancies at risk for complex I deficiency. We measured complex I activity in native CV and/or cultured CV in 23 pregnancies in 15 families. In accordance with the results of the investigations in CV, 15 children were born clinically unaffected. Two prenatally diagnosed unaffected fetuses and two prenatally diagnosed affected fetuses were lost prematurely with spontaneous or provoked abortions, respectively. Two affected children were born (prenatally found to be affected). In two pregnancies a discrepancy between native and cultured cells was found. We conclude that prenatal diagnosis for complex I deficiency can be reliably performed. Pitfalls were encountered in using cultured CV as a result of maternal cell contamination (MCC). Future research on pathogenic nuclear mutations underlying complex I deficiency will extend the possibilities for prenatal diagnosis at the molecular level. Copyright © 2001 John Wiley & Sons, Ltd.     

Demographic Consequences of Terrestrial Habitat Loss for Pool‐Breeding Amphibians: Predicting Extinction Risks Associated with Inadequate Size of Buffer Zones

Abstract: Much of the biodiversity associated with isolated wetlands requires aquatic and terrestrial habitat to maintain viable populations. Current federal wetland regulations in the United States do not protect isolated wetlands or extend protection to surrounding terrestrial habitat. Consequently, some land managers, city planners, and policy makers at the state and local levels are making an effort to protect these wetland and neighboring upland habitats. Balancing human land‐use and habitat conservation is challenging, and well‐informed land‐use policy is hindered by a lack of knowledge of the specific risks of varying amounts of habitat loss. Using projections of wood frog (Rana sylvatica) and spotted salamander (Ambystoma maculatum) populations, we related the amount of high‐quality terrestrial habitat surrounding isolated wetlands to the decline and risk of extinction of local amphibian populations. These simulations showed that current state‐level wetland regulations protecting 30 m or less of surrounding terrestrial habitat are inadequate to support viable populations of pool‐breeding amphibians. We also found that species with different life‐history strategies responded differently to the loss and degradation of terrestrial habitat. The wood frog, with a short life span and high fecundity, was most sensitive to habitat loss and isolation, whereas the longer‐lived spotted salamander with lower fecundity was most sensitive to habitat degradation that lowered adult survival rates. Our model results demonstrate that a high probability of local amphibian population persistence requires sufficient terrestrial habitat, the maintenance of habitat quality, and connectivity among local populations. Our results emphasize the essential role of adequate terrestrial habitat to the maintenance of wetland biodiversity and ecosystem function and offer a means of quantifying the risks associated with terrestrial habitat loss and degradation.     

植物线粒体基因转录水平表达研究方法的建立

以茎瘤芥雄性不育系为材料,在已有文献的基础上,对常规方法进行改进,使植物线粒体分离、线粒体切片观察、线粒体RNA提取、反转录方法、PCR扩增、northern杂交等方法系统化,建立了一整套比较有效的适合于植物线粒体基因转录水平表达分析的方法.图4参12