蒽醌染料中间体溴氨酸降解酶的特性

从污染地分离筛选出的菌株BX26对蒽醌染料中间体溴氨酸有显著的降解脱色作用,降解过程受降解酶的控制,试验结果表明,降解酶为溴氨酸诱导的胞外酶,该酶在温度高于50℃处理后失活,盐度对该酶失活有影响,盐度高于1%会显著降低该酶活力,酶对溴氨酸的催化脱色要有氧参加,氮气气氛中酶活受抑制。     

A mini review of fluoride-induced apoptotic pathways

Fluorine or fluoride can have toxic effects on bone tissue and soft tissue at high concentrations. These negative effects include but not limited to cytotoxicity, immunotoxicity, blood toxicity, and oxidative damage. Apoptosis plays an important role in fluoride-induced toxicity of kidney, liver, spleen, thymus, bursa of Fabricius, cecal tonsil, and cultured cells. Here, apoptosis activated by high level of fluoride has been systematically reviewed, focusing on three pathways: mitochondrion-mediated, endoplasmic reticulum (ER) stress-mediated, and death receptor-mediated pathways. However, very limited reports are focused on the death receptor-mediated apoptosis pathways in the fluoride-induced apoptosis. Therefore, understanding and discovery of more pathways and molecular mechanisms of fluoride-induced apoptosis may contribute to designing measures for preventing fluoride toxicity.     

O／W型乳化液的处理

采用药剂破乳－电解破乳工艺处理Ｏ／Ｗ型乳化液，药剂破乳选用聚合硫酸铁为破乳剂，破乳时最佳ＰＨ为８，聚合硫酸铁的最佳投量为１５００ｍｇ／Ｌ，电解破乳选用铁作阳极，铝作阴极，电流密度０．８６Ａ／ｄｍ＾２，极距２５ｍｍ，电解时间３ｈ。在上述条件下，破乳效果良好，出水清澈透明，ＣＯＤ总去除率可达到９６－９７％。     

Effect of acute exposure to PFOA on mouse liver cells in vivo and in vitro

Increasingly, epidemiological evidences indicate chemosynthetic perfluorooctanoic acid (PFOA), an environmental pollutant, induces potential adverse effect on human health after long-term exposure. However, less study has been performed for assessment of acute effect of PFOA exposure on metabolic homeostasis. In experimental designs, PFOA-exposed liver cells in vivo and in vitro were used to discuss underlying mechanism related to PFOA-induced metabolic dysfunction. In serological tests, PFOA-exposed mice showed increased treads of liver functional enzymes in alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin (T-BIL), trypsinase, low density lipoprotein-cholesterol (LDL-C), and insulin, while blood glucose, high density lipoprotein-cholesterol (HDL-C), and glucagon levels were reduced. In histocytological observations, PFOA-exposed liver showed visible cytoplasmic vesicles, and intact pancreatic islets were observed in PFOA-exposed pancreas. Additionally, increased insulin-positive cells and reduced glucagon-positive cells were detected in PFOA-exposed islets. As shown in immunoassays, PFOA-exposed liver resulted in elevations of cluster of differentiation 36 (CD36)-labeled cells and CD36 protein. In mouse liver cell study, PFOA-exposed cells showed increased cell apoptotic count, and increased phosphorylated levels of Bcl-2 and Bad in the cells. Furthermore, PFOA-exposed liver cells exhibited elevations of CD36-labeled cells and CD36 protein. Taken together, the present data demonstrate that acute exposure to PFOA-impaired liver function is associated with inducting CD36 expression and apoptosis, as well as disrupting key hormones in the pancreas.     

Urinary metabolomic profiling in rats exposed to dietary di(2-ethylhexyl) phthalate (DEHP) using ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS)

Di(2-ethylhexyl) phthalate (DEHP) is an omnipresent environmental chemical with widespread nonoccupational human exposure through multiple ways. Although considerable efforts have been invested to investigate mechanisms of DEHP toxicity, the key metabolic biomarkers of DEHP toxicity remain to be identified. The aim of this study was to assess the urinary metabonomics of dietary DEHP in rats using the technique of ultra-performance liquid chromatography quadrupole time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS). Fourteen female Wistar rats were divided into two groups and given increasing dietary doses of DEHP for 30 consecutive days. The urinary metabolite profile was studied using ultra-performance liquid chromatography coupled with quadrupole time-of-flight tandem mass spectrometry. Principal component analysis (PCA) and partial least squares-discriminant analysis (PLS-DA) enabled clusters to be clearly separated. Eleven principal urinary metabolites were identified as contributing to the clusters. The clusters in the positive electrospray ionization (ESI) mode were xanthurenic acid, kynurenic acid, nonate, N6-methyladenosine, and L-isoleucyl-L-proline. The clusters in the negative ESI mode were hippuric acid, tetrahydrocortisol, citric acid, phenylpropionylglycine, cPA(18:2(9Z, 12Z)/0:0), and LysoPC(14:1(9Z)). The urinary metabonomic changes indicated that exposure to dietary DEHP can affect energy-related metabolism, liver and renal function, fatty acid metabolism, and cause DNA damage in rats. The findings of this study on the urinary metabolites and metabolic pathways of DEHP may form the basis for future studies on the mechanisms of toxicity of this commonly found environmental chemical.     

Spatial variation and toxicity assessment for heavy metals in sediments of intertidal zone in a typical subtropical estuary (Min River) of China

Environmental Science and Pollution Research - Sediment samples were collected in five marshes (C1, Phragmites australis marsh; C2, P. australis and Cyperus malaccensis marsh; C3, C. malaccensis...     

Distribution and controls of heavy metals and organic matter in the surface sediments of the Southern Yellow Sea,China

Environmental Science and Pollution Research - Accurate and effective determination of the source of heavy metals is essential for the treatment of marine ecological environments. This article...     

文思湖底泥COD释放规律模拟研究

采用室内模拟实验方法,研究环境因子（温度、pH、扰动强度、供气量）对底泥释放COD的影响。结果表明,水温升高能加速底泥中有机质的释放;上覆水在弱酸至中性条件下底泥释放有机质最低;扰动上覆水体会加快有机质的释放。     

Molecular and physiological characterization of fluoroquinolone resistance in relation to uropathogenicity among Escherichia coli isolates isolated from Wenyu River, China

Increasing antibacterial resistance and pathogenicity in the environment is of growing concern due to its potential human risk. In the present study, 236 Escherichia coli isolates were collected from Wenyu River in China on drugless (48 isolates) and quinolone-containing plates (189 isolates). Their minimum inhibitory concentrations (MICs) were determined ranging from 0.125 μg mL⁻¹ to 128 μg mL⁻¹. Mutation points related to fluoroquinolone resistance were observed at S83 to L and D87 to N or Y in the GyrA subunit and S80 to R or I and E84 to G in the ParC subunit. Generally, MICs of LEV and GAT are dependent on the patterns of these mutation points. The profile with three mutation points was related to LEV-resistant E. coli isolates, and the (S83L, D87N + S80I) mutation profile was most prevalent (65.7%) in LEV-resistant isolates, while a large proportion of isolates, even those with three mutation points, were susceptive to GAT. The incidence of virulence factors in LEV-resistant isolates (44.7%, 59/132) was much higher than in nonresistant isolates (23.1%, 24/104) (χ² = 11.925, 1° of freedom, p < 0.001) indicating that fluoroquinolone-resistant E. coli would pose a potential risk. A similar distribution was also found in isolates resistant to GAT (χ² = 7.843, 1° of freedom, p = 0.0079).