Free market ideology and deregulation in Colorado’s oil fields: Evidence for triple movement activism?

Unconventional oil and gas extraction (UOGE) has spurred an unprecedented boom in onshore production in the US. Despite a surge in related research, a void exists regarding inquiries into policy outcomes and perceptions. To address this, support for federal regulatory exemptions for UOGE is examined using survey data collected in 2015 from two Northern Colorado communities. Current regulatory exemptions for UOGE can be understood as components of broader societal processes of neoliberalization. Free market ideology increases public support for federal regulatory exemptions for UOGE. Perceived negative impacts do not necessarily drive people to support increased federal regulation. Utilizing neo-Polanyian theory, interaction between free market ideology and perceived negative impacts is explored. Free market ideology appears to moderate people’s views of regulation: increasing the effect of perceived negative impacts while simultaneously increasing support for deregulation. To conclude, the ways in which free market ideology might normalize the impacts of UOGE activity are discussed.     

农药致慢性细胞毒性及基因毒性机制研究进展

大量流行病学研究和体内、体外检测分析表明,长期低剂量接触农药可以导致人体细胞和分子损伤,诱导细胞凋亡。农药致细胞及DNA损伤的机制主要与DNA加合物的形成、DNA单链和/或双链的断裂有关。此外,氧化应激参与农药致细胞及DNA损伤的过程,可能成为农药致细胞及DNA损伤的促发因素。从总体上看,其具体分子机制还不十分清楚,有待进一步研究。     

环境污染物导致氧化应激的关键信号通路及其检测方法

环境污染物能够以多种途径进入生物体内,在体内产生含氧自由基等活性氧物质,并通过多种信号通路及酶反应引起氧化应激,造成生物体内的脂质过氧化、蛋白质损伤、DNA表达改变、酶失活等,从而引发心血管疾病、风湿类疾病、感染及癌症等的发生。本文对环境污染物致氧化应激产生的原因、涉及的信号通路及酶反应、造成的危害,以及常见的基于细胞模型的氧化应激检测方法进行了综述,期望为评价环境污染物和检测氧化损伤提供参考。     

阿维菌素对中华绒螯蟹肝胰腺氧化胁迫效应和组织结构的影响

采用半静态染毒法,研究不同浓度(1.6、8.0、16.0μg·L-1)阿维菌素在胁迫中华绒螯蟹12、24、48、96 h时肝胰腺超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)积累量等氧化胁迫相关指标的变化;并在胁迫60 d时,记录各实验组和对照组中华绒螯蟹肝胰腺颜色的变化并进行组织病理观察。3个阿维菌素浓度组为实验组,空白组和溶剂组为对照组。结果表明在整个实验过程中空白组和溶剂组各个时间点各项指标之间无显著差异(P>0.05);低浓度(1.6μg·L-1)组SOD和CAT活力变化不显著(P>0.05);中浓度(8.0μg·L-1)组SOD和CAT活力变化趋势一致,持续被诱导,SOD活力在24 h以后显著高于空白组(P<0.01),CAT活力在48 h以后显著高于空白组(P<0.01);高浓度(16.0μg·L-1)组SOD和CAT活力在12 h~24 h之间变化趋势一致,表现为显著升高(P<0.05),但是在48 h之后,SOD活力显著下降(P<0.05);96 h时,高浓度组SOD活力显著低于空白组(P<0.01),而CAT活力显著高于空白组(P<0.01);在整个实验过程中各实验组MDA积累量逐渐增加,高浓度组氧化胁迫指标的变化幅度大于低浓度组。胁迫60 d时,取样观察可见对照组中华绒螯蟹肝胰腺正常,各实验组中华绒螯蟹肝胰腺发生了不同程度的病变,肝胰腺颜色由最开始的橘黄色变成了淡黄色、黄白色甚至白色,高、中、低各浓度组肝胰腺白化所占的比例分别是66.6%、57.1%和25.0%。组织病理分析显示,淡黄色肝胰腺的病理变化主要是B细胞数量减少,肝胰腺上皮细胞部分肿大并出现空泡;黄白肝病理观察可见肝胰腺上皮细胞中空泡数量增多,体积增大,且空泡内出现内容物,细胞核固缩;白肝的病理表现主要是基膜增厚,上皮细胞大量脱落,散落在管腔中,空泡数量进一步增多,肝胰腺的生理功能受损。由此得出,阿维菌素会对中华绒螯蟹肝胰腺造成氧化胁迫和组织损伤,且阿维菌素和对肝胰腺的氧化胁迫效应和组织结构损伤程度有一定的剂量-效应关系。     

The impact of pesticides on oxidative stress level in human organism and their activity as an endocrine disruptor

Pesticides cause serious environmental and health problems both to humans and animals. The aim of this review is to discuss selected herbicides and fungicides regarding their mode of action and their influence on basic oxidative stress parameters and endocrine disruption properties tested in selected cell cultures in vitro. Because of numerous difficulties which animal studies are subject to, cell cultures are an excellent experimental model reflecting human exposure to different pesticides through all relevant routes. This experimental model can be used to monitor aggregate and cumulative pesticide exposures.     

Effect of prochloraz fungicide on biotransformation enzymes and oxidative stress parameters in three-spined stickleback (Gasterosteus aculeatus L.)

The aim of this study was to characterize biomarker responses in three-spined sticklebacks exposed to prochloraz (Pcz). For this purpose, adult sticklebacks were exposed for 2 weeks to prochloraz at 0, 10, 50, 100 and 500 μg/L prior to one week of depuration in clean water. At days 7, 14 and 21, several hepatic biomarkers were measured including 7-ethoxyresorufin-O-deethylase (EROD), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT), total glutathione (GSH) content and thiobarbituric acid reactive substances (TBARS). Pcz induced a transient increase of antioxidant enzymes and a depletion of glutathione content during the first 7 days of exposure. This study showed that EROD activity and antioxidants were disrupted in a transient manner. GST was rapidly induced in a dose-dependent manner and this induction was persistent and observed also after depuration. GST appeared as a valuable biomarker to assess the exposure to Pcz.     

Corynebacterium glutamicum as an indicator for environmental cobalt and silver stress–A proteome analysis

Cobalt and silver are toxic for cells, but mechanisms of this toxicity are largely unknown. Analysis of Corynebacterium glutamicum proteome from cells grown in control and cobalt or silver enriched media was performed by two dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our results indicate that the cell adapted to cobalt stress by inducing five defense mechanisms: Scavenging of free radicals, promotion of the generation of energy, reparation of DNA, reparation and biogenesis of Fe-S cluster proteins and supporting and reparation of cell wall. In response to the detoxification of Ag⁺ many proteins were up-regulated, which involved reparation of damaged DNA, minimizing the toxic effect of reactive oxygen species (ROS) and energy generation. Overexpression of proteins involved in cell wall biosynthesis (1,4-alpha-glucan branching enzyme and nucleoside-diphosphate-sugar epimerase) upon cobalt stress and induction of proteins involved in energy metabolism (2-methylcitrate dehydratase and 1, 2-methylcitrate synthase) upon silver demonstrate the potential of these enzymes as biomarkers of sub-lethal Ag⁺ and Co toxicity.     

如何确定高加速寿命试验的应力极限

气锤驱动的高加速寿命试验,主要目的是确定试验样品的应力极限(包括工作极限和破坏极限),并通过改进试验所暴露的缺陷,按预期目标拓宽产品的应力极限。本文对一些应力极限的名词术语作了解释性说明,并具体论述了如何确定应力极限及快速温变循环试验的高低温温度极值。     

Cornmeal-induced resistance to ciprofloxacin and erythromycin in enterococci

Triclosan is used as an antibacterial agent in household items and personal care products. Since this compound is found in maternal milk of humans and bodies of wild animals, there is growing concern among some consumer groups and scientific community that triclosan is adverse for humans and wild animals. In order to estimate adverse actions of triclosan, the effects of triclosan on intracellular Zn²⁺ concentration and cellular thiol content were studied in rat thymocytes by the use of flow cytometer with appropriate fluorescent probes. Triclosan at 1-3 μM (sublethal concentrations) increased the intensity of FluoZin-3 fluorescence (intracellular Zn²⁺ concentration) and decreased the intensity of 5-chloromethylfluorescein (5-CMF) fluorescence (cellular thiol content). Negative correlation (r = −0.985) between triclosan-induced changes in FluoZin-3 and 5-CMF fluorescences was found. Removal of external Zn²⁺ did not significantly affect the triclosan-induced augmentation of FluoZin-3 fluorescence, suggesting an intracellular Zn²⁺ release by triclosan. These actions of triclosan were similar to those of H₂O₂ and triclosan significantly potentiated the cytotoxicity of H₂O₂. Therefore, the results may suggest that triclosan at sublethal concentrations induces oxidative stress that decreases cellular thiol content, resulting in an increase in intracellular Zn²⁺ concentration by Zn²⁺ release from intracellular store(s). Since recent studies show many physiological roles of intracellular Zn²⁺ in cellular functions, the triclosan-induced disturbance of cellular Zn²⁺ homeostasis may induce adverse actions on the cells.     

Effect of ingested titanium dioxide nanoparticles on the digestive gland cell membrane of terrestrial isopods

The aim of this study was to find out whether ingested titanium dioxide nanoparticles (nano-TiO₂) cause cell membrane damage by direct contact or by lipid peroxidation. We assessed lipid peroxidation and digestive gland cell membrane stability of animals fed on food dosed with nano-TiO₂. Conventional toxicity measures were completed to determine if cellular effects are propagated to higher levels of biological complexity. An invertebrate model organism (Porcellio scaber, Isopoda, Crustacea) was fed with food containing nanosized TiO₂ and the result confirmed that at higher exposure concentrations after 3 d exposure, nano-TiO₂ destabilized cell membranes but lipid peroxidation was not detected. Oxidative stress as evidenced by lipid peroxidation was observed at longer exposure durations and high exposure doses. These data suggest that cell membranes are destabilized by direct interactions between nanoparticles and cell membrane, not solely via oxidative stress.