丙烯腈诱导的氧化应激对大鼠睾丸NF-κB信号通路的影响

为探索丙烯腈(acrylonitrile,ACN)诱导的氧化应激对大鼠睾丸NF-κB信号通路的影响,将50只SPF级健康SD雄性大鼠按体重随机分为12.5、25、50 mg·kg~(-1)ACN染毒组,50 mg·kg~(-1)ACN+300 mg·kg~(-1)N-乙酰半胱氨酸(N-acetylcysteine,NAC)干预组(NAC干预组),对照组(给予等体积玉米油),每组10只,灌胃,1次/天,6天/周,共90 d。可见光分光光度法检测睾丸组织中超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、还原型谷胱甘肽/氧化型谷胱甘肽比值(glutathione/oxidized glutathione,GSH/GSSG)、丙二醛(malondialdehyde,MDA)。免疫荧光染色法检测睾丸核因子-κB(nuclear factorκB,NF-κB)激活及核转移。Western Blot检测睾丸p65、IκB蛋白表达。结果显示,低、高剂量染毒组大鼠睾丸GSH/GSSG比值、GSH-Px酶活性与对照组比较降低(P0.05)。中、高剂量染毒组大鼠睾丸MDA含量与对照组比较升高(P0.05)。NAC干预组大鼠睾丸MDA含量与高ACN组比较降低(P0.05);NAC干预组大鼠睾丸GSH/GSSG比值与高ACN组比较升高(P0.05);免疫荧光结果显示,高ACN组大鼠睾丸NF-κB被激活,并转移入细胞核。NAC干预组与高ACN组比较p65蛋白表达及核转移显著减少。Western Blot结果显示,高剂量染毒组大鼠睾丸p65蛋白表达与对照组比较升高(P0.05),IκB蛋白表达与对照组比较降低(P0.05);NAC干预组大鼠睾丸p65蛋白表达与高ACN组比较降低,IκB蛋白表达与高ACN组比较升高,差异有统计学意义(P0.05)。结果表明丙烯腈引起的氧化应激激活了大鼠睾丸生殖细胞NF-κB信号通路。     

截断阀室水淹后管道沉降的防护技术研究

为了保证长输天然气管道的安全运行,需要对其截断阀室遭受水淹后管道的不均匀沉降行为进行研究。应用ANSYS软件建立了管土非线性接触模型,通过对其进行分析建立了沉降量与最大Von Mises应力和椭圆度之间的映射关系,结果表明:不均匀沉降对管道强度的影响更明显,二者间基本呈线性关系,最大Von Mises应力随着沉降量的增大而增大,根据第四强度理论便可确定管道失效时的极限沉降量。同时还探讨了管径、内压、壁厚、埋深对管道应力状态的影响,降低内压、增大壁厚以及减小埋深和管径均可降低不均匀沉降时管道的最大Von Mises应力,但其中管径和壁厚的变化对管道最大Von Mises应力的影响更为显著。预期研究结果可以为山区管道的实时监测与防护措施制定提供一定的技术支持。     

Cd胁迫下杂交水稻对Cd的吸收及其动态变化

镉（Cd）是非必需的有毒元素,是农业环境和农产品的重要污染物,易被水稻吸收并在籽粒中积累。不同水稻品种拥有不同的独特基因,导致水稻籽粒吸收积累Cd的能力存在一定的差异。因此,开展不同水稻品种耐Cd特性及其不同生育期的吸收转运效率研究具有重要意义。本文采用水培试验,研究了两个水稻（Oryza sativa L.）品种：D83A/R527（低吸收累积Cd）和辐优838（高吸收累积Cd）在不同质量浓度Cd胁迫下籽粒Cd质量分数及不同生育时期水稻根、茎、叶内Cd的吸收积累量及其动态变化特点。结果表明,两种水稻品种在Cd胁迫下籽粒Cd积累量差异显著,辐优838在1.0 mg·L^-1 Cd质量浓度胁迫下籽粒Cd质量分数就已超过国家食品卫生标准;在1.0~3.0 mg·L^-1 Cd质量浓度胁迫下,D83A/R527籽粒内Cd质量分数仅为辐优838的50~60%。随着Cd处理浓度增加和生育时期推进,两种水稻各部位Cd吸收量均表现为逐渐增加,其增加幅度总体表现为：辐优838〉D83A/R527;不同部位中,根的积累效应最强,叶片吸收积累能力最低,辐优838茎、叶吸收积累效率分别是D83A/R527的1.5~2.0倍左右。在1.0~3.0mg·L^-1 Cd胁迫下,水稻Cd积累差异较为显著的时期为灌浆期,辐优838的根系向茎、叶的转移效率大于D83A/R527,且D83A/R527主要表现为由根系向茎Cd转移效率较高,叶片Cd积累相对较少。灌浆期是水稻籽粒干物质积累的重要时期,也是吸收累积Cd的重要时期,这为筛选低吸收积累水稻品种和调控Cd在水稻籽粒中的吸收累积奠定了重要理论基础。     

环境污染物对硬骨鱼肾间应激轴影响的研究进展

具备神经内分泌应激反应能力是一个健康有机体的基本特征,它可以使动物应对威胁其体内平衡的紧急情形。鱼类在遭受环境胁迫时,通过启动肾间应激轴分泌应激激素皮质醇,为机体动员和分配能量以维持体内平衡。虽然近来大多数研究的焦点一直是污染物对生殖轴线以及性类固醇激素的影响,但是污染物对其它内分泌系统包括肾间应激轴的干扰也越来越受到关注。环境污染物干扰肾间应激轴不仅损害鱼类正常的应激反应能力,还会进一步危害其生长、生殖、免疫等生理功能。本文在简要介绍硬骨鱼肾间应激轴结构组成及调控机制的基础上,综述了多种环境污染物对硬骨鱼肾间应激轴的干扰作用及其机制,展望了该领域今后的研究重点和方向。     

外源NO介导Cu~(2+)胁迫下番茄幼苗活性氧与内源NO代谢的研究

采用营养液培养方法,研究Cu~(2+)胁迫下外源一氧化氮(nitric oxide,NO)介导的番茄幼苗活性氧及NO代谢途径。结果表明:在Cu~(2+)胁迫下,番茄叶片和根系氧自由基含量增加,NO释放量以及硝酸还原酶(nitrate reductase,NR)和一氧化氮合酶(nitric oxide synthase,NOS)活性降低。外源NO能提高Cu~(2+)胁迫下番茄叶片NR和NOS活性,促进NO的产生,根系NOS活性及NO产量也同时上升。外源NO使精氨酸含量显著增加,而Hb(牛血红蛋白,NO清除剂)可部分抵消NO的促进作用,使Cu~(2+)+SNP+Hb处理下番茄精氨酸含量显著下降。可见,外源NO的加入可通过酶促和非酶促途径促进Cu~(2+)胁迫下NO的合成,介导NO信号调控网络,调节内源NO、精氮酸和活性氧代谢途径,从而缓解过多Cu~(2+)引起的氧化伤害。     

某水利枢纽坝区构造特征及其对岩溶发育规律的影响

某水利枢纽区构造基本格局形成于早白垩世的燕山运动,此时构造应力场以NE向为最大主应力方向,形成了规模较大的NE向百兴向斜;渐新世以来,区域表现为大面积的间歇性隆升,构造应力场转变以NW向为最大主应力方向,形成坝区占统治地位的NE向构造,在坚硬的岩层中形成大量节理裂隙,软弱岩层中则表现为塑性变形。这种构造特征对岩溶的发育具有控制性作用:(1)构造发育史控制了岩溶发育演化史,(2)构造运动的间歇性导致岩溶的多层性及继承性,(3)褶皱限制了岩溶呈NE向带状分布,(4)不同岩层内构造特征相异导致岩溶仅在某些岩层内较发育,(5)节理裂隙控制了岩溶发育的部位及形态规模。     

Ecological selection of bacterial taxa with larger genome sizes in response to polycyclic aromatic hydrocarbons stress

Polycyclic aromatic hydrocarbons(PAHs) are ubiquitous priority pollutants that cause great damage to the natural environment and health. Average genome size in a community is critical for shedding light on microbiome’s functional response to pollution stress within an environment. Here, microcosms under different concentrations were performed to evaluate the selection of PAHs stress on the average genome size in a community. We found the distinct communities of significantly larger genome size w...     

Determination of F2-isoprostanes in cultured human lung epithelial cells after exposure to metal oxide and silica nanoparticles by high-performance liquid chromatography/tandem mass spectrometry

The environmental impact of nanotechnology has caused a great concern. Many in vitro studies showed that many types of nanoparticles were cytotoxic. However, whether these nanoparticles caused cell membrane damage was not well studied. F₂-isoprostanes are specific products of arachidonic acid peroxidation by nonenzymatic reactive oxygen species and are considered as reliable biomarkers of oxidative stress and lipid peroxidation. In this article, we investigated the cytotoxicity of different nanoparticles and the degree of cellular membrane damage by using F₂-isoprostanes as biomarkers after exposure to nanoparticles. The human lung epithelial cell line A549 was exposed to four silica and metal oxide nanoparticles: SiO₂ (15 nm), CeO₂ (20 nm), Fe₂O₃ (30 nm), and ZnO (70 nm). The levels of F₂-isoprostanes were determined by using high-performance liquid chromatography/mass spectrometry. The F₂-isoprostanes’ peak was identified by retention time and molecular ion m/z at 353. Oasis HLB cartridge was used to extract F₂-isoprostanes from cell medium. The results showed that SiO₂, CeO₂, and ZnO nanoparticles increased F₂-isoprostanes levels significantly in A549 cells. Fe₂O₃ nanoparticle also increased F₂-isoprostanes level, but was not significant. This implied that SiO₂, CeO₂, ZnO, and Fe₂O₃ nanoparticles can cause cell membrane damage due to the lipid peroxidation. To the best of our knowledge, this is the first report on the investigation of effects of cellular exposure to metal oxide and silica nanoparticles on the cellular F₂-isoprostanes levels.     

Effects of benzo(a)pyrene on blood components,tumor markers,and oxidative status in mice

This study was carried out to investigate the effect of long-term exposure to benzo(a)pyrene (B(a)P) in mice. Hemogram, tumor markers, oxidative status, and B(a)P residues in liver tissue were evaluated. Sixty albino Swiss mice were randomly distributed equally into three groups; the control was given 0.1?mL corn oil once a week for 8 weeks. The other two groups were given 20 and 40?mg B(a)P per kg body weight once a week orally for the same period. B(a)P-treated mice suffered from depression and ascites, and macrocytic normochromic anemia was recorded at the 16th and 30th week. There was marked leukocytosis with lymphocytosis at the early stage of the experiment, followed by leukopenia, lymphopenia, and neutropenia at the end of the experiment. Monocytes and arginase activity were elevated throughout the experiment. Alpha feto-protein was detected only in the experimental groups in the 30th week of the experiment. A marked increase in lipid peroxides associated with a decrease in reduced glutathione and glutathione-S-transferase (GST) activity was observed in liver homogenate of the B(a)P-exposed animals. Residues of B(a)P were detected in liver tissue with a concentration parallel to the B(a)P dose level. In conclusion, B(a)P caused abnormal changes in the hemogram, evidence of tumor formation through B(a)P-induced oxidative stress, and it was accumulated in the liver tissue of mice.     

Oxidative stress mediated cytotoxicity of TiO2 nano anatase in liver and kidney of Wistar rat

This study examined the adverse effects of TiO₂ nanoparticle (nano-TiO₂) on the kidney and liver of Wistar rats. Changes of serum biochemical parameters and pathological lesions indicated that liver and kidney were significantly affected in animals treated with 50?mg?kg^?1 of nano-TiO₂. The inverse relationship between the level of reactive oxygen species and the activities of superoxide dismutase, catalase, and glutathione peroxidase indicates that nano-TiO₂ induces oxidative stress. A significant increase in the apoptosis of liver and kidney in a dose-dependent manner was also observed. The ultrastructural observations confirmed the internalization of nano-TiO₂ and their direct involvement in the mitochondria-mediated cytotoxicity. Data indicated that nano-TiO₂ induce oxidative stress which produces genotoxicity such as oxidative DNA damage, micronuclei (MN) induction, and cell apoptosis in liver and kidney.