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.     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.