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Effects of nitrogen dioxide and its acid mist on reactive oxygen species production and antioxidant enzyme activity in Arabidopsis plants

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Journal of Environmental Sciences 2015年第8期27卷 93-99页

作者： Xiaofang Liu Fen Hou Guangke Li nan sang College of Environment and Resource Research Center of Environment and Health Shanxi University College of Environmental Science and Engineering Nankai University

Nitrogen dioxide（NO2） is one of the most common and harmful air pollutants. To analyze the response of plants to NO2 stress, we investigated the morphological change, reactive oxygen species（ROS） production and antioxidant enzyme activity in Arabidopsis thaliana（Col-0） exposed to 1.7, 4, 8.5, and 18.8 mg/m3NO2. The results indicate that NO2 exposure affected plant growth and chlorophyll（Chl） content, and increased oxygen free radical（O2-）production rate in Arabidopsis shoots. Furthermore, NO2 elevated the levels of lipid peroxidation and protein oxidation, accompanied by the induction of antioxidant enzyme activities and change of ascorbate（As A） and glutathione（GSH） contents. Following this, we mimicked nitric acid mist under experimental conditions, and confirmed the antioxidant mechanism of the plant to the stress. Our results imply that NO2 and its acid mist caused pollution risk to plant systems. During the process, increased ROS acted as a signal to induce a defense response, and antioxidant status played an important role in plant protection against NO2/nitric acid mist-caused oxidative damage.

关键词： Nitrogen dioxide Nitric acid mist Arabidopsis thaliana Reactive oxygen species Antioxidant system

A comparison of the toxicity of landfill leachate exposure at the seed soaking and germination stages on Zea mays L.(maize)

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Journal of Environmental Sciences 2017年第5期29卷 206-213页

作者： Guangke Li Junyan Chen Wei Yan nan sang College of Environment and Resource Shanxi University Taiyuan 030006 China

To compare the toxicity of landfill leachate exposure at the early stages of seed soaking and germination on maize,a field experiment was conducted to evaluate the physiological aspects of growth,yield and potential clastogenicity of root-tip cells. The maizes were treated with leachate at levels of 2%,10%,20%,30% or 50%（V/V）. First,the change of physiological indexes,including chlorophyll（Chl）,Malondialdehyde（MDA）and Reactive oxygen species（ROS）levels,combined with yield all showed that soaking with leachate,but not germination,generated a greater ecological risk on maize. After a soaking treatment of maize with 50% leachate,the Chl,MDA and ROS levels during a vigorous growth period were 47.3%,149.8% and 309.7%,respectively,of the control,whereas the yield decreased to 68.6% of the control. In addition,our results demonstrated that the leachate at lower levels could promote growth. This is mainly embodied in that the yield of maize treated with 10%leachate at the soaking stage increased to 116.0% of the control. Moreover,the cytological analysis experiment also demonstrated that the ecological risk of leachate still exists in both cases. Furthermore,the gray relational analysis showed that the ear row number and tassel branch number were the major factors affecting the yield of maize treated with 50%leachate at the stages of soaking and germination,respectively. In general,these results are helpful in understanding the phytotoxicity of leachate,which provides additional reference data for risk assessment and management of leachate.

关键词： Landfill leachate Maize Phytotoxicity Seed soaking Germination

Coking wastewater increases micronucleus frequency in mouse in vivo via oxidative stress

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Journal of Environmental Sciences 2013年第10期25卷 2123-2129页

作者： Na Zhu Hongyan Li Guangke Li nan sang College of Environment and Resource Center of Environmental Science and Engineering Shanxi University

Coking wastewater has caused serious health risk in coal-producing areas of China, however its toxic effects have not been well understood. The genotoxicity induced by coking wastewater on mice in vivo and its possible oxidative mechanisms were investigated via observing the induction of micronuclei in polychromatic erythrocytes of mouse bone marrow, and subsequently determining the antioxidative enzyme activities （superoxide dismutase Cu, Zn-SOD, Se-dependent glutathione peroxidase, and catalase）, thiobarbituric acid reactive substance contents and protein carbonyl levels in brains and livers of mice. Results showed that the tested coking wastewater caused a significant increase of micronucleus frequencies in a concentration-dependent manner. Also, the sample increased lipid peroxidation and protein oxidation levels, which was accompanied by changes in antioxidative status. Interestingly, pre-treatment with an antioxidant （vitamin C） led to a statistical reduction in the micronucleus frequency caused by coking wastewater. This implies that coking wastewater induces evident genetic damage in mammalian cells, and exposure to polluted areas might pose a potential genotoxic risk to human beings; in the process, oxidative stress played a crucial role.

关键词： micronucleus oxidative stress coking wastewater mouse bone marrow

PM2.5 exposure induces age-dependent hepatic lipid metabolism disorder in female mice

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Journal of Environmental Sciences 2020年第3期32卷 227-237页

作者： Ruifeng Yan Tingting Ku Huifeng Yue Guangke Li nan sang College of Environment and Resource Research Center of Environment and HealthShanxi UniversityTaiyuanShanxi 030006China

Particulate matter exposure has been described to elevate the risk of lung and cardiovascular *** increasing number of recent studies have indicated positive correlations between PM2.5(the fraction of airborne particles with an aerodynamic diameter less than2.5 μm) exposure and the risk of liver ***,research on the effects of PM2.5exposure on liver fat synthesis,secretion,and clearance mechanisms under normal diet conditions is limited,and whether these effects are age-dependent is largely *** C57BL/6 mice at different ages(4 weeks(4 w),4 months(4 m),and 10 months(10 m))were treated with 3 mg/kg body weight of PM2.5 every other day for 4 ***,the ultrastructural changes of liver,the expression of genes involved in oxidative damage and lipid metabolism in the liver were *** of hepatic ultrastructure showed more and larger lipid droplets in the livers of 4-week-old and 10-month-old mice exposed to *** analysis showed that PM2.5 exposure increased the expression of genes related to lipid synthesis,but decreased the expression of genes involved in lipid transport and catabolism in the livers of 10-month-old *** findings suggest that exposure to PM2.5 disrupts the normal metabolism of liver lipids and induces lipid accumulation in the liver of female mice in an age-dependent manner,with older mice being more susceptible to PM2.5.

关键词： Fine particulate matter Liver Lipid metabolism Different ages

Confidentiality-aware message scheduling for security-critical wireless networks

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Journal of Systems Engineering and Electronics 2010年第1期21卷 154-160页

作者： Wei Jiang Guangze Xiong Xuyang Ding Zhengwei Chang nan sang College of Computer Science and Engineering University of Electronic Science and Technology of China Chengdu 610054 E R. China

Without considering security, existing message scheduling mechanisms may expose critical messages to malicious threats like confidentiality attacks. Incorporating confidentiality improvement into message scheduling, this paper investigates the problem of scheduling aperiodc messages with time-critical and security-critical requirements. A risk-based security profit model is built to quantify the security quality of messages; and a dynamic programming based approximation algorithm is proposed to schedule aperiodic messages with guaranteed security performance. Experimental results illustrate the efficiency and effectiveness of the proposed algorithm.

关键词： security-critical wireless networks confidentialityaware real-time message scheduling.

Endocannabinoid 2-arachidonoylglycerol protects inflammatory insults from sulfur dioxide inhalation via cannabinoid receptors in the brain

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Journal of Environmental Sciences 2017年第1期29卷 265-274页

作者： Ben Li Minjun Chen Lin Guo Yang Yun Guangke Li nan sang College of Environment and Resource Shanxi UniversityTaiyuanShanxi 030006China.

Sulfur dioxide（SO_2） pollution in the atmospheric environment causes brain inflammatory insult and inflammatory-related microvasculature ***,there are currently no effective medications targeting the harmful outcomes from chemical ***（eCBs） are involved in neuronal protection against inflammation-induced neuronal *** 2-arachidonoylglycerol（2-AG）,the most abundant eCBs and a full agonist for cannabinoid receptors（CB1 and CB2）,is also capable of suppressing proinflammatory stimuli and improving microvasculature ***,we indicated that endogenous 2-AG protected against neuroinflammation in response to SO_2 inhalation by inhibiting the activation of microglia and astrocytes and attenuating the overexpression of inflammatory cytokines,including tumor necrosis factor alpha（TNF-a）,interleukin（IL）-1β,and inducible nitric oxide synthase（iNOS）.In addition,endogenous 2-AG prevented cerebral vasculature dysfunction following SO_2 inhalation by inhibiting endothelin 1（ET-1）,vascular cell adhesion molecule-1（VCAM-1） and intercellular adhesion molecule 1（ICAM-1） expression,elevating endothelial nitric oxide synthase（eNOS） level,and restoring the imbalance between thromboxane A2（TXA2） and prostaglandin 12（PGI2）.In addition,the action of endogenous 2-AG on the suppression of inflammatory insult and inflammatory-related microvasculature dysfunction appeared to be mainly mediated by CB1 and CB2 *** results provided a mechanistic basis for the development of new therapeutic approaches for protecting brain injuries from SO_2 inhalation.

关键词： Sulfur dioxide Neuroinflammation Microvasculature dysfunction 2-Arachidonoylglycerol Cannabinoid receptors

Abnormal energy metabolism and tau phosphorylation in the brains of middle-aged mice in response to atmospheric PM2.5 exposure

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Journal of Environmental Sciences 2017年第12期29卷 145-153页

作者： Rui Gao Tingting Ku Xiaotong Ji Yingying Zhang Guangke Li nan sang College of Environment and Resource Research Center of Environment and HealthShanxi UniversityTaiyuan 030006China

In light of the accelerated aging of the global population and the deterioration of the atmosphere pollution, we sought to clarify the potential mechanisms by which fine particulate matter（PM_（2.5）） can cause cognitive impairment and neurodegeneration through the alteration of mitochondrial structure and function. The results indicate that PM_（2.5） inhalation reduces ATP production by disrupting the aerobic tricarboxylic acid cycle and oxidative phosphorylation, thereby causing the hypophosphorylation of tau in the cortices of middle-aged mice. Furthermore, excessive reactive oxygen species generation was involved in the impairment. Interestingly, these alterations were partially reversed after exposure to PM_（2.5） ended. These findings clarify the mechanism involved in mitochondrial abnormality-related neuropathological dysfunction in response to atmospheric PM_（2.5） inhalation and provide an optimistic sight for alleviating the adverse health outcomes in polluted areas.

关键词： Fine particulate matter(PM_(2.5)) Mitochondrial structure and function Energy metabolism Reactive oxygen species(ROS) Tau phosphorylation

Synergistic effects of particulate matter(PM_10) and SO_2 on human non-small cell lung cancer A549 via ROS-mediated NF-κB activation

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Journal of Environmental Sciences 2015年第5期27卷 146-153页

作者： Yang Yun Rui Gao Huifeng Yue Guangke Li Na Zhu nan sang College of Environment and Resource Research Center of Environment and Health Shanxi University

Since a real atmospheric scenario usually represents a system involving multiple pollutants, air pollution studies typically focused on describing adverse effects associated with exposure to individual pollutants cannot reflect actual health risk. Particulate matter（PM10） and sulfur dioxide（SO2） are two major pollutants derived from coal combustion processes and co-existing in coal-smoke air pollution, but their potentially synergistic toxicity remains elusive thus far. In this study, we investigated the cytotoxic responses of PM10 and SO2, singly and in binary mixtures, using human non-small cell lung cancer A549 cells, followed by clarifying the possible mechanisms for their interaction. The results indicated that the concomitant treatment of PM10 and SO2 at low concentrations led to synergistic injury in terms of cell survival and apoptosis occurrence, while PM10 and SO2 alone at the same concentrations did not cause damage to the cells. Also, radical oxygen species（ROS） production followed by nuclear factor kappa B（NF-κB） activation was involved in the above synergistic cytotoxicity, which was confirmed by the repression of the actions by an ROS inhibitor（NAC）. This implies that assessment of health risk should consider the interactions between ambient PM and gaseous copollutants.

关键词： PM10 SO2 Synergistic toxicity ROS NF-κB

Cardiac energy metabolism disorder mediated by energy substrate imbalance and mitochondrial damage upon tebuconazole exposure

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Journal of Environmental Sciences 2024年第2期136卷 270-278页

作者： Tingting Ku Jindong Hu Mengmeng Zhou Yuanyuan Xie Yutong Liu Xin Tan Lin Guo Guangke Li nan sang College of Environmental Science and Resources Research Center of Environment and HealthShanxi UniversityTaiyuan 030006China

Tebuconazole exposure has been described as an increasing hazard to human *** increasing number of recent studies have shown a positive association between tebuconazole exposure and cardiovascular disease risk,which is characterized by the reduction of adenosine triphosphate(ATP)***,researches on the damage of tebuconazole exposure to energy metabolism and the related molecular mechanisms are *** the present study,male C57BL/6 mice were treated with tebuconazole at different low concentrations for 4 *** results indicated that tebuconazole could accumulate in the heart and further induce the decrease of ATP content in the mouse ***,tebuconazole induced an obvious shift in substrate utilization of fatty acid and glucose by disrupting their corresponding transporters(GLUT1,GLUT4,CD36,FABP3 and FATP1)expression,and significantly repressed the expression of mitochondrial biogenesis(Gabpa and Tfam)and oxidative phosphorylation(CS,Ndufa4,Sdhb,Cox5a and Atp5b)related genes in a dosedependent *** investigation revealed that these alterations were related to the IRS1/AKT and PPARγ/RXRα*** findings contribute to a better understanding of triazole fungicide-induced cardiovascular disease by revealing the key indicators associated with this phenomenon.

关键词： Tebuconazole Cardiotoxicity Energy metabolic disorders Energy substrate Mitochondrial damage