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1.
Oxidative stress and DNA damages induced by cadmium accumulation   总被引:21,自引:0,他引:21       下载免费PDF全文
Experimental evidence shows that cadmium (Cd) could induce oxidative stress and then causes DNA damage in animal cells, however, whether such effect exists in plants is still unclear. In the present study, Vicia faba plants was exposed to 5 and 10 mg/L Cd for 4 d to investigate the distribution of Cd in plant, the metal effects on the cell lipids, antioxidative enzymes and DNA damages in leaves. Cd induced an increase in Cd concentrations in plants. An enhanced level of lipid peroxidation in leaves and an enhanced concentration of H2O2 in root tissues suggested that Cd caused oxidative stress in Vicia faba. Compared with control, Cd-induced enhancement in superoxide dismutase activity was significant at 5 mg/L than at 10 mg/kg in leaves, by contrast, catalase and peroxidaseactivities were significantly suppressed by Cd addition. DNA damage was detected by neutral/neutral, alkaline/neutral and alkaline/alkaline Comet assay. Increased levels of DNA damages induced by Cd occurred with reference to oxidative stress in leaves, therefore, oxidative stress induced by Cd accumulation in plants contributed to DNA damages and was possibly an important mechanism of Cd-phytotoxicity in Vicia faba plants.  相似文献
2.
以实验室培养的铜锈环棱螺(Bellamya aeroginosa)为受试生物,研究了2,2′, 4,4′-四溴联苯醚(BDE-47)污染沉积物对铜锈环棱螺肝胰脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和7-乙氧基—3-异吩唑酮—脱乙基酶(EROD)活性的影响,以揭示BDE-47与这些酶活性之间的剂量-效应和时间-效应关系.结果表明,不同水平BDE-47污染沉积物暴露后,铜锈环棱螺肝胰脏SOD和CAT活性表现出较为明显的剂量或时间依赖性效应,BDE-47可引起铜锈环棱螺肝胰脏的氧化应激,高剂量(≥160 ng·g-1)BDE-47的长时间暴露可导致SOD和CAT活性显著下降,提示细胞出现氧化损伤.SOD对BDE-47胁迫的敏感性高于CAT.铜锈环棱螺肝胰脏中SOD和CAT可以作为指示低水平BDE-47污染沉积物胁迫的生物标志物.BDE-47不能诱导铜锈环棱螺肝胰脏EROD活性,但高剂量(≥160 ng·g-1)或长时间BDE-47暴露则导致EROD活性显著降低.  相似文献
3.
This study aimed to develop original laboratory culture and sediment toxicity testing protocols for the freshwater gastropod Bellamya aeruginosa(Reeve),a new potential species for sediment toxicity testing.B.aeruginosa was successfully cultured with an effective culture system under proposed laboratory conditions.Optimal ad libitum feeding levels for larvae,juveniles,and adults were 2.0,6.0,and 16.0 mg fish food/(snail·day),respectively.Mean survival rates of juveniles were higher than 90%.The snails could ...  相似文献
4.
单壁碳纳米管对小鼠肝和肾氧化损伤的诱导   总被引:3,自引:3,他引:0       下载免费PDF全文
为了评价单壁碳纳米管(SWCNTs)对生物体的毒性效应,以昆明小鼠为受试动物,采用腹腔注射的染毒方法,研究了SWCNTs和标准碳黑(CB)对其肝和肾组织氧化损伤的诱导.实验结果表明:与对照组相比,SWCNTs和CB暴露显著的降低了小鼠肝和肾中还原性谷胱甘肽(GSH)的含量、抑制了超氧化物歧化酶(SOD)的活力、诱导了脂质过氧化终产物丙二醛(MDA)的产生、提高了DNA.蛋白质交联率(DNA.protein crosslinks,DPC),但在最高浓度(O.08 mg·d-1)暴露下,SWCNTs暴露组的影响程度要高于标准碳黑组.说明了SWCNTs暴露可以抑制小鼠肝和肾组织抗氧化系统,从而导致了器官的氧化损伤.并且这种氧化损伤的诱导部分是由于SWCNTs的特殊结构和金属元素的参与.  相似文献
5.
六价铬致小鼠DNA损伤及肝肾氧化应激的实验研究   总被引:2,自引:0,他引:2       下载免费PDF全文
为研究六价铬(Cr(Ⅵ))摄入后对机体造成的损伤,将重铬酸钾(K2Cr2O7)以25、50、100 mg·kg-1对小鼠进行灌胃,染毒时间为1 d、3 d和5 d.检测外周血淋巴细胞DNA损伤及肝肾组织活性氧自由基(ROS)水平、脂质过氧化产物丙二醛(MDA)含量,以及超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性.实验结果表明,经Cr(Ⅵ)染毒1 d、3 d和5 d后小鼠外周血淋巴细胞DNA损伤及肝ROS水平与对照组相比均有明显升高,肝脏抗氧化酶活性也有显著改变,但MDA含量差异不显著,而肾组织中各指标均未见有明显改变.由此认为,经口摄入Cr(Ⅵ)后能导致DNA损伤并且对肝脏造成氧化应激.  相似文献
6.
The effects of different cadmium (Cd) concentrations (0, 20, 60, and 100 μmol/L) on hydroponically grown Artemisia annua L. were investigated. Cd treatments applied for 0, 4, 12, 24, 72, 144, 216, and 336 hr were assessed by measuring the changes in photosynthetic pigments, electrolyte leakage, malondialdehyde (MDA) and antioxidants (ascorbic acid and glutathione), while the artemisinin content was tested after 0, 12, 144, 216, and 336 hr. A significant decrease was observed in photosynthetic pigment levels over time with increasing Cd concentration. Chlorophyll b levels were more affected by Cd than were chlorophyll a or carotenoid levels. The cell membrane was sensitive to Cd stress, as MDA content in all treatment groups showed insignificant differences from the control group, except at 12 hr treatment time. Ascorbic acid (AsA) content changed slightly over time, while glutathione (GSH) content took less time to reach a maximum as Cd concentration increased. Cd was found to promote synthesis and accumulation of artemisinin, especially at concentrations of 20 and 100 μmol/L. In conclusion, Cd stress can damage to photosynthetic pigments, and vigorously growing A. annua showed a strong tolerance for Cd stress. Appropriate amounts of added Cd aided synthesis and accumulation of artemisinin.  相似文献
7.
The interaction between zinc and cadmium was investigated in tomato plants (Solanum lycopersicum). Ten-day-old seedlings were treated with 10 mol/L CdCl2 associated to di erent concentrations of ZnCl2 (10, 50, 100, and 150 mol/L). Zn supply clearly reduced Cd accumulation in leaves and simultaneously increased Zn concentration. Cd induced oxidative stress in leaves as indicated by an increase in thiobarbituric acid-reactive substances (TBARS) level and chlorophyll breakdown. Furthermore, compared with control, Cdtreated plants had significantly higher activities of superoxide dismutase (SOD, EC 1.15.1.1), whereas, catalase (CAT, EC 1.111.1.6), ascorbate peroxidase (APX, EC 1.11.1.11), and glutathione reductase (GR, EC 1.6.4.2) activities were significantly suppressed by Cd addition. Zn supplementation, at low level, restored and enhanced the functional activity of these enzymes (SOD, CAT, APX and GR) as compared to Cd-alone-treated plants. The beneficial e ect of adequate Zn level on Cd toxicity was confirmed by a significant decrease in TBARS level and restoration of chlorophyll content. However, when Zn was added at high level in combination with Cd there was an accumulation of oxidative stress, which was higher than that for Cd or excess Zn alone treatments. These results suggested that higher Zn concentrations and Cd are synergistic in their e ect on plant growth parameters and oxidative stress.  相似文献
8.
纳米氧化锌对斑马鱼肝脏的毒性效应   总被引:1,自引:0,他引:1       下载免费PDF全文
采用半静态急性实验方法,研究斑马鱼在浓度为0、0.05、0.1、5、10、25、50 mg·L-1的纳米氧化锌(nano-ZnO)中暴露4、24、96 h后,nano-ZnO对肝中超氧化物歧化酶(SOD)、丙二醛(MDA)、过氧化氢酶(CAT)的影响,肝脏中Bcl-2、Bax、p53和MDM2的mRNA表达量的变化以及暴露7、15、30 d时肝组织解剖结构变化情况. 结果表明,与对照组相比,实验组表现为: ①肝组织出现组织水肿,部分细胞质空泡化、细胞核固缩;②肝巨噬细胞增多,窦间隙增大;③肝中SOD活性升高、MDA含量增加、CAT活性降低;④肝脏中Bax/Bcl-2和p53的mRNA的表达量均升高;⑤ MDM2 mRNA的表达量表现为在低浓度组中降低,高浓度组中则升高. 实验结果表明,nano-ZnO能引起斑马鱼肝脏发生氧化应激作用,使肝中抗氧化酶活性发生变化,并诱导肝脏中细胞凋亡相关基因的表达,使细胞发生凋亡且造成肝组织结构发生变化.  相似文献
9.
Increasing application of nanotechnology highlights the need to clarify and understand nanotoxicity. Mammalian and in vitro studies have raised concerns about the toxicity of titanium dioxide nanoparticles (TiO2-NPs), but there are limited data on ecotoxicity to aquatic organisms. In this work, the sub-acute toxicity of TiO2-NPs to carp (Cyprinus carpio) was assessed. Superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) activities and lipid peroxidation (LPO) levels in liver, gill and brain tissues of carps varied with concentration of TiO2-NPs suspensions and exposure time (up to 8 d). As a result, 100 and 200 mg/L TiO2-NPs caused statistically significant decrease in SOD, CAT and POD activities and significant increase in LPO levels in tissues (P < 0.05), suggesting that the fish exposed to these two concentrations of TiO2-NPs suffered from the oxidative stress. The extent of depletion of antioxidant enzymes activities and the elevation of LPO in the liver was the greatest, indicating that the liver might be the most susceptible organ to TiO2-NPs exposure. In addition, carps had gill pathologies including edema and thickening of gill lamellae as well as gill filaments, and liver pathologies including necrotic and apoptosis hepatocytes after exposed to 100 and 200 mg/L TiO2-NPs for 20 d. These results indicated a potential risk from TiO2-NPs released into the aqueous environment.  相似文献
10.
本研究以稀有鮈鲫(Gobiocypris rarus)为对象,研究了不同浓度CdSe/ZnS量子点(QDs)暴露下,稀有鮈鲫胚胎发育过程中自主运动频率、内心率和体长的变化,以及利用体内超氧化物歧化酶(SOD)和丙二醛(MDA)作为毒性指标,反映CdSe/ZnS QDs暴露对稀有鮈鲫胚胎发育的氧化应激作用.结果显示:CdSe/ZnS QDs对稀有鮈鲫胚胎72 hpf(hours post fertilization)的半致死浓度(LC50)为319.629 nmol·L-1,96 hpf的半致畸浓度(EC50)为203.312 nmol·L-1.CdSe/ZnS QDs暴露不仅影响稀有鮈鲫胚胎死亡率、畸形率、自主运动频率、孵化时间和孵化率,而且使其内心率减缓、体长缩短,导致胚胎卵凝结,心包囊肿,出现脊椎弯曲等多种毒性现象.同时发现,CdSe/ZnS QDs暴露导致稀有鮈鲫体内MDA含量增加以及SOD活力的降低.这表明CdSe/ZnS QDs对稀有鮈鲫胚胎发育具有致畸、致死作用,而氧化应激可能是引起其胚胎致畸、致死的重要机制之一.  相似文献
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