With increasing use of municipal solid waste landfills for waste disposal, the leachate generated has become a serious environmental concern. Therefore, it is important to set up simple and accurate methods for monitoring leachate toxicity. In the present study, the physiological and genetic toxicity of the leachate, generated from Xingou Municipal Landfill in China, were investigated with Triticum aestivum (wheat) bioassay. The results indicate that the lower leachate concentrations stimulated the germination, growth and cell division, and did not induce obvious increase in micronucleus (MN) frequency in root tips; while the higher concentrations inhibited the processes, and significantly augmented the MN frequency in a concentration-and time-dependent manner. In addition, pycnotic cells (PNC) and sister chromatid exchange (SCE) occurred in root tips at all leachate concentrations tested, and the frequencies had positive relation with the treatment concentration and time. The results imply that components of leachate from the landfill may be genotoxic in plant cells, and exposure to leachate in the aquatic environment may pose a potential genotoxic risk to organisms. The results also suggest that the wheat bioassay is efficient, simple and reproducible in monitoring genotoxicity of the leachate.

The genotoxicity of municipal landfill leachate was studied using the Vicia faba root-tip cytogenetic bioassay. Results show that landfill leachates collected in different seasons decreased the mitotic index (MI) and caused significant increases of micronucleus (MN) frequencies and anaphase aberration (AA) frequencies in a concentration-dependent manner (concentration expressed as 'chemical oxygen demand' measured by the method of potassium dichromate oxidation (CODCr)). In addition,a seasonal difference in genotoxicity induced by leachate was observed. The results confirm that leachate is a genotoxic agent in plant cells and imply that exposure to leachate in the aquatic environment may pose a potential genotoxic risk to organisms. The results also show that the V. faba cytogenetic bioassay is efficient, simple and reproducible in enotoxicity studies of leachate, and that there is a correlation between the genotoxicity and the chemical measurement (CODCr) of leachate.

The cytogenetic damage induced by municipal landfill leachate was studied using chromosomal aberration (CA) in mouse bone marrow assay. Results show that leachate samples collected in different seasons decreased the mitotic index (MI), and caused significant increases of CA frequencies in treatment concentration (Chemical oxygen demand (COD) measured by the method of potassium dichromate oxidation, CODCr)-dependent manners. Compared with the negative control, reductions of the MI of 54 and 38% were detected for the highest leachate concentration (CODCr 320mg/L) in mouse bone marrow treated with both samples. The frequencies of CA increased significantly with increasing concentrations of sample 1 from CODCr 40 to 320mg/L, and from 80 to 320mg/L after exposure to sample 2. In addition, aseasonal difference of MI and CA frequencies induced by leachate was observed. The results confirm that leachate is a genotoxic agent in mammalian cells, and imply that exposure to leachate in aquatic environment may pose a potential genotoxic risk to mammals and humans. The results suggest that the CA in mouse bone marrow bioassay is efficient in genotoxicity studies of leachate on mammals, and that there appears to be a correlation between the genotoxicity in mammal system and the chemical measurement (CODCr) of leachate. The results also indicate that different discharge guidelines and environmental quality standards should be established for eachates discharged from landfills to aquatic environment in different seasons.

生活垃圾填埋场渗滤液是指在垃圾堆放和填埋过程中由于发酵和雨水淋溶、冲刷以及地表水和地下水的浸泡而渗滤出来的污水，其中不仅含有大量的有机物、氨氮和重金属，同时含有多种微生物、致病菌和病毒等，是一种营养物质与有毒物质共存的高浓度难降解有机废水。渗滤液的形成和渗漏可造成填埋场周边地区地表水和地下水的严重污染，甚至危害公共健康。为此，本文研究了渗滤液对高等植物（玉米和大麦）和哺乳动物（昆明种小鼠）的毒性作用。结果表明，渗滤液对玉米和大麦种子萌发、幼苗生长和细胞有丝分裂均具有低浓度促进和高浓度抑制的效应，并可浓度和时间依赖性地诱导植物幼苗根尖细胞中微核、核固缩和核碎解、染色体后期异常、姐妹染色单体交换等遗传物质损伤的发生。哺乳动物实验结果表明，渗滤液可引起小鼠骨髓微核嗜多染红细胞中微核率浓度依赖 性地增加，改变不同组织器官（心、脑、肝、肺和肾）抗氧化酶活性，诱导脂质过氧化和蛋白氧化的发生。上述结果提示，生物毒性检测指标应纳入对渗滤液污染的控制和评价体系中。

焦化废水是煤高温干馏、煤气净化、副产品回收与精制过程中产生的难降解工业有机废水，其中含有大量的氨、氰、硫氰根、氟化物等无机污染物，同时还含有酚、油、胺、萘、吡啶、喹啉、葸等杂环及多环芳香族化合物（PAHs），组分复杂、污染物浓度高。这一水质特征决定了焦化废水的生物处理效果有限，理化处理成本高。在此基础上，有研究者提出利用植物-土壤系统进行修复，但其关键在于植物能否耐受焦化废水造成的环境胁迫。为此，本文以北方常见植物玉米为实验材料，探讨焦化废水对其生长和抗氧化系统的影响，旨在阐明焦化废水污染土壤植物修复的可行性。结果表明，一定浓度焦化废水可降低根尖细胞有丝分裂指数，影响植株生长；诱导超氧化物歧化酶（SOD）、过氧化物酶（POD）、过氧化氢酶（CAT）和抗坏血酸过氧化物酶（APX）活性增加，提高了抗坏血酸（AsA）和谷胱甘肽（GSH）含量；高浓度则可造成脂质过氧化和蛋白质氧化的损伤。结果提示，焦化废水胁迫可引起植物生长和体内抗氧化系统的变化，但此作用存在浓度和时间依赖性关系，为探讨焦化废水污染的植物修复提供了实验依据。

SO2 是一种常见的全球性大气环境污染物，前期研究提示其不仅能引起呼吸道疾患，极有可能还与一些中枢神经系统疾病的发生有关，但后者的分子机制尚不清楚。为此，本文采用动式熏气法研究了不同浓度SO2（7、14、28 和56mg/m3）吸入对大鼠海马组织炎性因子白介素-1β（IL-1β）和肿瘤坏死因子（TNF-α）水平、神经元胞内游离Ca2+浓度，即早基因（c-fos，c-jun 和COX-2）和凋亡相关基因（bcl-2，bax 和p53）表达的影响。结果表明：SO2 可造成海马组织IL-1β 和TNF-α水平显著增高，但低浓度下（7、14mg/m3）作用较为明显；SO2 可显著增加神经 元胞内钙离子浓度，上调即早基因c-fos，c-jun 和COX-2，凋亡基因bcl-2，bax和p53 mRNA 及其蛋白表达，且呈现出明显的剂量-效应关系，其中对COX-2 基因表达的作用最为明显。这一结果从整体水平上说明了SO2 对中枢神经系统的损伤效应，并提示其分子机制可能涉及炎性反应、钙离子稳态、即早基因和凋亡基 因表达。

In the present study, protein oxidation (PCO content) and DNA-protein crosslinks (DPC coefficient) were investigated in the viscera of mice exposed to a municipal landfill leachate at various concentrations for 7 days. The study was designed to investigate the injuries and a possible mechanism of landfill leachateinduced toxicity on mammals. The results indicate that the leachate sample changed the ratio of viscera to body weight in all organs tested, and the effect on the brain was more obvious than that on other organs. The leachate ingestion increased PCO levels in the brain, kidney, liver and spleen in a concentrationdependent manner, but did not affect the content in the heart. Also, the leachate sample enhanced DPC formation in the tested organs in a concentration-dependent manner, and the responses of the liver, kidney and spleen were more sensitive than that of the brain and heart. These findings provide further evidence that landfill leachate-induced toxicity on mammals might involve the formation of free radicals, either via autoxidation or by enzyme-catalyzed oxidation of pollutants in leachate, and then attack of proteins and nucleic acids via generated free radicals.

Recent studies implicate the possible neurotoxicity of SO2, wever, its mechanisms remain unclear. In the present study, we investigated SO2 derivative-induced effect on delayed rectifier potassium channels(IK) and cellular death/apoptosis in primary cultured hippocampal neurons. The results demonstrate that SO2 derivatives (NaHSO3 and Na2SO3, 3:1M/M) effectively augmented IK and promoted the activation of delayed rectifier potassium channels. Also, SO2 derivatives increased neuronal death percentage and contributed to the formation of DNA ladder in concentration-dependent manners. Interestingly, the neuronal death and DNA ladder formation, caused by SO2 derivatives, could be attenuated by the delayed rectifier potassium channel blocker (tetraethylammonium, TEA), but not byt het ransient outward potassium channel blocker(4-aminopyridine, 4-P). It implies that stimulating delayed rectifier potassium channels were involved in SO2 derivative-caused hippocampal neuronal insults, and blocking these channels might be one of the possibly clinical treatment for SO2-caused neuronal dysfunction.

Previous studiesprovideevidenceforthepossibleneurotoxicityof SO2, butlittleinformationis availableaboutitsmechanisms. Inthepresentstudy, SO2 inhalation-inducedeffectsontheprotein oxidation, DNA-proteincrosslinksandapoptosisinrathippocampuswerestudied, byexposingWistar rats to SO2 at 14, 28and56mg/m3. Theresultsindicatethattheproteincarbonylcontent, anindicatorof proteinoxidation, andDNA–proteincrosslinkcoefficientweresignificantlyaugmented with concentration-dependentproperties. Inaddition, SO2 inhalationatallconcentrationstestedcaused the increasesofcaspase-3activityandnumberofTUNELpositivestainingneuronandthestatistical difference asobservedafter28and56mg/m3 exposure, suggestingtheoccurrenceofapoptosis. The results implythatattackingprotein, nucleicacidsandlipidsbyfreeradicals, generatedvia SO2 derivatives in vivo, isoneofthemainmechanismsfor SO2-inducedinjuriesincentralneuronalsystem

The effects of the Xingou municipal landfill leachate on levels of thiobarbituric acid reactive substances (TBARS) and the activities of Cu,Zn-superoxide dismutase (Cu,Zn-SOD), Se-dependent glutathione peroxidase (Se-dependent GPx), and catalase (CAT) were investigated in brains and livers of Kunming albino mice of both sexes, using chemical oxygen demand (CODCr) as ameasure of leachate concentration. The results show that leachate caused lipid peroxidation and change of antioxidative status in brains and livers of mice. There was a sex difference in the response of antioxidative status, and female mice were more sensitive than male mice. Exposure to leachate at all concentrations tested caused significant increases of TBARS levels in brains and livers from mice of both sexes. For brains, Cu,Zn-SOD and Se-dependent GPx activities were significantly increased at high concentration (CODCr 240mg/L) for male mice, but the activities of both antioxidative enzymes were significantly increased at low concentration (CODCr 60mg/L) and decreased at high concentration (CODCr 240mg/L) for female mice; CAT activities remained unchanged for male mice and were significantly decreased for female mice at high concentration (CODCr 240mg/L). For livers, Cu,Zn-SOD and Se-dependent GPx activities were significantly increased at high concentrations (CODCr 120 and 240mg/L) for male mice, but the activities of both antioxidative enzymes were significantly increased at low concentration (CODCr 30 or 60mg/L) and decreased at high concentration (CODCr 240mg/L) for female mice; CAT activities were significantly increased for male mice at all concentrations tested and decreased for female mice at high concentrations (CODCr 120 and 240mg/L). These results suggest that leachate exposure can cause oxidative damage on brains and livers of mice. The results also suggest that leachate might induce toxicity in mammals by the free-radical-damage mechanism.