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。

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。

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.

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.