The induction of micronuclei (MN) in polychromatic erythrocytes (PCE) of mouse bone marrow by municipal landfill leachate was studied in vivo. Results showed that mouse exposure via drinking water containing various concentrations of leachate caused asignificant increase of MN frequencies in a concentration (Chemical oxygen demand measured with potassium dichromate oxidation, CODCr)-ependent manner. MN induction in female and male mice was different at higher concentrations. This implies that leachate is a genotoxic agent in mammalian cells and that exposure to leachate in an aquatic environment may pose a potential genotoxic risk to human beings.

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 effects of the Xingou landfill leachate on levels of thiobarbituric acid reactive substances (TBARS) and the activities of Cu, Znsuperoxide dismutase (Cu, Zn-SOD), Se-dependent glutathione peroxidase (Se-dependent GPx) and catalase (CAT) were investigated in hearts, kidneys and spleens of Kunming albino mice of both sexes. Exposure to leachate caused significant increases of TBARS levels in the organs tested from mice of both sexes. For hearts, Cu, Zn-SOD, Se-dependent GPx and CAT activities were significantly increased at high concentrations for male mice, but the activities of these antioxidant enzymes were significantly increased at low concentration and decreased at high concentrations for female mice. For kidneys, Cu, Zn-SOD and Se-dependent GPx activities were significantly increased at high concentrations for male mice, but the activities were significantly increased at low concentrations and the ratio of increase was reduced with the increasing of concentration for female mice; CAT activities remained unchanged for male mice and were significantly increased at all concentrations tested for female mice. For spleens, Cu, Zn-SOD and Se-dependent GPx activities were significantly increased at high concentrations for male mice, but the activities were significantly increased at low concentrations and decreased at high concentrations for female mice; CAT activities remained unchanged for male mice and were significantly increased at high concentrations for female mice. The results suggest that leachate exposure can cause oxidative damage on hearts, kidneys and spleens of mice, and there were sex difference and organ difference in the response of antioxidant status.

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.

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。