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.

Increasing evidence suggests that cyclooxygenase-2 (COX-2) is involved in synaptic transmission and plasticity, and prostaglandin E2 (PGE2) is a key molecule in COX-2-meduated synaptic modification. However, the precise mechanisms, in particular, which subtypes of PGE2 receptors (EPs) mediate the PGE2-induced synaptic response, are not clear. Recently, we demonstrated that EPs are expressed heterogeneously in the hippocampus, and EP2/4 are mainly expressed in presynaptic terminals. Here, we report that PGE2 increased synaptic stimulus-evoked amplitudes of EPSPs in hippocampal slices and frequency of miniature EPSCs (mEPSCs) in hippocampal neurons in culture. These actions were mimicked by an EP2 agonist and attenuated by protein kinase A inhibitors. Decrease of EP2 expression through silencing the EP2 gene eliminated PGE2-induced increase of the frequency of mEPSCs. COX-2 and microsomal PGE synthase-1 (mPGES-1) andmPGES-2are present in postsynaptic dendritic spines, because they are colocalized with PSD-95 (postsynaptic density-95), a postsynaptic marker. In addition, the frequency of mEPSCs was enhanced in neurons pretreated with interleukin-1 or lipopolysaccharide, which elevated expression of COX-2 and mPGES-1 and produced PGE2, and this enhancement was inhibited by a COX-2 inhibitor that inhibited production of PGE2. Our results suggest that PGE2 synthesized by postsynaptically localized COX-2 functions as a retrograde messenger in hippocampal synaptic signaling via a presynaptic EP2 receptor.

With increasing attention paid to the recycling use of aged refuse as vegetated soil, it is important to check its possible polluting risk and probe the tolerance of plant system to its stress. For this reason, several physiological responses in Zea mays[Gren Open L. Close][Red_L.Red Close] (maize) to the leaching samples of aged refuse in different particlesize [Gren Open (90-30, 30-150, 150-105, 105-90, Gren Close][Red Open(900-300, 300-150, 150-105, 105-90,and 90-0μm Red Close]and [Gren Open 900 Close][Red Open90-oRed Close] lm) were investigated in the present study, including growth, lipid peroxidation, protein oxidation and activities of antioxidant enzymes. The results indicate that the aged refuse affected the growth of maize seedlings, and elevated the levels of lipid peroxidation and protein oxidation in leaf tissues in a time-dependent manner, accompanying by the changes of antioxidant status. Also, above physiological responses varied as a function of particle-size distribution of the aged refuse, and statistical growth inhibition and oxidative stress occurred after the exposure of smaller particle-size samples, which contained higher level trace metals, the characteristic pollutants in the aged refuse. The results implicate that aged refuse might cause environmental stress on plant system, but the polluting risk mainly resulted from smaller particle-size samples. Therefore, the critical point of utilizing aged refuse as vegetated soil focused on analyzing its particle-size distribution, and screening out appropriate particle- size samples.

为了阐明大气污染物SO2对神经系统和心血管系统的毒作用机制，采用全细胞膜片钳技术研究了SO：衍生物（NaHSO，和Na2S0，分子比为1∶3）对大鼠海马、背根节神经元和心肌细胞膜上钠、钾、钙离子通道的影响。结果显示：（1）SO2衍生物可显著增大大鼠海马CAl区神经元钠电流，不影响钠通道的激活过程，但可使钠电流的失活曲线向去极化方向移动，延迟钠通道的失活过程；另外，SO2衍生物可显著增大瞬间外向钾电流（IA）和延迟整流钾电流（IK），不影响IA的激活过程，使IK 的激活过程向负电压方向移动，促进IK的激活过程，而使IA 的失活曲线向正电压方向移动，延迟IA的失活过程。（2）SO2 衍生物显著增大鼠背根节神经元钠电流（TTX-s钠电流和TTX-R钠电流），可使两种钠电流的激活和失活曲线均向去极化方向移动，但对失活的影响大于对激活的影响，即延迟钠通道的失活过程；SO2 衍生物显著增大背根节神经元瞬间外向钾电流（Toca）和延迟整流钾电流（Ik），不影响TOCA的激活过程，但可使Ik的激活曲线向超极化方向移动，促进Ik的激活。另外，还可使TOCs的失活曲线向去极化方向移动，即延迟TOCa的失活。（3）SO：衍生物可显著增大大鼠心肌细胞L一型钙电流（Ica，L），使Ica.L的激活和失活曲线均向去极化方向移动，但对失活的影响大于对激活的影响；SO2衍生物显著增大心肌细胞钠电流，不影响钠通道的激活过程，但可使钠电流的失活曲线向去极化方向移动，延迟钠通道的失活过程；SO2衍生物显著增大心肌细胞瞬间外向钾电流（I50），使I50的激活曲线向超极化方向移动，促进I50的激活过程，但可使I50的失活曲线向去极化方向移动，延迟I50的失活过程；此外，SO2衍生物还可显著增大心肌细胞内向整流钾电流（IK），但不影响其反转电位。结果表明，SO：衍生物可能通过影响神经元和心肌细胞膜上离子通道的活动而对中枢神经、传导神经以及心血管系统产生不利影响。提示大气SO：污染可能与神经系统和心血管系统疾病的发生有关。

The oxygenation of endogenous cannabinoids (eCBs) 2-arachidonoyl glycerol (2-AG) and arachidonoyl ethanolamide by cyclooxygenase-2 (COX-2) produces novel types of prostanoids: prostaglandin glycerol esters (PG-Gs) and prostaglandin ethanolamides (PG-EAs). However, the physiological function of COX-2 oxidative metabolites of eCBs is still unclear. Here we demonstrate that PGE2-G, a COX-2 oxidative metabolite of 2-AG, induced a concentration-dependentincrease in the frequencyof miniature inhibitorypostsynaptic currents (mIPSCs) in primary cultured hippocampal neurons, an effect opposite to that of 2-AG. This increase was not inhibited by SR141716, a CB1 receptor antagonist, but was attenuated by an IP3 or MAPK inhibitor. In addition, we also examined the effects of other prostanoids derived from COX-2 oxygenation of eCBs on mIPSCs. PGD2-G, PGF2α-G and PGD2-EA, but not PGE2-EA or PGF2α-EA, also increased the frequency of mIPSCs. The eCB-derived prostanoid-induced responses appeared to be different from those of corresponding arachidonic acid-derived prostanoids, implying that these effects are not mediated via known prostanoid receptors. We further discovered that the inhibition ofCOX-2 activity reduced inhibitory synaptic activity and augmented depolarization-induced suppression of inhibition (DSI), whereas the enhancement of COX-2 augmented the synaptic transmission and abolished DSI. Our results, which show that COX-2 oxidative metabolites of eCBs exert opposite effects to their parent molecules on inhibitory synaptic transmission, suggest that alterations in COX-2 activity will have significant impact on endocannabinoid signalling in hippocampal synaptic activity.