Antioxidant responses to benzo[a]pyrene, tributyltin and their mixture in the spleen of Sebasticus marmoratus

It has been reported that there is an interaction between Benzo[a]pyrene （BaP）, a widespread carcinogenic polycyclic aromatic hydrocarbon, and tributyltin （TBT）, an organometal used as an antifouling biocide. This study was therefore designed to examine the potential in vivo influence of BaP, TBT and their mixture on splenic antioxidant defense systems of Sebastiscus marmoratus. The fish were exposed to water containing environmentally relevant concentrations of BaP, TBT and their mixture. Spleens were collected for biochemical analysis after exposure for 7, 25, 50 d and after recovery for 7, 20 d. Cotreatment with BaP and TBT for 7 d potentiated the induction of glutathione peroxidase （GPx） activity by BaP or TBT alone. The cotreatment for 25 and 50 d resulted in inhibition of GPx activity, which was similar to the effect of TBT. Splenic glutathione S-transferase （GST） activities were significantly elevated in S. marmoratus exposed to BaP starting from 7 d and remained high up to 25 d. However, no further activity change was found with prolonged exposure. Cotreatment of BaP and TBT primarily inhibited the GST activity, which was similar to the effect of TBT. Cotreatment with BaP and TBT for 25 or 50 d potentiated the depletion of GSH （glutathione） by BaP or TBT alone. MDA （malondialdehyde） contents in spleen of S. marmoratus were not significantly altered compared with the control during the test period. Spleen, as an immune organ, is sensitive to exposure of BaP or TBT. It should have an effective mechanism to counteract oxidative damage. Antioxidative defense systems in spleen of S. marmoratus should be considered as potential biomarkers. Short-term exposure of BaP or TBT could result in induction of antioxidant defense system. A significant decrease of these indices, such as GSH, GST, GPx might indicate more severe contamination.     

基于人工免疫原理的事故预防研究

介绍生物免疫识别模式,分析事故预防过程的实质是抑制潜在危险转化成事故的控制过程,分析比较事故预防与生物免疫识别模式在作用、生存环境、动作触发源等的共性,构建了基于免疫识别模式的事故预防系统并建立了事故预防数学模型;定义事故预防系统的识别率、失效率、误判率并给出了数学表达式,指出监测生产系统各环节状态信息是否符合系统的安全要求就是识别潜在危险的过程,是事故预防的关键,基于人工免疫原理的事故预防数学模型具有较强的健壮性、自适应性和动态防护性等特点。     

基于智能优化算法的河流水质模型参数的优化简

为探索河流水质模型参数新的求解方法,根据有限的实测数据,分别应用免疫进化优化算法和免疫进化优选的捕食搜索算法,对河流水质模型计算公式中的多参数进行优化。将优化得到的计算公式用于国内外若干河流的河段中DO浓度值的拟合,并与实测结果进行了比较。结果表明,将免疫进化优化算法或免疫进化优选的捕食搜索算法优化得到的水质模型参数精度不仅较高,而且相对稳定,从而为河流水质模型参数的优化提供了一种新方法。     

气溶胶等效复折射率反演的免疫进化算法

通过Mie散射理论公式构建目标函数,利用免疫进化算法对气溶胶等效复折射率的实部和虚部进行协同优化,据此创新性地提出了气溶胶等效复折射率反演的新途径.基于成都市2017年9~12月逐时的气溶胶散射系数和吸收系数观测数据以及该时段同时次GRIMM180大气颗粒物监测仪的连续监测资料,研究结果表明,气溶胶等效复折射率反演的免疫进化算法不仅是普适的,而且还具有收敛速度快、计算稳定和求解精度高等特点.通过与其它气溶胶等效复折射率反演方法的对比分析,进一步论证了新方法的优势,这为气溶胶等效复折射率演变机理以及气溶胶吸湿性增长模型的后续研究提供了算法保障.     

二英类污染物生物分析方法研究进展

二英类物质具有致癌、致畸等毒理及健康效应.我国二英类物质污染源较多,分布较为广泛,因此二英监测任务十分紧迫.但是我国二英实验室相对较少,单纯的仪器分析方法不能满足监测需求,因此急需发展经济、简便、快速的生物检测方法.生物检测方法主要包含免疫类检测方法和基于芳香烃受体(AhR)信号通路的检测方法,本文着重对这两类生物检测方法的原理和进展等进行综述.     

Toxicological effects of mouse diet contaminated with tributyltin on the immune and neurological systems of C57BL/6 mice

Organotin compounds, widely used as antifouling agents, are known to bioaccumulate in the food chain. Among organotin compounds, tributyltin (TBT), a toxic and widespread contaminant, has become a serious factor in environmental pollution and is suspected of being immunotoxic in animals. The purpose of this study was to assess the effects of 80 µg of TBT per kilogram of body weight (kg bw), provided in food, on the immune and neurological systems of C57Bl/6 mice. Data showed that TBT increased the proliferation of T and B lymphocytes in both adult and juvenile female and juvenile male mice, but that it decreased the proliferation of both T and B lymphocytes in adult male mice. The macrophages activity in female and male juvenile mice was higher than in adults of both sexes. The natural killer cytotoxic activity was also increased in juvenile and adult males and females compared to the control groups. In the brain, we observed the presence of TBT in the hippocampus, the striatum, the cortex, and the cerebellum in both the male and female groups. The highest levels were observed in the cortex of females and males, while the lowest levels were found in the cerebellum. TBT also induced an increase in the levels of the antioxidant glutathione (GSH) in the striatum, the hippocampus and in cortical structures but not in the cerebellum where the levels of TBT are lower. Our findings indicate that TBT modulated the immune and nervous systems causing endocrine and nervous perturbations.     

The plausibility of a role for mercury in the etiology of autism: a cellular perspective

Autism is defined by a behavioral set of stereotypic and repetitious behavioral patterns in combination with social and communication deficits. There is emerging evidence supporting the hypothesis that autism may result from a combination of genetic susceptibility and exposure to environmental toxins at critical moments in development. Mercury (Hg) is recognized as a ubiquitous environmental neurotoxin and there is mounting evidence linking it to neurodevelopmental disorders, including autism. Of course, the evidence is not derived from experimental trials with humans but rather from methods focusing on biomarkers of Hg damage, measurements of Hg exposure, epidemiological data, and animal studies. For ethical reasons, controlled Hg exposure in humans will never be conducted. Therefore, to properly evaluate the Hg-autism etiological hypothesis, it is essential to first establish the biological plausibility of the hypothesis. This review examines the plausibility of Hg as the primary etiological agent driving the cellular mechanisms by which Hg-induced neurotoxicity may result in the physiological attributes of autism. Key areas of focus include: (1) route and cellular mechanisms of Hg exposure in autism; (2) current research and examples of possible genetic variables that are linked to both Hg sensitivity and autism; (3) the role Hg may play as an environmental toxin fueling the oxidative stress found in autism; (4) role of mitochondrial dysfunction; and (5) possible role of Hg in abnormal neuroexcitory and excitotoxity that may play a role in the immune dysregulation found in autism. Future research directions that would assist in addressing the gaps in our knowledge are proposed.     

亚硝酸盐氮胁迫对罗非鱼（GIFTOreoohromisniloticus）血清非特异性免疫酶活性的影响

试验设置了不同浓度亚硝酸盐氮（空白对照、0．75mg·L-1、1．50mg-L-1、3．00mg·L-1和5．00mg·L-1）,研究了亚硝酸盐氮胁迫对罗非鱼（GIFTOreochromisniloticus）血清非特异性免疫酶（溶菌酶、碱性磷酸酶、补体c3）活性的影响。结果表明：罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性均呈现出随亚硝酸盐氮浓度升高而降低的趋势,且当亚硝酸盐氮浓度小于1．50mg·L-1时,罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性与对照组相比差异不显著（P〉0．05）,说明低于1．50mg·L-1的亚硝酸盐氮不会对罗非鱼机体免疫力产生显著影响;而高于3．00mg·L-1的亚硝酸盐氮胁迫能够显著（P〈O．05）降低罗非鱼血清碱性磷酸酶、溶菌酶、补体C3活性,最大下降率分别达到31．75％、27．40％、14．43％,从而显示出高浓度亚硝酸盐氮（〉3．00mg·L-1）能够对罗非鱼机体产生强烈的氧化胁迫和免疫损伤,导致机体免疫力下降,增加罗非鱼对致病菌的易感性。本研究认为,3．00mg·L-1可能是亚硝酸盐氮胁迫引起罗非鱼机体免疫力显著降低的阈值。     

大气细颗粒物对小鼠T淋巴细胞亚群的影响

大气颗粒物对肺免疫系统有潜在毒性作用,打破免疫系统平衡,大气颗粒物成分中危害首当其冲的是大气细颗粒物(PM_(2.5)),为研究大气细颗粒物引起的机体T淋巴细胞中Th1/Th2免疫失衡方向。本研究通过免疫组化实验方法检测暴露后小鼠肺组织中T淋巴细胞的表达,进一步采用流式细胞术检测大气细颗粒物气管滴注后小鼠肺脏淋巴细胞中Th1/Th2比例。暴露组小鼠肺组织免疫组化研究结果提示浸润细胞区有大量的CD4~+T细胞,中高剂量暴露组小鼠肺组织中淋巴细胞亚群Th1/Th2比例向Th1偏移。大气细颗粒物影响免疫失衡,使T淋巴细胞向Th1漂移。