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。     

Soil factors associated with zinc deficiency in crops and humans

Zinc deficiency is the most ubiquitous micronutrient deficiency problem in world crops. Zinc is essential for both plants and animals because it is a structural constituent and regulatory co-factor in enzymes and proteins involved in many biochemical pathways. Millions of hectares of cropland are affected by Zn deficiency and approximately one-third of the human population suffers from an inadequate intake of Zn. The main soil factors affecting the availability of Zn to plants are low total Zn contents, high pH, high calcite and organic matter contents and high concentrations of Na, Ca, Mg, bicarbonate and phosphate in the soil solution or in labile forms. Maize is the most susceptible cereal crop, but wheat grown on calcareous soils and lowland rice on flooded soils are also highly prone to Zn deficiency. Zinc fertilizers are used in the prevention of Zn deficiency and in the biofortification of cereal grains.     

氮缺乏引起的非丝状菌活性污泥膨胀

采用SBR法处理啤酒废水,研究了进水中不同有机物与总氮的比值(以BOD/N计)条件对活性污泥膨胀的影响.结果表明,在进水BOD/N为100/4的条件下,污泥的沉降性能良好;在进水BOD/N分别为100/3和100/2时,均发生由高含水率的粘性菌胶团过量生长引起的非丝状菌膨胀.在进水BOD/N为100/0.94的条件下,发生的非丝状菌膨胀最为严重.试验中还研究了氮缺乏条件下污泥微生物对氮源和磷源的利用率以及COD去除率的变化.     

双峰驼骨质疏松症的流行特点及其与生物地球化学因子之间的关系

研究了双峰驼骨质疏松症的流行特点及与生物地球化学因子之间的关系，结果表明，在从腾格里沙漠西南端开始向巴丹吉林沙漠的西北方向延伸形成大约长600km，宽160km的狭长发病区域内，该病发病率为28．8％，致死率达60％,该区土壤、牧草中Cu、P含量极显著低于正常值（p＜0．01），牧草中m（Ca）：m（P）为50：1；病驼全血和被毛P含量亦低于健康驼（P＜0．01）．因此认为该病主要是由双峰驼食物链中P缺乏所致的一种骨营养不良症．     

Successful outcome of pregnancy after treatment of maternal anti-ro (SSA) antibodies with immunosuppressive therapy and plasmapheresis

In this short communication we describe a patient with anti-SSA and anti-SSB antibodies whose first child died of congenital complete heart block (CCHB). During her second pregnancy she was treated with prednisolone, azathioprine, and plasmapheresis, and levels of anti-SSA and anti-SSB antibodies fell significantly. The pregnancy evolved uneventfully and resulted in the birth of an unaffected male infant. This is the fourth reported case of a successful outcome of pregnancy after treatment with immunosuppressive drugs in a woman with a significant risk of recurrence of CCHB.     

The prognostic factors in the prenatal diagnosis of the echogenic fetal lung

The prenatal diagnosis of an echogenic fetal lung (EFL) is now often made in the early second trimester using high-resolution ultrasound. This ultrasound appearance is usually caused by a congenital cystic adenomatoid lung malformation (CCAM), an intrapulmonary lung sequestration or obstruction of a major airway. In order to provide prognostic guidelines to parents who may be considering termination of a fetus with these findings, we have analysed a series of 11 cases diagnosed in our centre over the past 2 years in conjunction with 60 cases from major published series. The data suggest that in the absence of non-immune hydrops fetalis (NIHF) or other anomalies, the outcome for the fetuses is excellent, with over 90 per cent survival. Neither early diagnosis (24 weeks) nor the presence of mediastinal shift is a poor prognostic indicator. In addition, it appears that if NIHF is absent at diagnosis, the chance that it will develop as the pregnancy continues is small (6 per cent). Furthermore, there is a significant (up to 30 per cent) chance that this ultrasound finding will resolve in utero. The development of in utero fetal surgical techniques may be the only hope for those hydropic fetuses who appear to have a dismal prognosis.     

Prenatal diagnostic procedure for leukocyte adhesion deficiency

Leukocyte adhesion deficiency (LAD) is a rare autosomal recessive disorder which leads to recurrent severe infections due to impaired leukocyte functions. The disorder is caused by an absence or deficiency of leukocyte cell adhesion molecules (LeuCAMs) on the leukocyte membranes. The diagnosis is established with monoclonal antibodies against the LeuCAMs. We have carried out a prenatal diagnostic procedure by means of cordocentesis in a mother who was 20 weeks pregnant and had previously given birth to a child with LAD. This previous child had the severe form of LAD with undetectable mRNA for the β chain, the common subunit of the LeuCAMs. We found that the fetal granulocytes expressed the LeuCAMs normally. At birth, the baby was physically normal and showed no signs of impaired leukocyte functions.