1,2-二氯乙烷染毒对小鼠脑组织氨基酸类神经递质的影响

探讨1,2-二氯乙烷(1,2-DCE)对小鼠脑组织氨基酸类神经递质的影响,为揭示1,2-DCE的神经毒性损伤机制提供实验参考数据。将昆明种小鼠随机分为4组,对照组和不同剂量1,2-DCE染毒组(0.25 mg/L、0.50 mg/L、1.00mg/L),每组10只小鼠。静式吸入染毒14 d,每天染毒2 h。染毒结束后取大脑组织,测定小鼠脑脏器系数;高效液相色谱法(HPLC)检测脑组织中谷氨酸(Glu)、天冬氨酸(Asp)、甘氨酸(Gly)、牛磺酸(Tau)及γ-氨基丁酸(GABA)的含量。结果小鼠脑脏器系数随染毒剂量的增加呈下降趋势,但各组间差异无统计学意义。各染毒组的Asp、Glu和Tau含量随染毒剂量的增加而升高,且中、高剂量染毒组与对照组比较差异有统计学意义;各染毒组的Gly含量随染毒剂量的增加也有升高的趋势,但与对照组比较差异无统计学意义;中剂量染毒组的GABA含量与对照组比较差异具有统计学意义,但高剂量组与对照组比较未见明显差异。提示亚急性1,2-DCE暴露可引起小鼠脑组织中氨基酸类神经递质含量的异常,其可能是1,2-DCE神经毒性损伤的主要机制之一。 更多还原     

亚慢性1,2-二氯乙烷染毒对小鼠空间学习记忆能力的影响

为探讨亚慢性1,2-二氯乙烷(1,2-DCE)染毒对小鼠空间学习记忆能力的影响及其可能机制,将昆明种小鼠随机分为4组,分别为对照组及1,2-DCE低、中、高剂量染毒组(0.225、0.45、0.9 g/m~3),每组5只。采用静式吸入方式染毒4周,染毒3.5 h/d。末次染毒结束后次日立即进行Morris水迷宫实验。处死小鼠,取大脑组织,采用高效液相色谱法(HPLC)检测脑组织中谷氨酸(G1u)、天冬氨酸(Asp)及γ-氨基丁酸(GABA)的含量。结果显示,在定位航行实验中,从训练第3天起高剂量组小鼠的逃避潜伏期均显著高于其他各组;训练第5天,中剂量组小鼠的逃避潜伏期与对照组和低剂量组相比,差异均有统计学意义;各剂量组游泳速度差异无统计学意义。空间探索实验中,各染毒组小鼠在目标象限停留时间随染毒剂量的增加而减少,但与对照组相比差异无统计学意义。高剂量染毒组小鼠脑组织中GABA含量显著高于其他各组,而各组间G1u和Asp含量差异均无统计学意义。提示亚慢性1,2-DCE染毒对小鼠空间学习能力的抑制性作用,可能与脑组织中抑制性氨基酸含量升高有关。     

亚急性1,2-二氯乙烷染毒致小鼠肝组织氧化损伤的研究

本研究的目的是探讨亚急性1,2-二氯乙烷(1,2-DCE)中毒致肝脏氧化损伤情况,为阐明1,2-DCE中毒性肝损伤的机制提供参考依据。将昆明种小鼠随机分成对照组和不同剂量1,2-DCE染毒组(0.35、0.7、1.2 mg/L),采用静式吸入方式染毒1周;然后,取血和肝组织,分别检测血中总胆红素(TB)和谷胱甘肽(GSH)含量,肝组织中丙二醛(MDA)、GSH含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性。结果中、高剂量染毒组小鼠的血浆中TB含量显著高于对照组小鼠;而中、高剂量染毒组小鼠的肝组织中GSH-Px活性和GSH含量及高剂量组的SOD活性显著低于对照组,高剂量染毒组小鼠的肝组织中MDA含量显著高于对照组。提示亚急性1,2-DCE中毒可引起肝组织的氧化性损伤。     

亚急性1,2-二氯乙烷中毒二例

2005年8月,我省某电厂安装冷却塔时发生一起亚急性1,2-二氯乙烷中毒事故,造成重度、轻度中毒各1例,报告分析如下。一、事故经过2005年8月初,一个农民工程队转包河南省某电厂的冷却塔安装工程,所用原料均由第一承包商提供,填料规格为500mm×1000mm、500mm×2000mm的S型及波浪型薄塑料板。填料的粘贴均由女工(20人)手工操作。作业在室外高温下进行,2人1组,用填料分别围挡起2m~2的场所,徒手用刷子蘸取黏合剂粘贴填料,刷至远端身体前倾,工作时暴露前臂,戴露手指的棉线手套,早期无其他防护措施。至第4     

1,2-二氯乙烷对小鼠睾丸细胞DNA的影响

目的研究1,2-二氯乙烷(1,2-DCE)对小鼠睾丸细胞DNA损伤作用,探讨1,2-DCE的生殖毒性。方法采用单细胞凝胶电泳方法,检测1,2-DCE不同染毒剂量(50,100,200,400 mg/kg)及染毒后不同时间(24,48,72 h)对小鼠睾丸细胞DNA的损伤情况。结果在受试剂量、时间范围内,小鼠睾丸细胞彗星率随1,2-DCE染毒剂量的增加而增加(P<0.01),彗尾的长度(除50 mg/kg染毒组)随剂量增加而延长(P<0.01),各剂量与彗星率和彗尾长度之间均存在剂量-反应关系(R彗星率=0.974 5,R彗尾长=0.970 6,P<0.01);染毒后24,48,72 h,各组小鼠睾丸细胞彗星率和彗尾的长度随染毒后时间的增加而增加(P<0.01)。结论1,2-DCE对小鼠睾丸细胞DNA具有明显的损伤作用。     

1,2-二氯乙烷对大鼠脑的影响

目的探讨1,2-二氯乙烷(DCE)对大鼠脑的影响。方法30只大鼠分2组,在一定剂量下连续染毒10d,试验期间和试验结束时分别对各组的大鼠进行体重、主要脑/体比测定、脑病理检查以及Cl-通道检查。结果DCE在该剂量连续经口染毒可引起大鼠体重增加减慢,脑/体比增大,部分脑组织受损,脉络丛Cl-通道不明显。结论一定剂量的DCE导致部分SD大鼠轻度脑损伤。     

亚急性重度1,2-二氯乙烷中毒致死2例报告

对2例1,2-二氯乙烷中毒死亡病例的临床资料及现场调查结果作一简要报道。     

一起印刷工亚急性1,2-二氯乙烷中毒事故调查

2007年5月，上海某塑胶有限公司发生一起亚急性1，2-二氯乙烷中毒事故，造成亚急性二氯乙烷中毒2例，现将事故报告分析如下：     

亚急性1,2-二氯乙烷重度中毒2例治疗体会

报道了2例因接触1,2-二氯乙烷而导致重度中毒．其中1例因为治疗恰当而达到临床治愈;另一例治疗后出现双眼视神经萎缩,并遗留脑病症状。所以治疗措施是关键。     

亚急性重度1,2-二氯乙烷中毒救治体会

目的探讨亚急性重度1,2-二氯乙烷中毒的救治。方法对1例以中毒性脑病为主要临床表现的亚急性重度1,2-二氯乙烷中毒患者采取以防治"脑水肿"为治疗重点的综合治疗。结果患者住院第4天由昏迷转为轻度意识障碍,出现头颈部、双上肢不自主的震颤伴构音困难,住院第6天意识清醒,头颈部震颤缓解,双上肢持续性震颤,住院治疗1个月余病情好转出院。结论及时、恰当的脱水治疗是救治亚急性重度1,2-二氯乙烷中毒的关键。     

1，2-二氯乙烷生物标志的研究

[目的]探讨1,2-二氯乙烷在尿中的代谢产物作为生物标志物,为预防1,2-二氯乙烷职业中毒提供依据。[方法]将SD大鼠分为染毒组和对照组,每组2只。用1,2-二氯乙烷对大鼠作灌胃染毒,然后收集尿样,经酸化、蒸发及甲酯化处理后用气相色谱-质谱（GC-MS）分析。[结果]在染毒大鼠的尿样中检出6种化合物：硫撑双乙酸二甲酯、2-甲硫基乙酸甲酯、磷酸三甲酯、2-甲氧基．2-戊烯二酸二甲酯、柠檬酸三甲酯和3,4-二甲氧基苯丙酸甲酯。其中硫撑双乙酸二甲酯和柠檬酸三甲酯的色谱信号较高,硫撵双乙酸已有文献报道是1,2．二氯乙烷代谢产物。[结论]硫撑双乙酸二甲酯作为接触1,2-二氯乙烷的生物标志物,值得进一步研究。柠檬酸三甲酯异常增高,可能与阻断三羧酸循环有关,有可能可作为1,2-二氯乙烷中毒的初步排查标志。     

1,2-二氯乙烷急性吸入染毒脑组织损伤形态学研究

为了研究 1 ,2 二氯乙烷 (1 ,2 -DCE)在静式吸入染毒条件下对脑组织的急性损害。采用连续静式吸入染毒大鼠 1 2h后 ,观察不同染毒剂量下受试动物脑组织的形态学变化 ;测定脑组织干湿重及含水量。结果显示 :染毒剂量为 2 .5g m3 时 ,脑组织在形态学上无明显变化 ,含水量为 80 .41 % ,与对照组 (79.82 % )相比 ,无明显差异 ;5 .0g m3 染毒组在形态学上出现轻微脑水肿 ,脑组织含水量为 82 .1 4 % ,与对照组相比有显著性差异 (P <0 .0 5) ;1 0 .0g m3 组脑组织在形态学上水肿明显 ,其含水量 (83 .65 % )与各组之间差异显著 (P <0 .0 5)。结果提示 :1 ,2 -DCE在短期大量吸入的情况下可导致动物出现脑水肿。     

Long-chain polyunsaturated fatty acids modulate interleukin-1beta-induced changes in behavior, monoaminergic neurotransmitters, and brain inflammation in rats

Recent evidence has suggested that an imbalance between membrane (n-3) and (n-6) fatty acids may contribute to the etiology of autoimmune and neurodegenerative diseases. In this study, the mechanisms by which eicosapentaenoic acid (EPA), gamma-linolenic acid (GLA), and arachidonic acid (AA) modulate neurotransmitters, behavior, and brain inflammation were evaluated in rats that received central saline or interleukin-1beta (IL-1) administrations. In rats treated with saline, only the AA-enriched diet significantly increased anxiety-like behavior in the elevated plus maze, which was associated with increased corticosterone secretion. AA also increased the turnover of dopamine (DA), noradrenaline (NA), and serotonin (5-HT) in the amygdala and increased the prostaglandin (PG)E(2) level in the hippocampus. IL-1 administration slowed rat learning in the water maze and increased anxiety-like behavior, changes which were associated with increased homovanillic acid and 5-HT turnover, decreased NA in the hippocampus and amygdala, decreased DA in the frontal cortex, and decreased IL-10 in limbic brain regions. Increased corticosterone secretion following IL-1 administration was accompanied by increased NA turnover in the hippocampus (P < 0.05) and increased PGE(2) concentration (P < 0.01) in the limbic brain regions. Of the 3 diets tested, only EPA attenuated IL-1-induced behavioral changes (P < 0.05 or 0.01), which was associated with the modulation of EPA on the neuroendocrine and immune changes induced by IL-1. GLA reduced hippocampal PGE(2) concentration in rats given IL-1 (P < 0.01). AA did not counteract any of the changes induced by IL-1. These results suggest that EPA, GLA, and AA play different roles in the neuroendocrine-immune network.     

锰对小鼠脑内四种氨基酸类神经递质的影响

将24只小鼠按体重随机均分为对照组及低、中、高染锰组,计算脑脏器系数,检测脑组织四种氨基酸含量及组织蛋白含量。与对照组相比,随染锰浓度提高,γ-氨基丁酸(GABA)含量逐渐降低,谷氨酸(Glu)和天冬氨酸(Asp)逐渐增高,呈剂量依赖趋势。中、高锰组Glu和Asp含量明显高于对照组。高锰组GABA明显低于对照组。锰可对小鼠脑内氨基酸类神经递质产生影响,其可能是锰神经毒性作用靶点之一。     

Effects of a single inhalative exposure to formaldehyde on the open field behavior of mice

The effects of formaldehyde on the explorative behavior and locomotor activity of mice after a single inhalative exposure were examined in an open field. Adult male mice were exposed to approximately 1.1 ppm, 2.3 ppm, or 5.2 ppm formaldehyde vapour for 2 hours and the open field test was carried out two hours after the end of exposure (trial 1) and repeated 24 hours thereafter (trial 2). The following behavioral parameters were quantitatively examined: numbers of crossed floor squares (inner, peripheral, total), sniffing, grooming, rearing, climbing, and incidence of fecal boli. The results of the first trial revealed that the motion activity was significantly reduced in all exposed groups. In the 1.1 ppm group, the frequency of rearing was reduced and that of floor sniffing increased. The exposure to the two higher formaldehyde concentrations caused a significant decrease in total numbers of floor squares crossed by the subjects, air sniffing, and rearing. The open field test on the next day (trial 2) showed that the frequencies of floor sniffing, grooming, and rearing in all formaldehyde groups were significantly altered. In the 2.5 ppm group, an increased incidence of fecal boli was observed. From the results obtained, we conclude that the exposure of male mice to formaldehyde vapour affects their locomotor and explorative activity in the open field, and that some open field parameters are still altered in the exposed animals even after 24 hours.     

肠道病毒71型感染乳鼠脑组织白介素1β与白介素6水平的研究

目的 检测肠道病毒71型(EV71)感染乳鼠脑组织白介素1β(IL-1β)与白介素6(IL-6)水平变化,探讨EV71致中枢损害可能的发病机制。方法 1日龄120只ICR乳鼠随机分为感染组及对照组。腹腔注射法建立EV71感染乳鼠模型。荧光定量RT-PCR法检测脑组织中EV71载量。光镜观察脑组织病理变化。酶联免疫吸附法(ELISA)检测脑组织匀浆液中IL-6与IL-1β含量。结果 感染组3 d、5 d与7 d乳鼠脑组织匀浆IL-1β浓度较对照组明显升高(P<0.01),感染组3 d、5 d、7 d与10 d乳鼠脑组织匀浆IL-6浓度较对照组明显升高,差异有统计学意义(P<0.01),感染组1 d与14 d乳鼠脑组织匀浆IL-1β及IL-6浓度与对照组相比差异无统计学意义(P>0.05)。结论 EV71感染乳鼠早期脑组织中IL-1β及IL-6含量明显升高,其介导的免疫反应可能是EV71致中枢损害可能的机制之一。     

ATP酶变化在1,2二氯乙烷致脑水肿过程中的作用研究

为探索Na+ K+ATP酶、Ca2 +、Mg2 +ATP酶在 1,2 -二氯乙烷 (1,2 DCE)致脑水肿过程中所起的作用 ,在复制脑水肿模型的基础上 ,检测受试动物脑组织中Na+ K+ATP酶、Ca2 +、Mg2 +ATP酶活力的变化。结果显示 ,随着染毒剂量的增加 ,Na+ K+ATP酶活力逐渐降低 ,最高剂量组与各组相比 ,具有显著性差异 ;Ca2 +、Mg2 +ATP酶活力显著下降 ,与其余各组相比 ,P <0 0 5。结果提示 :1,2 DCE引起了ATP酶活力的下降导致脑组织能量代谢障碍 ,从而可能引起“Ca2 +超载” ,ATP酶活力下降和“Ca2 +超载”可能是引起脑水肿的主要原因     

CYP2E1在1,2-二氯乙烷致脑氧化损伤中的作用

分别将昆明种小鼠随机分为对照组、单纯染毒组及低、中和高剂量二烯丙基硫化物(DAS)干预组。检测脑组织中CYP2E1蛋白和mRNA表达、MDA和GSH含量及SOD活性。单纯染毒组与对照组相比,小鼠脑组织中CYP2E1蛋白和mRNA表达及MDA含量显著升高,而GSH含量显著下降;DAS各干预组与单纯染毒组相比,CYP2E1蛋白和mRNA表达及MDA含量显著下降,GSH含量显著升高。提示1,2-DCE可诱导CYP2E1表达,导致脑组织氧化损伤。     

Decreased brain ascorbate levels in copper-deficient mice and in brindled mice

Mutant brindled mice, which exhibit signs of copper deficiency, were compared to their normal brothers as well as to age-matched suckling mice that were copper-deficient (-Cu) because their dams were consuming a copper-deficient diet, and a fourth group of copper-supplemented (+Cu) suckling mice, which served as dietary controls. Copper deficiency, genetic and dietary, resulted in mice with smaller brains (87 and 75%) and lower levels of the serum cuproprotein ceruloplasmin (10 and 6.1%) when compared to their respective controls. Brain ascorbic acid concentrations were determined in these mice by high performance liquid chromatography with electrochemical detection, and levels in brindled mice and -Cu mice were significantly lower (81 and 80%) than those measured in their respective controls. Injection of cupric chloride into -Cu pups raised brain ascorbate to levels found in +Cu mice and returned catecholamine levels to normal by raising norepinephrine from a major deficit (91%) and decreasing dopamine from an excess (22%). In another study, dietary copper deficiency was produced beginning at birth and continued for 7 weeks. These older -Cu mice had minor reductions in brain ascorbate (10%) and more severe reductions in norepinephrine levels (43%). Older +Cu mice had lower ascorbate and higher norepinephrine levels compared to suckling control mice.(ABSTRACT TRUNCATED AT 250 WORDS)