Revisiting the Hydrogen Storage Behavior of the Na-O-H System

Solid-state reactions between sodium hydride and sodium hydroxide are unusual among hydride-hydroxide systems since hydrogen can be stored reversibly. In order to understand the relationship between hydrogen uptake/release properties and phase/structure evolution, the dehydrogenation and hydrogenation behavior of the Na-O-H system has been investigated in detail both ex- and in-situ. Simultaneous thermogravimetric-differential thermal analysis coupled to mass spectrometry (TG-DTA-MS) experiments of NaH-NaOH composites reveal two principal features: Firstly, an H₂ desorption event occurring between 240 and 380 °C and secondly an additional endothermic process at around 170 °C with no associated weight change. In-situ high-resolution synchrotron powder X-ray diffraction showed that NaOH appears to form a solid solution with NaH yielding a new cubic complex hydride phase below 200 °C. The Na-H-OH phase persists up to the maximum temperature of the in-situ diffraction experiment shortly before dehydrogenation occurs. The present work suggests that not only is the inter-phase synergic interaction of protic hydrogen (in NaOH) and hydridic hydrogen (in NaH) important in the dehydrogenation mechanism, but that also an intra-phase H^δ+… H^δ– interaction may be a crucial step in the desorption process.     

鱼油抗大鼠动脉粥样硬化的实验研究

以大鼠高脂血症及动脉粥样硬化模型观察鱼油的作用，并与舒降之、诺衡比较。鱼油组血清总胆固醇（ＴＣ）、甘油三酯（ＴＧ）、低密度脂蛋白胆固醇（ＬＤＬ－Ｃ）及ＬＤＬ－Ｃ／ＴＣ显著低于高脂组（均为Ｐ＜０．０１）；生化与病理检查提示鱼油能防止肝内脂质沉积，减少肝组织脂质过氧化物水平；鱼油能明显抑制高脂饮食造成的早期动脉粥样硬化病变。鱼油降ＴＧ的作用与舒降之及诺衡无明显差异，降ＴＣ的效果优于诺衡（Ｐ＜０．０５），改变脂蛋白成分的作用不及舒降之与诺衡。研究表明鱼油能延缓大鼠高脂血症和动脉粥样硬化的发生与发展。     

血红素抑制内皮细胞损伤的形态学观察

目的 探讨血红素对人脐静脉内皮细胞氧化应激损伤的保护作用。方法 将培养的人脐静脉内皮细胞进行分组：对照组、损伤组、血红素组。观察各组细胞在光、电镜下形态学的改变。结果 在光镜下，血红素组细胞的生长状态明显优于损伤组；在电镜下，损伤组细胞核固缩，而血红素组细胞核幼稚，核仁明显。结论 在人脐静脉内皮细胞中，血红素对过氧化氢所造成的氧化应激损伤有明显的保护作用。     

中国仓鼠肺成纤维细胞和HeLa细胞DNA氧化损伤的自身修复能力与比较

目的:研究不同氧化相关因素对中国仓鼠肺成纤维细胞(CHL)和HeLa细胞DNA损伤的自身修复情况.方法:将CHL细胞和HeLa细胞用不同氧化相关因素处理一定时间[CHL细胞:过氧化氢(H2O2)25 min,重铬酸钾(K2Cr2O7)105 min,阿霉素(Dox)75 min;HeLa细胞:H2O2 25 min,K2Cr2O7 105 min],随后立即去毒培养0、0.5、1、2、3 h,以碱性单细胞凝胶电泳技术检测DNA链断裂情况.结果:①CHL细胞经H2O2、K2Cr2O7、Dox作用后引起DNA链断裂,去毒培养1 h链断裂修复明显(P<0.01);去毒培养2～3 h,前两毒剂的损伤组完全修复,而Dox组链断裂仍高于未损伤组;②HeLa细胞经H2O2、K2Cr2O7作用后引起DNA链断裂,去毒培养0.5 h链断裂明显修复(P<0.01),去毒培养1 h则完全修复;③CHL细胞和HeLa细胞损伤后修复的拖尾率与修复时间的回归系数显著不同(P<0.05).结论:两种细胞在氧化性DNA损伤后均迅速启动自身修复,但HeLa细胞比CHL细胞有更快的修复能力;同时这两种细胞由Dox所致损伤修复能力均较H2O2、K2Cr2O7所致的差.     

葛根素对抗H2O2引起血管平滑肌细胞凋亡及坏死

目的：研究葛根素对过氧化氢引起无血清培养的小牛主动脉血管平滑肌细胞凋亡和坏死的影响。方法：通过体外细胞培养，以噻唑兰（MTT）法测定细胞存活率，用流式细胞术检测细胞DNA含量及凋亡细胞百分率；DNA琼脂糖凝胶电泳法观察细胞凋亡过程中DNA断裂程度。结果：H2O2诱导无血清培养的平滑肌细胞凋亡，葛根素可显著降低平滑肌细胞中凋亡细胞百分率，并减少凋亡细胞DNA断裂，同时也减少其引起的平滑肌细胞坏死。结论：葛根素可对抗H2O2引起的无血清培养的血管平滑肌细胞凋凋亡及坏死。     

车前子对高脂血症大鼠脂质过氧化的影响

目的 :　探讨车前子对高脂血症大鼠脂质过氧化的影响。方法 :　采用大鼠血清及多脏器组织 ,观察车前子对高脂血症大鼠脂质过氧化的影响。结果 :　高脂对照组血清和心肌超氧化物歧化酶 ( SOD)活性显著降低 ,而脂质过氧化物 ( LPO)含量明显升高 ,血清和肝脏的过氧化氢酶( CAT)、谷胱苷肽过氧化物酶 ( GSH-Px)活性明显降低。补充车前子后显著升高血清及心肌组织SOD活性 2 2 %和 2 8% ,以及肝脏 GSH-Px活性 2 2 %。而使血清及心肌的 LPO含量分别下降 3 2 %和 1 7%。结论 :　 1 5 g/kg车前子可提高高脂血症大鼠体内抗氧化能力并免受自由基损伤     

硒对辐射所致过氧化脂质含量及谷胱甘肽过氧化物酶活性的影响

以肝、脾组织中过氧化脂质(LPO)含量及谷胱甘肽过氧化物酶(GSHL-Px)活性为指标探讨硒的辐射防护效应。实验结果表明:BALB/C纯系雄性小鼠经3Gy ~(60)Co γ射线照射后3天,肝、脾组织LPO生成量比未照射者均显著增多,而GSH-Px活性却都显著降低;但于照射前连续7天每日经口灌胃亚硒酸钠溶液0.2ml(含硒12.5μg)的实验组动物,肝、脾组织LPO含量均明显少于照射对照组,而GSH-Px活性都显著高于照射对照组,结果提示,通过降低LPO含量和增加GSH-Px活性,硒对小鼠可能有辐射防护作用。     

-Hydroperoxy diethyl peroxide, an unusual natural compound isolated from an ascidian (Phallusia mammillata): acute toxicity in DDY mice

-Hydroperoxy diethyl peroxide, a novel compound found in the tunic of ascidians, has two peroxide moieties per molecule. Since ascidians are a widely served food item in Japan, human exposure to this compound potentially exists in the seafood preparation industries. No toxicological data have so far been published on this compound, and so we determined the intraperitoneal 6-day LD₅₀ in mice and conducted histopathological examinations. The 6-day LD₅₀, was found to be 199 mg/kg with 95% confidence limits of 126–314 mg/kg. Histopathological examination revealed necrosis induced in a variety of cells that had been directly exposed to the compound. These cells included hepatocytes, parenchymal pancreatic cells and fat cells. It is concluded that direct contact with this compound is likely to elicit cellular necrosis of various organs. The specific toxicological effects are probably dependent on the route of exposure.