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1.
-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.  相似文献   
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日本大耳兔9只,其中6~8月龄5只,2~2.5年龄4只。均喂以2%654-2溶液1ml/天(即20mg)共43天。结果不分年龄统计,LPO含最下降0.827±1.048 nmol/ml(P<0.05)。Na~+-K~+-ATPase活性增加0.057±0.074μmol Pi/mg pro/hr(P<0.05)。认为654-2可能有抗衰老作用,并与普鲁卡因比较,讨论了其降低LPO的可能途径。  相似文献   
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中老年人脾肾虚证与血脂及抗氧化物关系的探讨   总被引:1,自引:0,他引:1  
采用前瞻性设计方案,利用现代先进的有针对性的指标,应用单因素及多因素综合分析方法,对773例中老年人进行脾肾虚证实质的研究。结果发现:中老年人肾虚证与脂质代谢紊乱、机体经物质减少、过氧化脂质增密切相关。同时发现,脾虚证到肾虚证是一个逐渐发展的病理过程,且有层次性。认为肾虚证脂质代谢紊乱程度高于脾虚证,脾虚证与机体抗氧化物减少无密切关系。  相似文献   
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Kainic acid (KA) administered systemically to rats produces seizures and brain damage. We measured an increase in reactive oxidant species (ROS) during KA-induced seizures in the extracellular fluid (ECF) of the piriform cortex, a brain region known to be subsequently damaged. Intracerebral microdialysis samples were collected and assayed for isoluminol-dependent chemiluminescence before and after injection of KA (16 mg/kg, ip). Hydrogen peroxide (H2O2) concentrations were calculated from catalase-sensitive chemiluminescence, the difference between total and catalase-resistant chemiluminescence. During generalized tonic-clonic seizures, both total and catalase-resistant chemiluminescence increased significantly in samples from brain ECF. Catalase-resistant chemiluminescence, most likely produced by ascorbic acid, increased for a full hour during sustained seizure activity. H2O2 concentrations showed a trend towards elevation during seizures. Increased ROS suggest that oxidative stress occurs in brain ECF during sustained seizure activity.  相似文献   
7.
Cytotoxic Effect of Brain Macrophages on Developing   总被引:3,自引:0,他引:3  
Brain macrophages are transiently present in different regions of the central nervous system during development or in the course of tissue remodelling following various types of injuries. To investigate the influence of these phagocytes on neuronal growth and survival, brain macrophages stemming from the cerebral cortex of rat embryos were added to neuronal primary cultures. A neurotoxic effect of brain macrophages was demonstrated by the reduction of the number of neurons bearing neurites within two days of contact between the two cell types. Neuronal death and phagocytosis were also directly observed in video recordings of living cultures. This toxicity involved the production by brain macrophages of reactive oxygen intermediates, as shown by the protective effect of catalase, a scavenger of H2O2. In addition, the respiratory bursts of brain macrophages were stimulated in the presence of neurons. These results suggest that brain macrophages could favour the appearance of neuroregressive events which occur either during neurogenesis or in neurodegenerative diseases, implying intracerebral recruitment of mononuclear phagocytes.  相似文献   
8.
目的 在体观察过氧化氢(H2O2)对豚鼠耳蜗功能及形态的影响。方法 实验动物分为4组,分别灌流人工外淋巴液(artificial perilymph,APL),50μMH2O2,100μMH2O2和200μMH2O2(H2O2均溶于APL中),并用Pl和H033342双染色方法观察H2O2引起的内耳细胞损伤情况。结果 所有H2O2灌流组复合动作电位((CAP)阈移和耳蜗微音电位(CM)幅度变化与人工外淋巴液组比较差异有显著性,且各H2O2组的变化呈现出浓度依赖性;Pl和H033342双染色方法发现外毛细胞是H2O2攻击的主要靶细胞,而Hensen细胞未见任何损伤痕迹。结论 H2O2可导致耳蜗功能下降及耳蜗毛细胞损伤:Hensen细胞较毛细胞可能具有更强的抗氧化能力。  相似文献   
9.
2-吡啶甲醇及2-吡啶甲醛的合成   总被引:2,自引:0,他引:2  
以 2 -甲基吡啶为原料、过氧化氢为氧化剂制备 2 -吡啶甲醇和 2 -吡啶甲醛,工艺方法经济、安全  相似文献   
10.
To determine the role of the phospholipase D (PLD) pathway in injury and survival of alveolar epithelial cells, A549 cells were exposed to H2O2 (500 μM) which resulted in time-dependent injury and bi-phasic increase of PLD activity at 5 min and at 3 h, respectively. n-Butanol (0.5%) inhibited PLD activation, attenuated cell injury at 5 min of H2O2 exposure, but enhanced injury at 3 h of exposure. This activation was inhibited by treatment with catalase (500 units/ml). Exogenous phosphatidic acid mimicked the effects of PLD activation, and diphenyliodonium (NADPH oxidase inhibitor) reversed the decline in cell viability induced by H2O2 exposure. Propranolol (phosphatidic acid phospholydrolase inhibitor) and quinacrine (phospholipase A2 inhibitor) had weak effects on H2O2-induced PLD activation but reversed H2O2-induced injury. We speculate that PLD activation at the initiation of H2O2 exposure predominantly results in NAPDH oxidase activation, which mediates A549 cell injury, but turns to mediating cell survival as the H2O2 attack continues, which might be mainly due to the accumulation of intracellular phosphatidic acid.  相似文献   
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