Reactive oxidant species in piriform cortex extracellular fluid during seizures induced by systemic kainic acid in rats

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.     

Cumulative biochemical effects of repeated subclinical hydrogen sulfide intoxication in mouse brain

Summary Adult female NMRI mice exposed four times to 100 ppm hydrogen sulfide vapour for 2 h at 4-day intervals showed increasing inhibition of the cerebral cytochrome oxidase activity. Cerebral RNA decreased significantly after the fourth exposure. This change was accompanied by the reduced orotic acid uptake in the RNA fraction. At the same time, 2,3-cyclic nucleotide 3-phosphohydrolase activity used as a marker for glia increased. Acetylcholine esterase activity remained unchanged. The initial exposures also caused an increase in the superoxide dismutase activity and an increase in the glutathione concentration. The latter effects were abolished in the third and fourth exposures. The present data seem to indicate that the biochemical effects of repeated subclinical hydrogen sulfide intoxications are cumulative.     

膳食蛋白质对荷瘤小鼠生长的影响

将72只昆明种雌性小鼠随机分为高蛋白饲养组和低蛋白饲养组,分别在两组中设立对照组和实验组,实验组小鼠接种艾氏腹水瘤。3周喂养实验表明:高蛋白各组小鼠体重高于低蛋白组,且高蛋白荷瘤组小鼠瘤径大于低蛋白组瘤组。高蛋白组和低蛋白组,荷瘤小鼠肝过氧化氢酶和超氧化物歧化酶活性均低于对照组(P<0.01;P<0.05),而荷瘤小鼠肝过氧化脂质明显高于对照组(P<0.05)。结果提示:患瘤早期,可能存在一个“营养适宜期”,患瘤后期增加营养,要采取谨慎态度。     

Cytotoxic Effect of Brain Macrophages on Developing

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.     

不同浓度乙醇对内皮细胞分泌作用的影响

目的 研究不同浓度乙醇对内皮细胞的保护作用。方法 应用过氧化氢损伤培养的人脐静脉内皮细胞,并与不同浓度乙醇进行孵育,检测内皮细胞产生的内皮素及一氧化氮。结果低、中浓度乙醇明显减少损伤的内皮细胞产生的内皮素。同时实验还提示长时间高浓度乙醇对内皮细胞有明显损伤作用;不同浓度的乙醇均抑制内皮细胞产生一氧化氮。结论低、中浓度乙醇使内皮细胞在受损时生成的内皮素明显减少。     

原花青素对大鼠心肌缺血再灌注损伤的保护作用

目的：观察原花青素（procyanidin,PC）对大鼠心肌缺血再灌注损伤的保护作用，方法：结扎大鼠冠状动脉左前降支（LAD）40min，复灌120min后复制出大鼠心肌缺血再灌注损伤模型，观察PC对大鼠心肌酶学，心梗面积和脂质过氧化的影响。结果：PC能减少心肌细胞磷酸肌酶激酶（CPK）和乳酸脱氢酶（LDH）的释放，明显缩小心肌梗死面积，能显提高大鼠血清和心肌组织中超氧化物歧化酶（SOD）活性，降低心肌和血清脂质过氧化代谢产物丙二醛（MDA）含量，结论：PC对大鼠心肌缺血再灌注损伤有保护作用，其机制可能与清除自由基，抑制脂质过氧化反应有关。     

金粉蕨素拮抗血管内皮细胞氧化应激损伤及机制

目的 :研究金粉蕨素 (onychin ,Ony)对血管内皮细胞氧化应激损伤的影响及可能机制。方法 :培养人脐静脉血管内皮细胞株 (ECV30 4 ) ,经Ony处理后 ,用过氧化氢 (H2 O2 )对其损伤 ;用MTT比色法和乳酸脱氢酶测定法分别检测损伤组和处理组细胞增殖活性和功能状态 ;用Western Blot法检测磷酸化ERK1 2和p38、P90RSK蛋白的表达。结果 :不同浓度的Ony(0 .3、1、3、10 μmol·L-1)促进H2 O2 损伤的内皮细胞增殖 ,减少LDH释放 ,并呈浓度依赖性。Ony(3μmol·L-1)抑制H2 O2 诱导的磷酸化p38表达 ,30min时最明显 ,但并不影响H2 O2 对ERK的激活以及ERK下游蛋白激酶P90RSK的表达。而阳性对照药genistein虽可增加内皮细胞增殖活性和减少功能损伤 ,但明显抑制H2 O2 诱导的磷酸化ERK表达及其下游蛋白激酶P90RSK。结论 :Ony拮抗血管内皮细胞氧化应激损伤可能与抑制p38磷酸化有关。     

过氧化氢对豚鼠耳蜗功能及形态的影响

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。     

Responses of antioxidant systems in the hepatocytes of common carp (Cyprinus carpio L.) to the toxicity of microcystin-LR.

The freshwater, bloom-forming cyanobacterium (blue-green alga) Microcystis aeruginosa produces a peptide hepatotoxin, which causes the damage of animal liver. Recently, toxic Microcystis blooms frequently occur in the eutrophic Dianchi Lake (300 km2 and located in the South-Western of China). Microcystin-LR from Microcystis in Dianchi was isolated and purified by high performance liquid chromatography (HPLC) and its toxicity to mouse and fish liver was studied (Li et al., 2001). In this study, six biochemical parameters (reactive oxygen species, glutathione, superoxide dismutase, catalase, glutathione peroxide and glutathione S-transferase) were determined in common carp hepatocytes when the cells were exposed to 10 microg microcystin-LR per litre. The results showed that reactive oxygen species (ROS) contents increased by more than one-time compared with the control after 6 h exposure to the toxin. In contrast, glutathione (GSH) levels in the hepatocytes exposed to microcystin-LR decreased by 47% compared with the control. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxide (GSH-Px) increased significantly after 6 h exposure to microcystin-LR, but glutathione S-transferase (GST) activity showed no difference from the control. These results suggested that the toxicity of microcystin-LR caused the increase of ROS contents and the depletion of GSH in hepatocytes exposed to the toxin and these changes led to oxidant shock in hepatocytes. Increases of SOD, CAT and GSH-Px activities revealed that these three kinds of antioxidant enzymes might play important roles in eliminating the excessive ROS. This paper also examined the possible toxicity mechanism of microcystin-LR on the fish hepatocytes and the results were similar to those with mouse hepatocytes.     

菲啰啉对不同氧化剂和多柔比星所致CHL细胞DNA链断裂的影响

目的 为了研究菲啰啉对2种氧化剂和抗癌药多柔比星诱发细胞DNA损伤的影响, 并初步探讨其损伤机制。方法 用不同浓度菲啰啉预处理CHL细胞30 min, 再分别加入3种不同染毒受试物,共同培养一定时间(0.3 mmol·L^-1重铬酸钾：105 min； 0.5 μmol·L^-1多柔比星：5 min； 0.4 mmol·L^-1过氧化氢(H₂O₂)：25 min)后, 用碱性单细胞凝胶电泳方法(ASCGE)测定DNA链断裂情况, 并同时以菲啰啉与二甲亚砜(DMSO，0.33 mol·L^-1)比较对H₂O₂致DNA损伤中·OH的产生和清除。结果 3种染毒受试物均可明显引起CHL细胞DNA链断裂；而当3 μmol·L^-1菲啰啉预处理后, 可使重铬酸钾、H₂O₂所致DNA迁移长度和细胞拖尾率明显降低, 并超过DMSO降低H₂O₂的损伤作用, 当菲啰林浓度升至12 μmol·L^-1时, 可完全消除这两种因素所致的DNA链断裂损伤；10 μmol·L^-1菲啰啉可抑制多柔比星所致DNA损伤, 但浓度直至60 μmol·L^-1仍不能完全消除多柔比星的损伤作用。结论 菲啰啉对2种氧化剂和多柔比星所致DNA损伤均有不同程度的防护作用,同时提示重铬酸钾和H₂O₂所致的DNA损伤主要与需过渡金属离子参与的·OH产生有关, 而多柔比星所致损伤仅部分与此有关。