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第14届国际自由基大会纪要
由国际自由基学会(Society for Free Radical Research International,SFRRI)授权,中国生物物理学会自由基生物学和医学专业委员会承办,中国生物化学与分子生物学会临床应用生物化学与分子生物学分会、解放军总医院和中华预防医学会自由基生物医学专业委员会协办,SFRRI、亚洲自由基学会(SFRR Asia)、美国加州氧自由基学会(OCC),国家自然科学基金委员会、中国科学院生物物理研究所资助的第14届国际自由基大会于2008年10月18至22日在北京成功召开.
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AIM To study the relationship between the lipid peroxide (LPO) and superoxide dismutase (SOD) and thepathogenesis of gastrointestinal cancers.METHODS We investigated the SOD activity and LPO levels in blood and mucosa of patients withesophageal (EC), gastric (GC) and colorectal cancer (CC), gastric ulcer (GU) and compared with normalesophagus (NE), stomach (NS) and colon (NC). respectively, 287 patients who underwent endoscopy werestudied. SOD activity of the tissue and blood was determined using SUN's adrenaline auto oxidation method.LPO levels were determined according to YU's method.RESULTS The SOD activity and LPO level in blood and mucosa are shown in the Table 1 (x±Sx).Table 1 SOD and LPO in blood and tissues of patients with gastrointestinal cancers SOD(U/mg protein) LPO(U/mg)Groups n Tissue blood Tissue BloodNormal stomachGastric ulcerGastric cancerNormal esophagusEsophageal cancerNormal colonColon cancer 60 42 43 32 52 28 30 1.90±0.18 0.64±0.40a 0.37±0.24a 1.17±0.70 0.39±0.30a 0.81±0.36 0.31±0.17b 33.70±1.73 25.50±0.67b 27.86±1.02b 30.80±3.78 28.23±10.63 20.97±4.77 19.35±7.32 0.01±0.004 0.05±0.010b 0.06±0.021b 0.014±0.005 0.061±0.033b 0.012±0.003 0.069±0.015b 0.83±0.01 0.11±0.02 0.12±0.03 0.08±0.02 0.11±0.02 0.08±0.03 0.11±0.02aP<0.001, bp<0.01 vs corresponding normal controls, respectively.CONCLUSION SOD activity of the tissue is significantly decreased in EC. GC and CC. LPO levels weresignificantly higher than those of corresponding normal tissue. These results suggest that mucosal SOD andLPO levels are closely related to the pathogenesis of the gastrointestinal cancers.
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实验性急性坏死性胰腺炎并发肺损伤大鼠血液、肺组织中氧自由基代谢变化
急性坏死性胰腺炎(Acute necrotizing pancreatitis, ANP)常并发肺损伤,其发生机制尚不甚清楚,本实验旨在探讨氧自由基(Oxygen free radical, OFR)在大鼠并发肺损伤中的作用.实验中用SD大鼠32只,雌雄不限,体重250~300 g,由陕西省中医研究院提供,随机分成:对照组(n=16);实验组(n=16).
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抗氧化剂在新生鼠高氧肺损伤治疗中的作用研究
目前,普遍认为:高氧肺损伤与氧自由基(oxygen free radical,OFR)的活性、炎性细胞的激活[1]以及细胞因子的释放有关.SOD抗氧化作用的安全性及疗效已得到了肯定[2].U74389G作为一种合成21-氨基类固醇的抗氧化剂,是甲基强的松龙提取物,没有激素活性,具有高亲脂性,易穿过细胞膜,是有效的铁离子螯合剂及有效的脂质过氧化物阻碍者.有报道[3],U74389G通过抑制高氧肺氧自由基、减轻炎症而减轻肺损伤,本研究观察了抗氧化剂U74389G及SOD对高氧暴露新生大鼠肺内组织氧自由基的产生、脂质过氧化物丙二醛(malondialdehyde,MDA)的产生、SOD的活性、肺的病理改变及对肺细胞凋亡的影响而阐述高氧肺损伤的机理,以探讨两者的抗氧化作用及两者的疗效比较.
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In this study, we hypothesized that total flavonoid of Litsea coreana leve (TFLC) protects against focal cerebral ischemia/reperfusion injury. TFLC (25, 50, 100 mg/kg) was administered oral y to a rat model of focal ischemia/reperfusion injury, while the free radical scavenging agent, edaravone, was used as a positive control drug. Results of neurological deficit scoring, 2,3,5-triphenyl tetrazolium chloride staining, hematoxylin-eosin staining and biochemical tests showed that TFLC at different doses significantly al eviated cerebral ischemia-induced neurological deficits and histopathological changes, and reduced infarct volume. Moreover, it suppressed the increase in the levels of nitrates plus nitrites, malondialdehyde and lactate dehydrogenase, and it diminished the reduction in gluta-thione, superoxide dismutase and catalase activities induced by cerebral ischemia/reperfusion in-jury. Compared with edaravone, the protective effects of TFLC at low and medium doses (25, 50 mg/kg) against cerebral ischemia/reperfusion injury were weaker, while the protective effects at high dose (100 mg/kg) were similar. Our experimental findings suggest that TFLC exerts neuroprotective effects against focal cerebral ischemia/reperfusion injury in rats, and that the effects may be asso-ciated with its antioxidant activities.
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中药对心脏手术心肌缺血再灌注损伤的保护作用
随着心脏外科的迅速发展,对于体外循环(cardiopulmonarybypass,CPB)中心肌保护的要求越来越高.CPB心内直视手术过程中,造成心脏损伤原因,除手术本身外,心肌缺血再灌注损伤(myocardial ischemia reperfusion iniury,MIRI)也是其重要的因素.目前认为,CPB再灌注过程中氧自由基(oxygen free radical,0FR)的暴发性产生是造成心肌损伤的重要因素.
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雪莲黄酮对大鼠创伤性脑水肿的治疗机制研究
Background: A large amount of free radical formation and lipid peroxidization play an important role in development of traumatic cerebrodema.xuelianhuangtong showed a strong effect antiinflammatory and antiperoxidization ,and might have an therapeutic effect on treatment of cerebrodema.No report about this was published.
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参麦注射液对自由基损伤后海马神经细胞凋亡的影响
参麦注射液是中医院急症常备之药,治疗气阴两虚证,疗效确切.我们采用胞形态学、细胞化学方法,试图阐明参麦注射液对胎鼠海马神经细胞氧自由基损伤后发生凋亡的影响,现将研究结果报告于下.
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被动吸烟对大鼠胰腺损伤的研究
吸烟是一种呈全世界流行的生活习惯.有研究发现,吸烟与胰腺癌(PC)和慢性胰腺炎(CP)发展有关[1,2].本研究采用香烟烟雾染毒法模拟被动吸烟状态,观察吸烟所致大鼠胰腺损伤并探讨香烟中氧自由基(oxygen free radical,OFR)在胰腺损伤中的作用.
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急性乙醇性胃黏膜损伤中三磷酸腺苷合成酶6和8亚基的表达
乙醇是导致胃黏膜损伤的一个常见因素,它可通过多种机制损伤胃黏膜,氧自由基(oxygen free radical,OFR)对胃黏膜的氧化应激作用是其中的一个重要方面.线粒体是细胞内易受乙醇作用而损伤的细胞器,其中线粒体DNA(mitochondrial,mtDNA)又是细胞内乙醇相关氧化应激的主要目标.
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2-(2-乙缩醛)邻苯二甲酸酯对小鼠睾丸、肝脏、肾脏和胰腺的短期影响
Aim: To determine the biochemical effect of di-(2-ethylhexyl) phthalate (DEHP) on testes, liver, kidneys and pancreas on day 10 in the process of degeneration of the seminiferous epithelium. Methods: Diets containing 2% DEHP were given to male Crlj:CD1(ICR) mice for 10 days. The dose of DEHP was 0.90 ± 0.52 mg/mouse/day. Their testes, livers, kidneys and pancreata were examined for detection of mono-(2-ethylhexyl) phthalate (MEHP), nitrogen oxides (NOx) produced by peroxidation of nitric oxide (NO) with free radicals, and lipid peroxidation induced by the chain reaction of free radicals. Results: Histological observation and serum analysis showed the presence of severe spermatogenic disturbance, Leydig cell dysfunction, liver dysfunction and dehydration. Unexpectedly, the concentration of MEHP in the testes was extremely low compared with that in the liver. However, the concentration of the NOx in the testes was as high as the hepatic concentration. Furthermore, free radical-induced lipid peroxidation was histochemically detected in the testes but not in the liver. Conclusion: The results indicate that DEHP-induced aspermatogenesis is caused by the high sensitivity of the testicular tissues to MEHP rather than the specific accumulation or uptake of circulating MEHP into the testes.
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别嘌醇治疗新生儿缺氧缺血性脑病疗效评价
1 文献来源[1]Van Bel F,Shadid M,Moison RM,et al.Effect of allopurinol on postasphyxial free radical formation,cerebral hemodynamics,and electrical brain activity.Pediatrics,1998,101(2):185-193
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氧自由基与分泌性中耳炎
分泌性中耳炎(secretory otitis media,SOM)是以鼓室积液及听力下降为主要特征的中耳非化脓性炎性疾病.关于SOM的发病机理至今未明确,其中以各种原因所致咽鼓管功能障碍受重视.关于-氧化氮(nitric oxide,NO)、一氧化氮合酶(nitric oxide synthase,NOS)及氧自由基(oxygen free radical,OFR)在SOM中作用的研究较少,本文就此做简要概述.
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氧自由基对精子功能的影响
氧自由基(oxygen free radical,OFR)又叫活性氧簇(reactive oxygen species, ROS),是近年来研究较多的体内信息基团和效应基团研究较多.作为机体氧代谢过程中产生的一类化学基团,其广泛存在于心血管、神经、免疫、消化、生殖及呼吸系统器官的细胞内.正常情况下,ROS的生成与清除处于动态平衡,以维持机体结构的完整和功能正常.如果ROS浓度过高可以导致细胞病理的改变.生殖细胞跟机体其它细胞一样容易受到ROS的损伤.所以在精子发生、发育、成熟、贮藏各个阶段都需要抗氧化物的保护.近又有实验证实ROS有信号传递的作用,而且在生殖过程的某些关键环节中,这种信使ROS有很重要的调节作用.
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AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na+-K+-ATPase and Ca2+-ATPase in model group was decreased. Contrast to the model group, the activity of Na+-K+-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2+-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na+-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2+-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.