昆虫体内抗氧化系统研究进展

昆虫为了减轻和防止活性氧损伤,已形成了复杂的氧化应激机制。可通过酶促如超氧化物歧化酶、过氧化物酶、过氧化氢酶等和非酶促谷胱甘肽、抗坏血酸和胡萝卜素等清除活性氧的系统以清除过量的活性氧。本文论述了昆虫在氧化胁迫下所具有的一套抗氧化系统。对其系统组成抗氧化酶和抗氧化剂的主要成分的抗氧化活性进行了综述。     

松果菊苷抗衰老作用机理研究

研究了中国传统药物肉苁蓉提取物松果菊苷(echinacoside,ECH)体外清除活性氧自由基和体内抗氧化、抗衰老作用的机理。运用电子顺磁共振(electron paramagretic resonance,EPR)自旋捕捉方法研究ECH对体外产生的羟自由基(^ OH)、超氧阴离子自由基(O2^-)和脂自由基(L^ )的清除能力;并以D-半乳糖衰老小鼠为实验模型,采用低温EPR技术直接检测小鼠心、肝、肾、脑组织活性氧物种(reactive oxygen species,ROS)水平;生化方法检测小鼠全血谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)和脑组织单胺氧化酶(monoaminoxidase,MAO)活性及肝组织丙二醛(malondialdehvde,MDA)含量;EPR自旋捕捉方法检测血清超氧化物歧化酶(supemxide dismutase,SOD)活力;跳台法检测小鼠记忆力。结果表明ECH能较好抑制体外^ OH,O2^-和L^ 自由基,同时能够提高GSH-Px和SOD活性,降低MDA含量,因此对D-半乳糖所致衰老引起的活性氧自由基损伤具有一定修复作用。由于抑制了MAO活性而提高小鼠的记忆力。由此可以认为ECH抗脂质过氧化及改善衰老的作用与其抗氧化活性有关。     

NaHCO3胁迫下外源海藻糖对南蛇藤几种与抗逆性有关的生理生化指标变化的影响

NaHCO3胁迫下叶面喷施海藻糖(trehalose,TR)的南蛇藤叶中活性氧(O2和H2O2)产生速率、丙二醛(MDA)含量以及电解质外渗率显著下降(P<0.05),超氧化物歧化酶(SOD),过氧化氢酶(CAT)、过氧化物酶(POD),抗坏血酸过氧化物酶(APX)和谷胱甘肽还原酶(GR)活性以及抗坏血酸(AsA)和还原型谷胱甘肽(GSH)含量明显提高.显示外源海藻糖可在一定程度上提高NaHCO3胁迫下的南蛇藤叶细胞膜保护功能,减少叶中活性氧的积累,抑制脂质过氧化,从而提高南蛇藤抗NaHCO3胁迫的能力.     

慢性镉暴露对背角无齿蚌肝脏的氧化损伤效应

目的:探明氯化镉(CdCl2)暴露对背角无齿蚌肝脏中抗氧化酶活力及脂质过氧化的影响。方法:根据背角无齿蚌96 h镉离子(Cd²⁺)半致死剂量设置1个对照组和2个处理组(0.1和0.5 mg/L),分别检测镉暴露4周及镉清除4周期间背角无齿蚌肝脏中抗氧化酶[超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)、过氧化氢酶(CAT)]的活力和脂质过氧化物丙二醛(MDA)的含量。结果:不同浓度Cd²⁺暴露对背角无齿蚌抗氧化酶活力及脂质过氧化产生不同程度的影响,低浓度Cd²⁺暴露的毒性效应较弱,高浓度Cd²⁺暴露可显著抑制肝脏SOD活力,诱导GPx活力升高,在暴露后期显著抑制CAT活力,MDA含量随着暴露时间的延长而显著升高。结论:慢性Cd²⁺暴露可影响背角无齿蚌肝脏抗氧化酶活力,引起脂质过氧化损伤,且作用机制与急性毒性不同。     

夜间低温胁迫对番茄叶片活性氧代谢及AsA-GSH循环的影响

以番茄品种‘辽园多丽’为试材,利用人工气候室模拟设施生产中的夜间低温胁迫环境,研究9℃和6℃夜低温对番茄叶片活性氧代谢和AsA-GSH循环的影响。结果显示:9℃和6℃夜间低温胁迫3～9d可诱导番茄叶片中超氧阴离子(O2.-)产生速率、过氧化氢(H2O2)和丙二醛(MDA)含量上升;抑制过氧化物酶(POD)、过氧化氢酶(CAT)的活性,增加超氧化物歧化酶(SOD)和AsA-GSH循环中抗坏血酸过氧化物酶(APX)、脱氢抗坏血酸还原酶(DHAR)、谷胱甘肽还原酶(GR)的活性,并提高还原型抗坏血酸(AsA)、还原型谷胱甘肽(GSH)、氧化型谷胱甘肽(GSSG)的含量。研究表明,在夜间低温胁迫过程中,增加的番茄叶片中SOD活性和AsA-GSH循环清除活性氧的能力并未与氧还原的速率一致,从而导致番茄叶片中活性氧的累积,使细胞膜系统受到一定破坏,在6℃处理的植物中尤为明显。     

两种莪术类药用植物姜黄素提取物对小鼠抗氧化活性研究

本研究通过对两种莪术类药用植物姜黄素提取物,结合3种姜黄素的含量分析其对小鼠的抗氧化药效。通过高效液相色谱法测定总姜黄素提取物中3种姜黄素的含量。选取48只雌性小鼠,随机分成4组分别灌胃提取液(含1组喂基础饲料)。正常饲喂14 d后,小鼠采血测定SOD (超氧化物歧化酶)、CAT (过氧化氢酶)、GSH-Px (谷胱甘肽过氧化物酶)、XOD (黄嘌呤氧化酶)及NO (一氧化氮)、MDA (丙二醛)含量。结果表明,经姜黄素提取液灌胃的小鼠,SOD、CAT、XOD活性升高,NO含量下降;GSH-PX活性普遍升高,MDA含量普遍下降;2种莪术抗氧化活性具有差异性,浓度或含量与抗氧化活性不具有正相关关系;产地不同,也是影响体内抗氧化活性的因素之一。     

无瓣海桑果实提取物对衰老小鼠学习 记忆能力的影响及其机制研究

无瓣海桑果实为真红树无瓣海桑的果实。研究无瓣海桑果实不同提取物对D-半乳糖所致衰老小鼠学习记忆能力影响及其作用机制。采用Morris水迷宫实验测量无瓣海桑果实不同提取物对小鼠的学习记忆能力影响,HE染色观察各组小鼠脑部神经细胞的变化情况,并测定脑组织超氧化物歧化酶(SOD)活力、谷胱甘肽过氧化物酶(GSH-Px)活力、一氧化氮(NO)含量和单胺氧化酶(MAO)活力。结果表明:与模型组相比,无瓣海桑果实不同提取物处理组小鼠在水迷宫实验中逃避潜伏期明显缩短(P0.05),目标象限停留时间明显增加(P0.05)。无瓣海桑果实不同提取物处理组小鼠脑部神经细胞损伤与模型组相比明显减少,小鼠脑部SOD酶活力和GSH-Px酶活力提高(P0.05),NO含量和MAO活力在脑部显著降低(P0.05)。无瓣海桑果实不同提取物对D-半乳糖致衰老小鼠学习记忆能力有改善作用,无瓣海桑果实不同提取物通过提高小鼠脑内源抗氧化酶(SOD、GSH-Px)活力,降低脑部NO含量和MAO活力来提高D-半乳糖致衰老小鼠的学习记忆能力。     

云芝提取物对改善小鼠胃肠功能的作用

以大黄水煎剂建立小鼠胃肠功能损害模型,探讨云芝提取物和其中的白桦脂酸对小鼠胃肠功能的影响以及白桦脂酸对小鼠在脂质过氧化方面的影响。研究结果表明云芝提取物和白桦脂酸能够较为显著地提高胃蛋白酶活性,增加胃泌素和胃酸分泌量（P<0.01）;同时白桦脂酸高低剂量组能够明显降低小鼠血浆中丙二醛的含量,提高超氧化物歧化酶、谷胱甘肽过氧化物酶的活性以及肝脏匀浆中谷胱甘肽过氧化物的含量（P<0.01）。说明云芝提取物和白桦脂酸能够有效地改善小鼠的胃肠功能,且抗脂质过氧化是云芝活性成分白桦脂酸治疗作用机制之一。     

外源亚精胺对盐胁迫下黄瓜(Cucumis sativus L.)叶绿体活性氧清除系统和结合态多胺含量的影响

采用营养液水培,研究了外源亚精胺(Spd)对NaCl胁迫下抗盐能力不同的两个黄瓜品种幼苗生长、叶绿体中活性氧清除系统、转谷酰胺酶(TGase)活性、结合态多胺含量及植株光合速率的影响.结果表明,外源Spd能提高NaCl胁迫下叶绿体中TGase活性、叶绿体结合态腐胺(Put)、Spd、精胺(Spm)及总多胺含量;提高超氧化物歧化酶(SOD)、抗坏血酸过氧化物酶(APX)和谷胱甘肽还原酶(GR)活性,提高抗坏血酸(AsA)、类胡萝卜素(Car)、还原型谷胱甘肽(GSH)含量及还原型谷胱甘肽/氧化型谷胱甘肽(GSH/ GSSG)比值,降低脱氢抗坏血酸/抗坏血酸(DAsA/AsA)比值;同时显著降低叶绿体过氧化氢(H2O2)和丙二醛(MDA)含量,提高植株净光合速率,缓解NaCl胁迫对幼苗生长的抑制.表明Spd对黄瓜盐害的缓解作用之一可能是通过提高叶绿体结合态多胺含量和叶绿体活性氧清除能力,从而缓解盐胁迫对叶绿体膜的伤害.     

黄芩素-7-甲醚对高原缺氧小鼠脑组织保护作用研究

研究黄芩素-7-甲醚对高原缺氧小鼠脑组织的保护作用及机制。用50只小鼠进行常压耐缺氧实验,测定黄芩素-7-甲醚的有效剂量。然后将88只小鼠随机分为正常对照组、缺氧模型组、芦丁组和黄芩素-7-甲醚组,连续灌胃给药5天,最后一个给药60 min后,置于模拟海拔8000 m氧舱内停留12 h,检测脑组织中含水量、过氧化氢(H2O2)、一氧化氮(NO)、丙二醛(MDA)、乳酸脱氢酶(LDH)、抗氧化酶以及Nrf2和HO-1蛋白的表达情况。结果发现:低压低氧能够诱导小鼠脑含水量、脑组织中H_2O_2、NO和MDA含量以及LDH活性显著增加,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性显著减低,Nrf2和HO-1蛋白表达增强。经黄芩素-7-甲醚预处理后能够显著降低高原缺氧小鼠脑组织中H_2O_2、MDA和NO含量以及LDH活性,提高抗氧化酶的活性,同时进一步增加Nrf2和HO-1蛋白的表达。以上结果表明:黄芩素-7-甲醚能够缓解高原缺氧导致脑组织氧化应激损伤,作用机制可能与清除自由基,激活Nrf2/ARE/HO-1信号途径,提高抗氧化酶活性有关。     

Protective effect of chelerythrine on gentamicin-induced nephrotoxicity

Despite their beneficial effects, aminoglycosides including gentamicin (GEN) have considerable nephrotoxic side-effects. The toxicity of GEN at the level of the kidney seems to relate to the generation of reactive oxygen species (ROS). ROS have been reported to be involved in the activation of protein kinase C (PKC). The unique structural aspects of PKC cause it to function as a sensor for oxidative stress. It seems likely that the increased NAD(P)H oxidase-derived superoxide (O2) production is at least in part mediated by PKC. We investigated the effects of chelerythrine, a commonly used PKC inhibitor, on GEN-induced changes of renal malondialdehyde (MDA), nitric oxide (NO) generation, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities, glutathione (GSH) content, and serum creatinine (Cr), blood urea nitrogen (BUN) levels. Morphological changes in the kidney were also examined. GEN administration to control rats increased MDA and NO generation but decreased CAT, SOD and GSH-Px activities, and GSH content. Chelerythrine administration with GEN caused significantly decreased MDA, NO generation and increased CAT, SOD and GSH-Px activities, and GSH content when compared with GEN alone. Chelerythrine also significantly decreased serum Cr and BUN levels. Morphological changes in the kidney including tubular necrosis were evaluated qualitatively. Both biochemical findings and histopathological evidence showed that administration of chelerythrine reduced the GEN-induced kidney damage. We propose that chelerythrine acts in the kidney as a potent scavenger of free radicals to prevent the toxic effects of GEN via the inhibition of a PKC pathway.     

镉对长江华溪蟹精巢抗氧化酶活性及脂质过氧化的影响

在实验条件下,将健康性成熟雄性长江华溪蟹Sinopotamon yangtsekiense暴露于0、7.25、14.5、29、58和116 mg/L浓度的镉(Cd2+)溶液中,分别于1 d、3 d、5 d和7 d时测定精巢中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氧酶(CAT)活性及脂质过氧化产物丙二醛(MDA)的含量.结果显示,不同时间段3种酶活性和MDA含量均具有浓度和时间效应关系,表明急性镉暴露对精巢有明显的毒性作用,其作用机制与抗氧化酶活力变化和脂质过氧化加剧有关.     

全氟辛烷磺酸钾对小鼠肾脏的氧化性损伤

目的:以小鼠肾脏细胞中的活性氧(ROS)、丙二醛(MDA)、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力为指标,探讨全氟辛烷磺酸钾(PFOS-K)对小鼠肾脏的氧化性损伤作用。方法:以剂量为6mg/kg·bw、12 mg/kg·bw、24 mg/kg·bw 3个浓度的PFOS-K混悬液,每天分别给小鼠经口灌胃一次,连续染毒20天后检测肾脏脏器系数,以及肾脏中ROS、MDA、GSH含量的变化和SOD、GSH-Px、CAT活性的改变。结果:与阴性对照组相比,在6-24 mg/kg·bw剂量范围内,PFOS-K使小鼠体重下降、肾脏重量增加、肾脏脏器系数增大,且表现出一定的剂量-效应关系(r小鼠体重=-0.905,r肾脏湿重=0.938,r脏器系数=0.936)。PFOS-K使小鼠肾脏内活性氧(ROS)及丙二醛(MDA)含量增多(rROS=0.990,rMDA=0.997)、谷胱甘肽(GSH)含量减少(rGSH=-0.994),超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活力降低(rSOD=-0.917,rGSH-Px=-0.986,rCAT=-0.991)。结论:本试验条件下,PFOS-K致使小鼠肾脏肿大,影响了肾脏的发育;造成了肾脏的氧化性损伤,肾组织内抗氧化酶系统遭到破坏,氧化应激反应增强,具有氧化损伤作用。     

The contradictory effects of nitric oxide in caerulein-induced acute pancreatitis in rats

This study was planned to observe the effects of nitric oxide synthesis on the antioxidative defense enzymes and pancreatic tissue histology in caerulein-induced acute pancreatitis. Acute pancreatitis was induced by intraperitoneal injections of 50 microg/kg caerulein, L-arginine used for NO induction and N(omega)-nitro-L-arginine methyl ester (L-NAME) used for NO inhibition. In the caerulein group acinar cell degeneration, interstitial inflammation, oedema and haemorrhage were detected. Pancreatic damage scores were decreased with both NO induction and inhibition (p<0.05). MDA, GSH-Px, CAT, GSH and SOD activities were significantly changed in the caerulein group and indicated increased oxidative stress. Both NO induction and inhibition decreased this oxidative stress. It is concluded that both nitric oxide induction and inhibition ameliorated caerulein-induced acute pancreatitis. The findings indicate that a certain amount of NO production has beneficial effects in experimental acute pancreatitis, but uncontrolled over-production of NO may be detrimental.     

乙酰唑胺对氧惊厥潜伏期的影响

为探讨脑血流调节与氧惊厥的关系,在复制大鼠氧惊厥模型的基础上,采用行为学方法测定氧惊厥潜伏期,并测定不司部位脑组织氧化与抗氧化指标,采用腹腔注射不同剂量脑血管扩张药物乙酰唑胺,观察脑血管扩张对氧化状态以及氧惊厥潜伏期的影响。观察结果为:(1)与生理盐水组相比,乙酰唑胺200、20 mg/kg体重组腹腔给药后氧惊厥潜伏期(纯氧6 ATA暴露)明显缩短(P<0.01),乙酰唑胺2 mg/kg体重组无明显改变(P>0.05);(2)腹腔给乙酰唑胺(20 mg/kg体重)或生理盐水后,各组各部位脑组织GSH-PX无显著差异(P>0.05),但随暴露时间的延长,其活力呈现先升高后降低的趋势;与对照组相比,乙酰唑胺6min组和生理盐水16min组皮层丙二醛(maleic dialdehyde,MDA)含量均明显增多(P<0.01),乙酰唑胺16 min组海马MDA含量明显增多(P<0.01)。结果表明,乙酰唑胺可缩短氧惊厥潜伏期,加重脑组织氧化损伤。     

腹腔注射乙酰唑胺对大鼠氧惊厥潜伏期的影响

为探讨脑血流调节与氧惊厥的关系,本研究在复制大鼠氧惊厥模型的基础上,采用行为学方法测定氧惊厥潜伏期,并测定脑皮质氧化指标内二醛（maleic dialdehyde,MDA）含量,采用腹腔注射不同剂量脑血管扩张药物乙酰唑胺（acetazolamide,ACZ）,以及联合注射ACZ及其拈抗刺吲哚美辛（indomethacin,IND）后,观察脑血管扩张对氧化状态以及氧惊厥潜伏期的影响。结果观察到：（1）腹腔注射ACZ（不小于7．5mg／kg体重）后,氧惊厥潜伏期明显缩短（P〈0．05）,剂量越大,缩短越明显。腹腔注射IND对氧惊厥潜伏期无显著影响。腹腔注射IND（20mg／kg体重）,30min后再注射ACZ（7．5mg／kg体重）,ACZ的氧惊厥潜伏期缩短作川被对抗（P〈0．05）。（2）腹腔注射ACZ7．5mg／kg后,与各组相比,6及16min暴露后,脑组织MDA含量明显增多（P〈0．01,P〈0．05）;腹腔注射IND对脑皮质MDA含量无显著影响;在预注射IND,再注射ACZ后,MDA含量显著降低（P〈0．01,P〈0．05）。结果表明,ACZ外周注射加重氧化损伤,缩短氧惊厥潜伏期;而IND可以对抗其氧惊厥潜伏期缩短作用以及氧化损伤加重作用,碳酸酐酶活力变化很可能是通过影响脑血管状态而影响氧化损伤以及氧惊厥潜伏期。     

叶黄素酯对四氧嘧啶所致小鼠氧化损伤的保护性研究

目的研究万寿菊花中提取的叶黄素酯体内对四氧嘧啶所致的小鼠氧化损伤的影响。方法采用分光光度法测定模型组肝组织超氧化物歧化酶（SOD）、丙二醛（MDA）、过氧化氢酶（CAT）、谷脱甘肽（GSH）、血清中天门冬氨酶氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、肝糖原,脑、心脏、股四头肌SOD、MDA的活性。结果叶黄素酯可抑制由于氧化损伤所致的小鼠肝SOD、MDA、CAT、GSH和血清中AST、AIJT的异常升高;降低脑、心脏、股四头肌SOD、MDA水平;降低血糖,提高肝糖元水平。结论叶黄素可通过影响组织、血清中相关酶活性而对四氧嘧啶所致的小鼠氧化损伤有一定的保护作用。     

Protective effects of melatonin and caffeic acid phenethyl ester against retinal oxidative stress in long-term use of mobile phone: A comparative study

There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Melatonin and caffeic acid phenethyl ester (CAPE), a component of honeybee propolis, were recently found to be potent free radical scavengers and antioxidants. Mechanisms of adverse effects of EMR indicate that reactive oxygen species may play a role in the biological effects of this radiation. The present study was carried out to compare the efficacy of the protective effects of melatonin and CAPE against retinal oxidative stress due to long-term exposure to 900 MHz EMR emitting mobile phones. Melatonin and CAPE were administered daily for 60 days to the rats prior to their EMR exposure during our study. Nitric oxide (NO, an oxidant product) levels and malondialdehyde (MDA, an index of lipid peroxidation), were used as markers of retinal oxidative stress in rats following to use of EMR. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in retinal tissue. Retinal levels of NO and MDA increased in EMR exposed rats while both melatonin and CAPE caused a significant reduction in the levels of NO and MDA. Likewise, retinal SOD, GSH-Px and CAT activities decreased in EMR exposed animals while melatonin and CAPE caused a significant increase in the activities of these antioxidant enzymes. Treatment of EMR exposed rats with melatonin or CAPE increased the activities of SOD, GSH-Px and CAT to higher levels than those of control rats. In conclusion, melatonin and CAPE reduce retinal oxidative stress after long-term exposure to 900 MHz emitting mobile phone. Nevertheless, there was no statistically significant difference between the efficacies of these two antioxidants against to EMR induced oxidative stress in rat retina. The difference was in only GSH-Px activity in rat retina. Melatonin stimulated the retinal GSH-Px activity more efficiently than CAPE did.     

The contradictory effects of nitric oxide in caerulein-induced acute pancreatitis in rats

This study was planned to observe the effects of nitric oxide synthesis on the antioxidative defense enzymes and pancreatic tissue histology in caerulein-induced acute pancreatitis. Acute pancreatitis was induced by intraperitoneal injections of 50 µg/kg caerulein, L-arginine used for NO induction and N^ω-nitro-L-arginine methyl ester (L-NAME) used for NO inhibition. In the caerulein group acinar cell degeneration, interstitial inflammation, oedema and haemorrhage were detected. Pancreatic damage scores were decreased with both NO induction and inhibition (p<0.05). MDA, GSH-Px, CAT, GSH and SOD activities were significantly changed in the caerulein group and indicated increased oxidative stress. Both NO induction and inhibition decreased this oxidative stress. It is concluded that both nitric oxide induction and inhibition ameliorated caerulein-induced acute pancreatitis. The findings indicate that a certain amount of NO production has beneficial effects in experimental acute pancreatitis, but uncontrolled over-production of NO may be detrimental.