134只家兔红细胞脂质过氧化物的正常值

脂质过氧化作用是指发生在不饱和脂肪酸共价键上的一系列自由基反应。关于这方面的研究涉及面相当广,包括某些疾病的病理过程如肿瘤,化学中毒,感染,炎症反应,自身免疫病,辐射损伤及心血管系统疾病等以及衰老、吞噬杀菌等生理过程。 自由基的损伤作用主要是引发细胞膜的脂质过氧化作用而造成机体细胞的损伤,脂质过氧化反应可以     

丹参酮对心肌肌质网脂质过氧化过程中脂类自由基的清除作用

应用自旋捕集方法和化学发光方法研究天然抗氧化剂丹参酮（Ｔａｎｓｈｉｎｏｎｅ）对心肌肌质网膜脂质过氧化过程中产生的脂类自由基的清除作用。发现在一定的浓度范围内,丹参酮对脂质过氧化有较好的保护作用,在丹参酮浓度大于１ｍｇ／ｍｇ蛋白时,对脂类自由基清除率可达６０％。丹参酮对肌质网膜脂质过氧化的保护机理可能是通过清除脂类自由基而阻断脂质过氧化的链式反应,而不是清除氧自由基而防止脂质过氧化的启动。     

Egr-1在小鼠和人组织中的表达及其与细胞增殖的关系

目的：探讨早期生长反应基因－1（Egr-1）在小鼠和人体组织和细胞中的表达及其与细胞增殖的联系,方法：应用原位杂交和免疫组织化学法对小鼠和人的不同组织进行Egr-1检测。结果：Egr-1mRNA和Egr-1蛋白阳性信号呈棕褐色。位于细胞浆和细胞核,生长活跃和增生的细胞可见相对的Egr-1表达。结论：Egr-1mRNA和Egr-1蛋白的高表达主要在生长活跃和增生的细胞,与细胞增殖有密切的关系。     

高血糖、蛋白质糖化与脂质过氧化反应

 高血糖、蛋白质糖化与脂质过氧化反应孙贺英,柳洁,高应,王惠云（山西职工医学院生化组,太原０３００１２）（山西省人民医院内分泌科）（山西医学院生化组）血糖持续性升高是糖尿病的重要临床特征。近年来报道糖尿病患者体内自由基反应明显增强,脂质过氧化产物增加。...     

脂质过氧化对细胞与机体的作用

脂质过氧化作用是指发生在不饱和脂肪酸共价键上的一系列自由基反应。近几年来,关于脂质过氧化作用的研究涉及面相当广,包括某些疾病的病理过程如肿瘤、化学中毒、感染、炎症反应、自身免疫病、辐射损伤及心血管系统疾病等以及衰老、吞噬杀菌等生理过程。人们试图从分子水平探讨这些过程的机理。本文将要讨论脂质过氧化的产生、对机体的作用、生物体抗氧化作用,及其与衰老、细胞损伤和某些疾病的关系。     

大白鼠中缝背核的组织结构及其向尾壳核复合体的定位投射

本实验应用Nissl法、单胺荧光组织化学法和逆行荧光标记与单胺荧光组织化学结合技术对大白鼠中缝背核的组织结构及其向尾壳核（CP）复合体的定位投射进行了观察。结果表明,中缝背核（NRD）可分为五个细胞群:尾侧细胞群、背内侧细胞群、腹内侧细胞群、外侧细胞群和前侧细胞群;大量的5-羟色胺细胞分布于NRD的各个细胞群,少量儿茶酚胺（CA）细胞只见于外侧细胞区。在CP复合体注射逆行荧光化合物快兰（Fast Blue 253/50以下简称FB）之后,中缝背核内出现不少FB标记的5—HT细胞,这些投射于CP复合体的细胞主要位于背内侧细胞群和腹内侧细胞群。本实验结果为进一步研究NRD的功能提供了形态学依据。     

植物脱水素的结构和功能

脱水素（DHN）属于LEA蛋白（late embrygenesis abundant protein）第二家族成员,具有广泛的生物学功能,如防止细胞脱水,稳定细胞膜,结合金属离子,清除羟基自由基防止膜脂过氧化,保护冷敏感性酶活性,作为分子伴侣和结合DNA／RNA的特性等。本文介绍脱水素的结构,在植物器官、组织和亚细胞中的定位以及功能的研究进展。     

野菊花总黄酮的对佐剂性关节炎大鼠抗炎免疫及机制探讨

为了了解野菊花总黄酮（total flavonoids of Chrysanthemum,TFC）对佐剂性关节炎（adjuvant arthritis,AA）大鼠炎症和免疫反应的调节作用,探讨TFC对AA大鼠病变机体一些细胞因子、ERK信号转导通路对腹腔巨噬细胞（peritoneal macrophages,PMCP）的影响,阐明TFC调节AA大鼠抗炎免疫活性的信号转导机制,本研究通过电子显微镜、免疫组织化学法、细胞凋亡检测及分子生物学的多种研究方法探讨AA大鼠滑膜组织和滑膜细胞的凋亡情况及其Caspase-3机制。     

扬子鳄小胃黏膜的组织化学和细胞学

扬子鳄（Alligator sinensis）的小胃是在胃幽门部与十二指肠的交接处由胃幽门括约肌和十二指肠括约肌突入管腔形成的一个小腔,其生理功能一直不清楚。本文采用组织化学、电子显微镜和免疫组织化学技术对扬子鳄小胃黏膜的组织化学成分、细胞超微结构及细胞类型进行了较全面的研究。小胃黏膜上皮PAS反应呈强阳性,AB染色呈弱阳性,主要分泌中性糖蛋白和少量的含硫酸性糖蛋白。电子显微镜下,扬子鳄小胃黏膜上皮主要由表面黏液细胞组成,偶见内分泌细胞。小胃腺部则70％-90％为内分泌细胞,其余为少量的腺黏液细胞和泌酸胃酶细胞。应用7种胃肠激素的抗血清在小胃黏膜中检测出了5-羟色胺（5-HT）、胃泌素（Gas）、胰高血糖素（Glu）、生长抑素（SS）、P-物质（SP）和血管活性肠肽（VIP）细胞,以Glu细胞密度最高,VIP细胞密度最低。未检测到胰多肽（PP）细胞。本研究结果表明,从组织化学成分和细胞类型看,扬子鳄的小胃与胃同源;从细胞超微结构和内分泌细胞所占百分比例看,扬子鳄的小胃已出现了明显的特化,泌酸胃酶细胞中未见泌酸小管,可能没有泌酸功能。内分泌细胞含量丰富,可能在调节胃肠道功能中发挥重要作用[动物学报54（6）：1044—1050,2008]。     

抗氧化剂对脂质过氧化反应混合物引起人培养细胞DNA损伤的影响

 <正> 脂质过氧化反应(LPR)中产生的自由基和过氧化物可引起多种细胞损伤,特别是对DNA的损伤可能是许多癌肿的重要原因。Akasaka等将E.coli与鼠肝微粒体脂质过氧化反应混合物(LPRM)孵育,使有DNA修复缺陷的细菌株突变率增加。我们将人羊膜FL细胞与大鼠肝微粒体LPRM共同培养,看能否诱发程序外DNA合成(UDS),并分组加入抗氧化剂观察其影响。     

Oxidative Damage of U937 Human Leukemic Cells Caused by Hydroxyl Radical Results in Singlet Oxygen Formation

The exposure of human cells to oxidative stress leads to the oxidation of biomolecules such as lipids, proteins and nuclei acids. In this study, the oxidation of lipids, proteins and DNA was studied after the addition of hydrogen peroxide and Fenton reagent to cell suspension containing human leukemic monocyte lymphoma cell line U937. EPR spin-trapping data showed that the addition of hydrogen peroxide to the cell suspension formed hydroxyl radical via Fenton reaction mediated by endogenous metals. The malondialdehyde HPLC analysis showed no lipid peroxidation after the addition of hydrogen peroxide, whereas the Fenton reagent caused significant lipid peroxidation. The formation of protein carbonyls monitored by dot blot immunoassay and the DNA fragmentation measured by comet assay occurred after the addition of both hydrogen peroxide and Fenton reagent. Oxidative damage of biomolecules leads to the formation of singlet oxygen as conformed by EPR spin-trapping spectroscopy and the green fluorescence of singlet oxygen sensor green detected by confocal laser scanning microscopy. It is proposed here that singlet oxygen is formed by the decomposition of high-energy intermediates such as dioxetane or tetroxide formed by oxidative damage of biomolecules.     

Chemiluminescence study on the peroxidation of linoleic acid initiated by the reaction of ferrous iron with hydrogen peroxide

Linoleic acid was used as a model system to study lipid peroxidation initiated by the reaction of ferrous iron with hydrogen peroxide. Low-level chemiluminescence of the peroxidation was measured with a high-sensitivity single-photon counter. It was found that the luminescence primarily comes from the dimol reaction of singlet oxygen and that the peak intensity of emission is a quadratic function of the concentration of either Fe2+ or H2O2, provided that the other Fenton reagent is in great excess. Under the same conditions, analysis on reaction kinetics shows a linear relationship between the maximal level of the initiator formed by the Fenton reaction and the initial concentration of Fe2+ or H2O2. This implies that the peak intensity of the chemiluminescence may be a good index of the maximal level of the initiator.     

The requirement for iron (III) in the initiation of lipid peroxidation by iron (II) and hydrogen peroxide

The initiation of lipid peroxidation by Fe2+ and H2O2 (Fenton's reagent) is often proposed to be mediated by the highly reactive hydroxyl radical. Using Fe2+, H2O2, and phospholipid liposomes as a model system, we have found that lipid peroxidation, as assessed by malondialdehyde formation, is not initiated by the hydroxyl radical, but rather requires Fe3+ and Fe2+. EPR spin trapping with 5,5-dimethyl-1-pyrroline-N-oxide and the bleaching of para-nitrosodimethylaniline confirmed the generation of the hydroxyl radical in this system. Accordingly, catalase and the hydroxyl radical scavengers mannitol and benzoate efficiently inhibited the generation and the detection of hydroxyl radical. However, catalase, mannitol, and benzoate could either stimulate or inhibit lipid peroxidation. These unusual effects were found to be consistent with their ability to modulate the extent of Fe2+ oxidation by H2O2 and demonstrated that lipid peroxidation depends on the Fe3+:Fe2+ ratio, maximal initial rates occurring at 1:1. These studies suggest that the initiation of liposomal peroxidation by Fe2+ and H2O2 is mediated by an oxidant which requires both Fe3+ and Fe2+ and that the rate of the reaction is determined by the absolute Fe3+:Fe2+ ratio.     

The involvement of iron in lipid peroxidation. Importance of ferric to ferrous ratios in initiation

Intense lipid peroxidation of brain synaptosomes initiated with Fenton's reagent (H2O2 + Fe2+) began instantly upon addition of Fe2+ and preceded detectable OH. formation. Although mannitol or Tris partially blocked peroxidation, concentrations required were 10(3)-fold in excess of OH. actually formed, and inhibition by Tris was pH dependent. Lipid peroxidation also was initiated by either Fe2+ or Fe3+ alone, although significant lag phases (minutes) and slowed reaction rates were observed. Lag phases were dramatically reduced or nearly eliminated, and reaction rates were increased by a combination of Fe3+ and Fe2+. In this instance, lipid peroxidation initiated by optimal concentrations of H2O2 and Fe2+ could be mimicked or even surpassed by providing optimal ratios of Fe3+ to Fe2+. Peroxidation observed with Fe3+ alone was dependent upon trace amounts of contaminating Fe2+ in Fe3+ preparations. Optimal ratios of Fe3+:Fe2+ for the rapid initiation of lipid peroxidation were on order of 1:1 to 7:1. No OH. formation could be detected with this system. Although low concentrations of H2O2 or ascorbate increased lipid peroxidation by Fe2+ or Fe3+, respectively, high concentrations of H2O2 or ascorbate (in excess of iron) inhibited lipid peroxidation due to oxidative or reductive maintenance of iron exclusively in Fe2+ or Fe3+ form. Stimulation of lipid peroxidation by low concentrations of H2O2 or ascorbate was due to the oxidative or reductive creation of Fe3+:Fe2+ ratios. The data suggest that the absolute ratio of Fe3+ to Fe2+ was the primary determining factor for the initiation of lipid peroxidation reactions.     

Retardation of cell aging by lipid peroxidation

Different concentrations of Fe e+/vitamin C mixtures were used as initiators of lipid peroxidation in diploid fibroblasts from cultured human embryonic lung. Malondialdehyde (MDA) formation in the cell cultures was correlated directly with the concentrations of Fe²⁺ and vitamine C. Lipid peroxidation was associated with an increase in life-span, decrease in the population doubling time and increase in cellular DNA synthesis. The effects of lipid peroxidation varied inversely with the MDA level. These data showed that low levels of lipid peroxidation retarded several biological properties of cultured cells that are associated with cell aging.     

NADPH-dependent lipid peroxidation capacity in unfixed tissue sections: characterization of the pro-oxidizing conditions and optimization of the histochemical detection

Summary Factors which influence the iron-stimulated lipid peroxidation in rat liver have been studied by incubating unfixed cryostat sections with a pro-oxidant system and using an optimized histochemical detection method for lipid peroxidation products with 3-hydroxy-2-naphthoic acid hydrazide and Fast Blue B. We used a method that was slightly different from the one described previously. The final reaction product was exclusively localized in the cytoplasm of liver parenchymal cells with a homogeneous distribution within the liver lobule. The absorbance maximum, as measured cytophotometrically, was found to be 550 nm. Maximum lipid peroxidation was observed when the pro-oxidant system contained 0.2 mm NADPH, 1 mm ADP and 15 μm FeCl₂. Some reaction product was found when NADPH was omitted. Iron concentrations higher than 180 μm prevented the formation of lipid peroxidation products in certain areas of the sections, whereas ADP concentrations higher than 1 mm inhibited the reaction in the whole section. A pH dependency was also observed, with the highest lipid peroxidation at pH 7.2. Optimum lipid peroxidation was induced by incubating for 30 min at 37°C with the pro-oxidant system. A linear relationship was found between the thickness of the sections (up to 20 μm) and the amount of lipid peroxidation products. The addition of scavengers of O2- (superoxide dismutase), hydrogen peroxide (catalase) and OH · (mannitol) to the first step medium did not affect the amount of final reaction product. These findings appear to confirm the hypothesis proposed for events occurring in isolated microsomes, leading to the formation of hydroperoxides and ultimately lipid peroxidation-derived carbonyls. The present method is a useful tool for studying the capacity of lipid peroxidation in tissues under different (patho)physiological conditions.     

Comparison of two methods used to analyse lipid peroxidation from Vaccinium myrtillus (L.) during snow removal, reacclimation and cold acclimation.

Malondialdehyde (MDA) concentration is a widely used method to analyse lipid peroxidation in biological material. In plant tissues, however, certain compounds (anthocyanins, carbohydrates) may interfere with measurements which may lead to an overestimation of the MDA levels. Two methods were compared for analysing lipid peroxidation, either uncorrected or corrected for interfering compounds. The comparison was performed in three separate experiments with respect to cold treatments (snow removal in winter, reacclimation in summer and cold acclimation in autumn) in bilberry (Vaccinium myrtillus L.). During winter and autumn the methods seem to measure different compounds, but during active growth in the summer the difference between the methods was less. This is obviously due to carbohydrates which act as cryoprotectants and increase in concentration during cold acclimation as well as due to the anthocyanins. It is thus suggested that the validity of the uncorrected method to measure MDA and thereby lipid peroxidation is best in plant tissue which is in an active growth state.     

Oxidative stress in plant cell culture: a role in production of beta-thujaplicin by Cupresssus lusitanica suspension culture

Oxidative stress is a common physiological stress that often challenges plants. Reactive oxygen species (ROS) are major factors in oxidative stress that significantly affect plant cell growth and secondary metabolism. Here we used beta-thujaplicin production by Cupressus lusitanica cell culture as an example to demonstrate the common occurrence of oxidative stress in cultivated plant cells and its effect on multiple aspects of cell culture process. C. lusitanica cells cultivated under Fe(2+) stress generate a significant level of ROS, and oxidative stress also occurs at late stages of C. lusitanica cell cultures under normal conditions. ROS production inhibited cell growth, induced lipid peroxidation and cell death, and enhanced ethylene and beta-thujaplicin production. It is demonstrated that Fe(2+) stress enhances ROS production via the Fenton reaction and promotes beta-thujaplicin production via ROS-induced lipid peroxidation that may activate cyclic oxylipin and ethylene pathways. Results further indicate that H(2)O(2) is a positive signal for beta-thujaplicin production, whereas superoxide anion radical (O(2) (- )) negatively affects beta-thujaplicin induction and strongly induces cell death. The study suggests that evaluating the oxidative stress and plant responses in a cell culture process is very necessary and important for understanding biochemical processes and for gaining the maximal productivity of target secondary metabolites.     

Histological and Histochemical Uses of Periodic Acid

Periodic acid acts upon the 1,2 glycol linkage (-CHOH -CHOH-) of carbohydrates in tissue sections to produce aldehyde (RCHO+RCHO) which can be colored with Schiff s reagent. The method can be used on frozen or paraffin sections and is useful as a reaction for carbohydrates of tissues: glycogen (in paraffin section only), mucin, basement membrane, reticulin, the colloid of the pituitary stalk and thyroid, some of the acidophile cells of the human anterior hypophysis, the granular cells of the renal arteriole, etc.

In abnormal tissues, it colors many of the “hyaline” materials— amyloid infiltrations, arteriolosclerotic hyaline, colloid droplets, mitotic figures, etc.

The histochemical uses of the periodic-acid-Schiff's reagent (PAS) need careful control because of the possibility of attachment of iodate or periodate to tissue constitutents, producing a recoloration of the Schiff's reagent. Whenever possible the positive reacting material should be further identified by other methods since Lison showed other substances besides aldehydes can recolorize SchifFs reagent.     

Lipid peroxidation in mitochondria and microsomes from adult and fetal rat tissues

Pregnant female Wistar rats that received a control (100 ppm Zn) or a Zn-deficient diet (1.5 ppm Zn) from d 0 to 21, or nonpregnant normally fed female rats without or with five daily oral doses of 300 mg/kg salicylic acid were used for the experiments. In isolated mitochondria or microsomes from various maternal and fetal tissues, lipid peroxidation was determined as malondialdehyde formation measured by means of the thiobarbiturate method. Zn deficiency increased lipid peroxidation in mitochondria and microsomes from maternal and fetal liver, maternal kidney, maternal lung microsomes, and fetal lung mitochondria. Lipid peroxidation in fetal microsomes was very low. Zn deficiency produced a further reduction of lipid peroxidation in fetal liver microsomes. Salicylate increased lipid peroxidation in liver mitochondria and microsomes after addition in vitro and after application in vivo. The increase of lipid peroxidation by salicylate may be caused by two mechanisms: an increased cellular Fe uptake that, in turn, can increase lipid peroxidation and chelating Fe, in analogy to the effect of ADP in lipid peroxidation. The latter effect of salicylate is particularly expressed at increased Fe content.