Journal of free radicals in biology & medicine最新文献_第2页

Calcium efflux from sarcoplasmic reticulum microsomes due to oxidation and sulfhydryl-binding agents 氧化和巯基结合剂引起的肌浆网微粒体的钙外排

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80006-X

Nancy M. Scherer, David W. Deamer

{"title":"Calcium efflux from sarcoplasmic reticulum microsomes due to oxidation and sulfhydryl-binding agents","authors":"Nancy M. Scherer, David W. Deamer","doi":"10.1016/S0748-5514(86)80006-X","DOIUrl":"10.1016/S0748-5514(86)80006-X","url":null,"abstract":"<div>Calcium permeability of sarcoplasmic reticulum (SR) microsomes was measured after aging or after exposure to peroxydisulfate or to sulfhydryl-binding agents. Under conditions where the Ca2+-ATPase was active, the maximum net release of Ca2+ was not significantly different between control and oxidized SR. However, when calcium uptake was prevented by EGTA or apyrase, the Ca2+ permeability of oxidized microsomes was 2 to 3 times greater than control of low (10−9, 10−7 M) but not high (10−6 M) levels of external calcium. The observation that vesicles preincubated with 5 mM dithiothreitol loaded up to 3 times as much calcium and had a slightly lower calcium permeability coefficient than control vesicles suggested that suflhydryl oxidation might modulate calcium flux. This hypothesis was tested by exposing to sulfydryl-binding agents:silver, arsenite, and p-chloromercuri-phenylsulfonic acid. Sulfhydryl-binding agents initiated a rapid release of calcium from microsomes, and release was halted by dithiothreitol. Inhibition of calcium transport could not entirely account for the apparent increase in permeability because the calcium permeability of SR treated with sulfhydryl-binding agents was 5 times greater than that of SR exposed to Ca2+-ATPase inhibitors. These results suggest that oxidation may increase the calcium permeability of SR. by allowing calcium loss through a channel that can be gated by sulfhydryl oxidation.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 4","pages":"Pages 249-254"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80006-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14167878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

The role and mechanism of metal ions and their complexes in enhancing damage in biological systems or in protecting these systems from these systems from the toxicity of O2− 金属离子及其络合物在增强生物系统损伤或保护这些系统免受O2−毒性中的作用和机制

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/0748-5514(86)90117-0

Sara Goldstein, Gidon Czapski

{"title":"The role and mechanism of metal ions and their complexes in enhancing damage in biological systems or in protecting these systems from these systems from the toxicity of O2−","authors":"Sara Goldstein, Gidon Czapski","doi":"10.1016/0748-5514(86)90117-0","DOIUrl":"10.1016/0748-5514(86)90117-0","url":null,"abstract":"<div>Cooper complexes of 1,10-phenanthroline and some substituted 1,10-phenanthroline cleave DNA in the presence of a reducing agent and molecular oxygen. Generally, the damage is attributed to hydroxyl radicals which are formed through the Haber-Weiss reaction. It is assumed that this reaction occurs with the ternary metal complexes with the biological target and the mechanism is defined as the “site specific mechanism.” In these systems, O2− drives the cycle through the reduction of copper(II). On the other hand, these same copper complexes catalyze the dismutation of O2− and thus should protect the systems from O2− toxicity. In this article, the toxicity of these complexes is explained on kinetic grounds. A general discussion on the various factors which could cause the metal ions or their complexes to act either as protectors from O2− toxicity or as sensitizers of toxic effects of O2− is given.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 1","pages":"Pages 3-11"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0748-5514(86)90117-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14154116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 151

Increased spontaneous chemiluminescence from liver homogenates and isolated hepatocytes upon inhibition of o2− and h2o2 utilization 抑制o2 -和h2o2的利用后，肝脏匀浆和分离肝细胞的自发化学发光增加

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80062-9

Julio F. Turrens, Cecilia Giulivi, Alberto Boveris

{"title":"Increased spontaneous chemiluminescence from liver homogenates and isolated hepatocytes upon inhibition of o2− and h2o2 utilization","authors":"Julio F. Turrens, Cecilia Giulivi, Alberto Boveris","doi":"10.1016/S0748-5514(86)80062-9","DOIUrl":"10.1016/S0748-5514(86)80062-9","url":null,"abstract":"<div>The intracellular steady-state concentrations of hydrogen peroxide or Superoxide anion were increased by inhibiting either catalase, glutathione peroxidase, or Superoxide dismutase activities. Catalase was inhibited with aminotriazole while glutathione peroxidase activity was blocked by eliminating reduced glutathione after addition of either iodoacetamide diethylmaleate or phorone. The concentration of aminotriazole that stimulated chemiluminescence in 50% (60 mM) was very similar to the Ki for catalase activity (70 mM). Cyanide, an inhibitor of both catalase and Superoxide dismutase, stimulated chemiluminescence in 50% at a concentration (0.15 mM) which is much closer from the Ki for Superoxide dismutase (0.25 mM) than from the Ki for catalase (15 μM). The Superoxide dismutase inhibitor diethyldithiocarbamate also increased chemiluminescence six- to ten-fold. Depletion of reduced glutathione stimulated spontaneous chemiluminescence when its concentration decreased below 4.5 μmol · g liver−1. The results shown herein suggest that the changes in the intracellular steady-state concentration occurring after inhibition of any antioxidant enzyme are responsible for the increased spontaneous chemilumi-nescence. Spontaneous chemiluminescence from intact cells may be used as a noninvasive method for monitoring intracellular free radical metabolism.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 2","pages":"Pages 135-140"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80062-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14161704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

Photosensitization by antitumor agents 2: Anthrapyrazole-photosensitized oxidation of ascorbic acid and 3,4-dihydroxyphenylalanine 抗肿瘤药物的光敏作用2:蒽吡唑-抗坏血酸和3,4-二羟基苯丙氨酸的光敏氧化

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80071-X

Krzysztof Reszka, Pawel Kolodziejczyk, J. William Lown

引用次数: 15

Lipid hydroperoxides initiate the autoxidation of sulfite with concomitant production of superoxide 脂质氢过氧化物引发亚硫酸盐的自氧化，同时产生超氧化物

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80073-3

Eric P. Brestel , William F. Petrone , Reuben A. Cohen

引用次数: 7

The effects of paraquat on Escherichia coli:Distinction between bacteriostasis and lethality 百草枯对大肠杆菌的作用:抑菌与致死的区别

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80005-8

Jeffrey Kitzler, Irwin Fridovich

引用次数: 11

Progressive loss of the macrophage respiratory burst in oxygen toxicity 氧中毒中巨噬细胞呼吸破裂的进行性丧失

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80061-7

Gearald Harrison , Henry Jay Forman

{"title":"Progressive loss of the macrophage respiratory burst in oxygen toxicity","authors":"Gearald Harrison , Henry Jay Forman","doi":"10.1016/S0748-5514(86)80061-7","DOIUrl":"10.1016/S0748-5514(86)80061-7","url":null,"abstract":"<div>The respiratory burst of rat alveolar macrophages stimulated by a variety of agents declines as a function of time of exposure to hyperoxia. Previous studies have evaluated this effect in terms of the stimulated O2⨪ production of a population of cells. The present study was designed to determine whether this decline is due to a “turning off” of the respiratory burst activity of some cells within the alveolar macrophage population or a general suppression of the activity of all cells. The phorbol myristate acetate (PMA) initiated respiratory burst of individual rat alveolar macrophages was monitored using the reaction of nitroblue tetrazolium (NBT), which results in the formation of a precipitate on active cells. The formazan staining was evaluated using black and white photographs of the cells and comparison to a scale constructed from photographed cells of four differing intensities of staining. Frequency distributions indicated that when the respiratory burst capability in the population of alveolar macrophages is impaired approximately 50% by oxygen exposure and/or culture in plastic vessels with artificial media, there is a gradual shift in NBT reduction rather than an “all or nothing” mechanism, in which the distribution would have reflected a shift from darkly stained cells to the very lessened or negligible staining observed at the end stage of oxygen toxicity.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 2","pages":"Pages 129-134"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80061-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14936131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Importance of the polyunsaturated fatty acid to vitamin E ratio in the resistance of rat lung microsomes to lipid peroxidation 多不饱和脂肪酸与维生素E之比在大鼠肺微粒体抗脂质过氧化中的重要性

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80042-3

Robert A. Leedle , Steven D. Aust

{"title":"Importance of the polyunsaturated fatty acid to vitamin E ratio in the resistance of rat lung microsomes to lipid peroxidation","authors":"Robert A. Leedle , Steven D. Aust","doi":"10.1016/S0748-5514(86)80042-3","DOIUrl":"10.1016/S0748-5514(86)80042-3","url":null,"abstract":"<div>Rat lung microsomes and liposomes made from isolated lung microsomal lipids were found to be much more resistant to lipid peroxidation than those from liver in both enzymatic and nonenzymatic systems. The polyunsaturated fatty acid (PUFA) content of isolated lung microsomal lipids was 28% of total fatty acids, while liver was 54%. The vitamin E (α-tocopherol) content of isolated lung microsomal lipids was 2.13 nmol/μmol lipid phosphate and that of liver was 0.43. Individually, neither the lower PUFA content nor higher vitamin E levels could account for the resistance of lung microsomal lipids to peroxidation. Distearoyl-L-a-phosphatidylcholine and/or α-tocopherol were added to liver microsomal lipids to achieve different PUFA to vitamin E ratios at PUFA contents of 28% or 54%, and the resulting liposomes were subjected to an NADPH-dependent lipid peroxidation system utilizing cytochrome P450 reductase, EDTA-Fe+3, and ADP-Fe+3. Liposomes having PUFA to vitamin E ratios less than approximately 250 nmol PUFA/nmol vitamin E were resistant to peroxidation, whereas lipid peroxidation, as evidenced by malondialdehyde production, occurred in liposomes having higher ratios. When lipid peroxidation occurred, 40%–60% of the liposomal vitamin E was irreversibly oxidized. Irreversible oxidation did not occur in the absence of lipid peroxidation. These studies indicated that the low PUFA to vitamin E ratio in lung microsomes and isolated microsomal lipids was sufficient to account for the observed resistance to lipid peroxidation.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 5","pages":"Pages 397-403"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80042-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14719410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

Immunogenicity of polyethylene glycol-modified superoxide dismutase and catalase 聚乙二醇修饰的超氧化物歧化酶和过氧化氢酶的免疫原性

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80031-9

Mary L. Nucci, Joann Olejarczyk, Abraham Abuchowski

引用次数: 34

Biochemical changes in the intestine associated with anoxia and reoxygenation: In vivo and in vitro studies 肠道中与缺氧和再氧化相关的生化变化:体内和体外研究

Journal of free radicals in biology & medicine Pub Date : 1986-01-01 DOI: 10.1016/S0748-5514(86)80032-0

Andrew T. Canada, Robert F. Werkman , Charles M. Mansbach II , Gerald M. Rosen

{"title":"Biochemical changes in the intestine associated with anoxia and reoxygenation: In vivo and in vitro studies","authors":"Andrew T. Canada, Robert F. Werkman , Charles M. Mansbach II , Gerald M. Rosen","doi":"10.1016/S0748-5514(86)80032-0","DOIUrl":"10.1016/S0748-5514(86)80032-0","url":null,"abstract":"<div>In ischemia/reperfusion injury, it is hypothesized that superoxide is responsible for the component of injury due to reperfusion. The superoxide is hypothesized to result from the aerobic oxidation of purines produced by the ischemia-mediated breakdown of high-energy phosphates. This oxidation is catalyzed by xanthine oxidase proposed to be rapidly formed as a result of ischemia-mediated protease conversion from xanthine dehydrogenase. In vivo experiments with the intestine of either rats or guinea pigs were unable to confirm the rapid conversion of xanthine dehydrogenase to xanthine oxidase as a result of ischemia. In vitro experiments with isolated guinea pig enterocytes did show a significant increase in xanthine oxidase activity after these cells were first placed in an anaerobic environment for 60 min and then reoxygenated; however, the magnitude of the increase is such that the biological importance of this finding remains uncertain. Using a variety of techniques, including spin trapping, hydroxylamine oxidation, and vanadate NADPH oxidation, we explored the possibility that superoxide was produced as a result of anoxia followed by reoxygenation in the in vitro enterocyte system. From these experiments, we determined that superoxide is generated as a result of anoxia/reoxygenation. However, from xanthine oxidase inhibition experiments using pterinaldehyde, only a small percentage of the total superoxide produced comes from the action of this enzyme on purines.</div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 5","pages":"Pages 327-334"},"PeriodicalIF":0.0,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80032-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14169708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13