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Protection by metal complexes with SOD-mimetic activity against oxidative gastric injury induced by indometacin and ethanol in rats

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ANNALS OF CLINICAL BIOCHEMISTRY 2001年第6期38卷 694-700页

作者： El-Missiry, MA El-Sayed, IH Othman, AI Mansoura Univ Fac Sci Dept Zool Mansoura 35516 Egypt

We have investigated the protective effect or oral administration of copper and manganese complexes with superoxide dismutase (SOD)-mimetic activity against oxidative gastric mucosal injury induced by the non-steroidal antiinflammatory drug indometacin with ethanol in the rat. The total area of the gastric lesions and lipid peroxidation were significantly increased 1 h after oral administration of indometacin (15 mg/kg) and ethanol, indicating in acute oxidative injury. The activities of SOD, catalase (CAT), glutathione-S-transferase (GST) and glutathione content were significantly decreased in the gastric mucosa by indometacin plus ethanol. Manganese or copper complexes showed SOD-mimetic activity. Pretreatment with these complexes protected against gastric mucosal lesions and decreased lipid peroxides, as well as attenuating the decrease in the activities or SOD, CAT and GST in gastric mucosa. These findings suggest that active oxygen species and lipid peroxidation play an important role in the pathogenesis of gastric mucosal injury induced by indometacin. In addition, we have shown that Mn and Cu complexes have gastroprotective properties against ulceration induced by indometacin plus ethanol. The present results suggest that appropriate copper or manganese complex supplementation may potentially provide prophylaxis or therapy for some pathologies associated with excessive free radical production and inhibited SOD activity.

关键词：消炎药非甾类/毒性铜/药理学乙醇/毒性自由基/代谢胃黏膜/药物作用胃黏膜/损伤胃黏膜/代谢吲哚美辛/毒性脂质过氧化作用/药物作用锰/药理学分子模拟有机金属化合物/药理学氧化还原超氧化物歧化酶/药理学动物男(雄)性大鼠

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Modulation of glutathione and antioxidant enzymes by Ocimum sanctum and its role in protection against radiation injury

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Indian Journal of Experimental Biology 1999年第3期37卷 262-268页

作者： Devi, P. Uma Ganasoundari, A. DepartmentofRadiobiology KasturbaMedicalCollegeManipalIndia.info@mahe.ernet.in

Aqueous extract (OE) of the leaves of Ocimum sanctum, the Indian holy basil, has been found to protect mouse against radiation lethality and chromosome damage and to possess significant antioxidant activity in vitro. Therefore a study was conducted to see if OE protects against radiation induced lipid peroxidation in liver and to determine the role, if any, of the inherent antioxidant system in radioprotection by OE. Adult Swiss mice were injected intraperitoneally (ip) with 10 mg/kg of OE for 5 consecutive days and exposed to 4.5 Gy of gamma radiation 30 min after the last injection. Glutathione (GSH) and the antioxidant enzymes glutathione transferase (GST), reductase (GSRx), peroxidase (GSPx) and superoxide dismutase (SOD), as well as lipid peroxide (LPx) activity were estimated in the liver at 15 min, 1, 2, 4 and 8 hr post-treatment. LPx was also studied after treatment with a single dose of 50 mg/kg of OE with/without irradiation. OE itself increased the GSH and enzymes significantly above normal levels whereas radiation significantly reduced all the values. The maximum decline was at 30-60 min for GSH and related enzymes and at 2 hr for SOD. Pretreatment with the extract checked the radiation induced depletion of GSH and all the enzymes and maintained their levels within or above the control range. Radiation significantly increased the lipid peroxidation rate, reaching a maximum value at 2 hr after exposure (approx. 3.5 times that of control). OE pretreatment significantly (P<0.0001) reduced the lipid peroxidation and accelerated recovery to normal levels. The results indicate that Ocimum extract protects against radiation induced lipid peroxidation and that GSH and the antioxidant enzymes appear to have an important role in the protection.

关键词：抗氧化剂/代谢自由基清除剂/药理学谷胱甘肽/代谢脂质过氧化作用/药物作用罗勒植物提取物/药理学辐射损伤实验性/预防和控制动物女(雌)性男(雄)性小鼠

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The effect of conjugated linoleic acid on the antioxidant enzyme defense system in rat hepatocytes

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LIPIDS 1999年第8期34卷 833-839页

作者： Cantwell, H Devery, R O'Shea, M Stanton, C Dublin City Univ Sch Biotechnol Dublin 9 Ireland TEAGASC Dairy Prod Res Ctr Fermoy Cork Ireland

Short-term effects of physiological concentrations of conjugated linoleic acid (CLA) on membrane integrity, metabolic function, cellular lipid composition, lipid peroxidation, and antioxidant enzymes were examined using rat hepatocyte suspension cultures. Incubation with CLA (5-20 ppm) for 3 h decreased the ability of hepatocyte plasma membranes to exclude trypan blue by approximately 25%, and caused leakage of cytosolic lactate dehydrogenase (LDH) into the medium. The significant decrease (P < 0.02) in hepatocyte viability as measured by LDH leakage during cell incubation with 10 and 20 ppm CLA was not associated with significant changes in cellular ATP content. Protein synthesis in hepatocytes was elevated (P < 0.05) in the presence of 5 and 10 ppm CLA, but at a higher concentration (20 ppm), protein synthesis was similar to that of control cells. Gluconeogenesis was maintained in cells incubated with lower concentrations of CLA (5 and 10 ppm) but was decreased (P < 0.02) at the higher concentration. Incubation with 20 ppm CLA for 3 h did not affect the specific activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme of cholesterol synthesis. Both cis-9,trans-11/trans-9,cis-11, and cis-10,trans-12/trans-10,cis-12 isomers of CLA were incorporated to a similar level into hepatocytes. Levels ranged from 3.9 to 4.1%, respectively, of total fatty acids in neutral lipids, and from 0.7 to 0.8%, respectively, of total fatty acids in phospholipids. Cellular lipid peroxidation remained unchanged in the presence of CLA (5-20 ppm), despite significant inhibition (P < 0.05) of superoxide dismutase. Catalase activity was maintained near control levels in the presence of 5 and 10 ppm CLA but was significantly decreased in the presence of 20 ppm CLA. Glutathione peroxidase activity was significantly decreased in the presence of 10 ppm CLA. The apparent sensitivity of the antioxidant enzyme defense system of liver cells to CLA, coupled with the lack o

关键词：腺苷三磷酸/代谢抗氧化剂/代谢过氧化氢酶/药物作用细胞存活/药物作用胆固醇/生物合成脂肪酸类/代谢糖原异生/药物作用谷胱甘肽过氧化酶/药物作用亚油酸类/药理学脂质过氧化作用/药物作用肝/细胞学肝/酶学蛋白质生物合成大鼠 Sprague-Dawley 超氧化物歧化酶/药物作用动物男(雄)性大鼠

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Increased lipophilicity and subsequent cell partitioning decrease passive transcellular diffusion of novel, highly lipophilic antioxidants

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期288卷 1317-1326页

作者： Sawada, GA Barsuhn, CL Lutzke, BS Houghton, ME Padbury, GE Ho, NFH Raub, TJ Pharmacia & Upjohn Inc Drug Absorpt & Transport Kalamazoo MI 49007 USA Pharmacia & Upjohn Inc Discovery Technol Kalamazoo MI 49007 USA Pharmacia & Upjohn Inc Pharmaceut Kalamazoo MI 49007 USA Pharmacia & Upjohn Inc Drug Metab Res Kalamazoo MI 49007 USA

Oxidative stress is considered a cause or propagator of acute and chronic disorders of the central nervous system. Novel 2,4-diamino-pyrrolo[2,3-d]pyrimidines are potent inhibitors of iron-dependent lipid peroxidation, are cytoprotective in cell culture models of oxidative injury, and are neuroprotective in brain injury and ischemia models. The selection of lead candidates from this series required that they reach target cells deep within brain tissue in efficacious amounts after oral dosing. A homologous series of 26 highly lipophilic pyrrolopyrimidines was examined using cultured cell monolayers to understand the structure-permeability relationship and to use this information to predict brain penetration and residence time. Pyrrolopyrimidines were shown to be a more permeable structural class of membrane-interactive antioxidants where transepithelial permeability was inversely related to lipophilicity or to cell partitioning. Pyrrole substitutions influence cell partitioning where bulky hydrophobic groups increased partitioning and decreased permeability and smaller hydrophobic groups and more hydrophilic groups, especially those capable of weak hydrogen bonding, decreased partitioning, and increased permeability. Transmonolayer diffusion for these membrane-inter active antioxidants was limited mostly by desorption from the receiver-side membrane into the buffer. Thus, in this case, these in vitro cell monolayer models do not adequately mimic the in vivo situation by underestimating in vivo bioavailability of highly lipophilic compounds unless accepters, such as serum proteins, are added to the receiving buffer.

关键词：抗氧化剂/化学抗氧化剂/药理学细胞系细胞膜通透性/药物作用扩散氢离子浓度脂质过氧化作用/药物作用氧化性应激嘧啶类/药理学吡咯类/药理学吡咯烷类/药理学构效关系动物狗

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Inhibition of lipid peroxidation by pindolol

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PHARMACOLOGY & TOXICOLOGY 1999年第3期84卷 130-134页

作者： Miura, T Muraoka, S Fujimoto, Y Hokkaido Coll Pharm Otaru Hokkaido 04702 Japan

Among beta-blockers, including atenolol, metaproterenol, pindolol and propranolol, only pindolol strongly inhibited lipid peroxidation induced by xanthine oxidase-hypoxanthine in the presence of adenosine-5'-phosphate-Fe3+. In the reaction system, superoxide predominantly reduced iron because superoxide dismutase strongly prevented the iron reduction. However, pindolol had no effect on the superoxide-dependent iron reduction. Adding superoxide dismutase immediately stopped the lipid peroxidation, indicating that superoxide is closely connected with forming the initiator of xanthine oxidase-hypoxanthine-induced lipid peroxidation. On the other hand, pindolol also inhibited lipid peroxidation, whereas it did not react with superoxide, indicating that it inhibited xanthine oxidase-hypoxanthine-induced lipid peroxidation by an independent mechanism of superoxide. Pindolol sharply scavenged 2,2'-azino-bis-(3-ethylbenzothiazoline-6-sulfonate) radical cations, but the ability of pindolol to scavenge peroxyl radicals of 2,2'-azobis(2-amidinopropane)-dihydrochloride and 2,2'-diphenyl-p-picrylhydrazyl radicals was low. In addition, pindolol did not scavenge hydroxyl radicals at physiologically significant concentrations. These results suggest that the ability of pindolol to inhibit lipid peroxidation was due to scavenging carbon-centered radicals rather than peroxyl radicals.

关键词：腺苷二磷酸/代谢肾上腺素能β受体拮抗剂/药理学药物相互作用红细胞/代谢自由基清除剂/药理学马次黄嘌呤/药理学铁/代谢脂质过氧化作用/药物作用高铁肌红蛋白/代谢氧化还原吲哚洛尔/药理学超氧化物歧化酶/代谢黄嘌呤氧化酶/药理学动物牛

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Genotoxic effects of benzyl isothiocyanate, a natural chemopreventive agent

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MUTAGENESIS 1999年第6期14卷 595-603页

作者： Kassie, F Pool-Zobel, B Parzefall, W Knasmüller, S Inst Canc Res A-1090 Vienna Austria Fed Res Ctr Nutr Inst Hyg & Toxicol Karlsruhe Germany

Benzyl isothiocyanate (BITC) is contained in cruciferous plants which are part of the human diet. Numerous reports indicate that BITC prevents chemically induced cancer in laboratory animals and it has been postulated that BITC might also be chemoprotective in humans. On the other hand, evidence is accumulating that this compound is a potent genotoxin in mammalian cells by itself. To further elucidate the potential hazards of BITC, we investigated its genotoxic effects in different in vitro genotoxicity tests and in animal models. In in-vitro experiments [differential DNA repair assay with Escherichia coli, micronucleus assay with human HepG2 cells and single cell gel electrophoresis (SCGE) assay with hepatocytes and gastrointestinal tract cells] pronounced dose-dependent genotoxic effects were found at low dose levels (less than or equal to 5 mu g/ml). In contrast, substantially weaker effects were obtained in in vivo experiments with laboratory rodents: in the differential DNA repair assay with E. coli cells, only moderate genotoxic effects were seen in indicator cells recovered from various organs of mice after treatment with high doses (between 90 and 270 mg/kg), while in SCGE assay with rats a change in the DNA migration pattern was seen at a dose level of 220 mg/ kg body wt. These findings indicate that BITC is detoxified under in vivo test conditions. This assumption was supported by the results of in vitro experiments which showed that the genotoxic effects of BITC are markedly reduced by bovine serum albumin and human body fluids such as saliva and gastric juice. Additional experiments carried out on the mechanistic aspects of the genotoxicity of BITC showed that this compound causes formation of thiobarbituric acid-reactive substances in HepG2 cells and that its DNA damaging properties are diminished by alpha-tocopherol, vitamin C, sodium benzoate and beta-carotene, indicating the possible involvement of free radicals in the genotoxicity of BITC. The doses

关键词：抗诱变药/药理学细胞培养的剂量效应关系药物电泳琼脂凝胶自由基清除剂/代谢异硫氰酸盐类/代谢异硫氰酸盐类/毒性脂质过氧化作用/药物作用小鼠近交系微核试验诱变力试验/方法大鼠近交F344 沙门菌鼠伤寒/药物作用血清白蛋白牛/代谢肿瘤细胞培养的成年人动物人类男(雄)性小鼠大鼠

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Radiation protection by the Ocimum flavonoids orientin and vicenin: Mechanisms of action

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RADIATION RESEARCH 2000年第4期154卷 455-460页

作者： Devi, PU Ganasoundari, A Vrinda, B Srinivasan, KK Unnikrishnan, MK Kasturba Med Coll & Hosp Dept Radiobiol Manipal 576119 Karnataka India Coll Pharm Manipal 576119 Karnataka India

In previous studies, flavonoids, orientin and vicenin, that were isolated from the leaf extract of Ocimum sanctum, were found to protect mice against radiation injury. Several flavonoids are known to be good antioxidants. Therefore, the effect of orientin and vicenin on radiation-induced lipid peroxidation in vivo and their antioxidant activity in vitro were studied. Adult mice were injected intraperitoneally with 50 mu g/kg of orientin or vicenin and exposed whole-body to 3 Gy of gamma radiation. Lipid peroxidation was measured in the liver 15 min to 8 h postirradiation. The antioxidant activity of orientin/vicenin (10-500 mu M) was studied by measuring inhibition of hydroxyl radicals generated by the Fenton reaction (Fe3+-EDTA-ascorbic acid-H2O2) in vitro. The compounds were also tested for possible pro-oxidant and iron chelation activities at the above concentrations in the irt vitro system. Orientin and vicenin provided almost equal protection against radiation-induced lipid peroxidation in mouse liver. Both compounds showed a significantly greater free radical-inhibiting activity irt vitro than DMSO. Neither orientin nor vicenin showed any pro-oxidant activity at the concentrations tested. Both compounds inhibited free radical formation in the absence of EDTA. Free radical scavenging appears to be a likely mechanism of radiation protection by these flavonoids. (C) 2000 by Radiation Research Society.

关键词：抗氧化剂/分离和提纯抗氧化剂/药理学芹菜素类黄酮物质/分离和提纯类黄酮物质/药理学自由基清除剂/分离和提纯自由基清除剂/药理学 γ射线葡糖苷类/分离和提纯葡糖苷类/药理学羟自由基铁螯合剂/分离和提纯铁螯合剂/药理学脂质过氧化作用/药物作用脂质过氧化作用/辐射效应肝/化学肝/药物作用肝/辐射效应医学印度传统分子结构植物提取物/化学植物叶/化学植物药用/化学辐射防护剂/分离和提纯辐射防护剂/药理学硫巴比妥酸反应物/分析全身照射动物女(雌)性男(雄)性小鼠

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Oxidative effects of nickel on bone marrow and blood of rats

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JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A 1999年第8期58卷 475-483页

作者： Chen, CY Sheu, JY Lin, TH Kaohsiung Med Coll Sch Technol Med Sci Kaohsiung Taiwan Kaohsiung Med Coll Grad Inst Med Kaohsiung Taiwan Foo Yin Inst Technol Dept Med Technol Kaohsiung Taiwan

This study was undertaken to examine the oxidative effects of nickel (Ni) on rat blood and bone marrow. Treatment with either 100, 250, or 500 mu mol/kg Ni ip significantly enhanced lipid peroxidation in serum and bone marrow after 24 h. The concentrations of Ni and Fe in serum and bone marrow cells were also significantly increased after NiCl2 administration. After treatment with NiCl2, the activities of glutathione peroxidase (GPx) and levels of alpha-tocopherol in bone marrow cells were markedly reduced. There was an inverse association thiobarbituric acid elevated (TBA)-chromogen product with decreased GPx activity and alpha-tocopherol levels in bone marrow cells of NiCl2-treated rats. The concentrations of a-tocopherol in blood significant reduced with 100 and 250 mu mol/kg Ni but returned to control at the 500-mu mol/kg dose. Data suggest that lipid peroxidation may be a contributing factor in Ni-induced tissue oxidative stress.

关键词：方差分析骨髓细胞/化学骨髓细胞/药物作用骨髓细胞/酶学色谱法高压液相剂量效应关系药物环境污染物/代谢环境污染物/毒性谷胱甘肽过氧化酶/血液谷胱甘肽过氧化酶/药物作用谷胱甘肽过氧化酶/代谢铁/分析铁/血液脂质过氧化作用/药物作用镍/分析镍/血液镍/代谢镍/毒性大鼠 Sprague-Dawley 维生素E/血液维生素E/代谢动物男(雄)性大鼠

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Why is glycated LDL more sensitive to oxidation than native LDL? A comparative study

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PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS 2000年第4期63卷 177-186页

作者： Sobal, G Menzel, J Sinzinger, H Univ Vienna Radiopharmacol Unit Dept Nucl Med A-1090 Vienna Austria Univ Vienna Inst Immunol A-1090 Vienna Austria

It is well established that oxidative modification of low-density lipoprotein (LDL) plays a causal role in human atherogenesis and the risk of atherosclerosis is increased in patients with diabetes mellitus. To examine the influence of different agents which may influence LDL-glycation and oxidation, experiments including glycation with glucose, glucose 6-phosphate, metal chelators (EDTA) and antioxidants (BHT) were perfomed. The influence of time dependence on the glycation process and the alteration of the electrophoretic mobility of LDL under diverse glycation and/or oxidation conditions was also investigated. The formation of conjugated dienes and levels of lipid peroxides in these different LDL-modifications were estimated. The copper-induced oxidation of LDL in vitro was determined by measurement of thiobarbituric acid reactive substances (TBARS) and expressed as nmol MDA/mg of LDL protein. We found that glycated LDL is more prone to oxidation than native LDL. Using native LDL, the maximal oxidation effect was found to reach a value of 49.72 nmol MDA/mg protein after 8 h. The maximum oxidation of the 31 days, glycated LDL with glucose was 71.76 nmol MDA/mg protein amounting to 144.33 % of the value found for native LDL. In the case of glucose 6-phosphate glycation, the maximum oxidation under the same conditions amounted to 173.77 % of the value found for native LDL. To measure the extent of glycation, fluorescence of advanced glycation end products (AGEs) was determined (370 nm excitation and 440 nm emission). The most potent glycation agent was glucose 6-phosphate leading to the formation of very high amounts of AGEs. This process was promoted in the absence of EDTA, which prevents the oxidative cleavage of modified Amadori products (ketoamines) to AGEs. We therefore conclude that both processes, glycation and oxidation, result in the modification of LDL, The lower the glycation-rate (+/ - EDTA) as measured by relative fluorescence units RFU (generation of A

关键词：抗氧化剂/药理学动脉硬化/代谢螯合剂/药理学铜/药理学依地酸/药理学电泳琼脂凝胶荧光葡萄糖/代谢葡糖-6-磷酸盐/代谢糖基化动力学脂质过氧化作用/药物作用脂蛋白类 LDL/血液脂蛋白类 LDL/代谢氧化还原/药物作用氧化性应激/药物作用硫巴比妥酸反应物/分析成年人女(雌)性人类男(雄)性中年人

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Singlet oxygen toxicity is cell line-dependent: A study of lipid peroxidation in nine leukemia cell lines

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PHOTOCHEMISTRY AND PHOTOBIOLOGY 1999年第6期70卷 858-867页

作者： Schafer, FQ Buettner, GR Univ Iowa Free Rad Res Inst Iowa City IA 52242 USA Univ Iowa ESR Facil Iowa City IA 52242 USA

Singlet oxygen (O-1(2)) can be quenched by water, lipids, proteins, nucleic acids and other small molecules. Polyunsaturated fatty acids (PUFA) of tells principally quench O-1(2) by chemical mechanisms, producing lipid hydroperoxides, while proteins physically and chemically quench O-1(2) Because cell lines can have different PUFA and protein levels, we hypothesized that O-1(2) toxicity will vary between cell Lines. We used Photofrin(R) as a source of O-1(2). Exposure of nine different leukemia cell lines (CEM, HEL, HL-60, K-562, KG-1, L1210, Molt-4, THP-1 and U-937) to Photofrin and light results in changes In membrane permeability (trypan blue) that vary with cell Line. The greater the lipid content of the cell line, the less susceptible they are to membrane damage. when the cell media was supplemented with docosahexaenoic acid (DHA, 22:6), the overall unsaturation of cellular lipids increased, Photofrin and light resulted in increased radical formation in these supplemented cells compared to controls;however, there was no difference in membrane permeability between DHA-supplemented and control cells, Lipid-derived radical formation (electron paramagnetic resonance spin trapping) was cell Line dependent: but no correlation between lipid content of cells and radical formation was found. However, we found that the greater the protein content of cells the more they were protected against membrane damage induced by Photofrin photosensitization, This suggests that cellular proteins are a hey target for O-1(2)-mediated toxicity. A remarkable observation is that cell size correlates inversely with ability of cells to cope with a given Bur of O-1(2).

关键词： HL-60细胞/药物作用 HL-60细胞/代谢 K562细胞/药物作用 K562细胞/代谢白血病L1210/药物疗法白血病L1210/代谢白血病实验性/药物疗法白血病实验性/代谢脂质过氧化作用/药物作用氧/毒性肿瘤细胞培养的动物人类小鼠

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