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Oxygen consumption through metabolism and photodynamic reactions in cells cultured on microbeads

PHYSICS IN MEDICINE AND BIOLOGY 2000年第1期45卷 103-119页

作者： Schunck, T Poulet, P Univ Strasbourg 1 Inst Phys Biol Fac Med UPRESA 7004 CNRS F-67085 Strasbourg France

Oxygen consumption by cultured cells, through metabolism and photosensitization reactions, has been calculated theoretically. From this result, we have derived the partial oxygen pressure P-O2 in the perfusion medium Bowing across sensitized cultured cells during photodynamic experiments. The P-O2 variations in the perfusate during light irradiation are related to the rate of oxygen consumption through photoreactions, and to the number of cells killed per mole of oxygen consumed through metabolic processes. After irradiation, the reduced metabolic oxygen consumption yields information on the cell death rate, and on the photodynamic cell killing efficiency. The aim of this paper is to present an experimental set-up and the corresponding theoretical model that allows us to control the photodynamic efficiency for a given cell-sensitizer pair, under well defined and controlled conditions of irradiation and oxygen supply. To demonstrate the usefulness of the methodology described, CHO cells cultured on microbeads were sensitized with pheophorbide a and irradiated with different light fluence rates. The results obtained, i.e. oxygen consumption of about 0.1 mu M s(-1) m(-3) under a light fluence rate of 1 W m(-2), 10(5) cells killed per mole of oxygen consumed and a decay rate of about 1 h(-1) of living cells after irradiation, are in good agreement with the theoretical predictions and with previously published data.

关键词： CHO细胞细胞死亡/药物作用细胞死亡/辐射效应叶绿素/类似物和衍生物叶绿素/药理学仓鼠亚科光微球体模型理论氧耗量/药物作用氧耗量/辐射效应分压光化学疗法光敏感药/药理学动物

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Geometry and charge determine pharmacological effects of steroids on N-methyl-D-aspartate receptor-induced Ca²⁺ accumulation and cell death

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期293卷 747-754页

作者： Weaver, CE Land, MB Purdy, RH Richards, KG Gibbs, TT Farb, DH Boston Univ Sch Med Dept Pharmacol Mol Neurobiol Lab Boston MA 02118 USA

Modulation of N-methyl-D-aspartate (NMDA) receptor function by a series of sulfated steroids and dicarboxylic acid ester analogs of pregnenolone sulfate and pregnanolone sulfate was investigated in cultured hippocampal neurons. The "bent" steroid ring structure associated with 5 beta-stereochemistry favors receptor inhibition, whereas the more planar ring structure of the pregn-5-enes and 5 alpha-pregnanes favors potentiation of NMDA-induced [Ca2+] increases and neuronal cell death. The nature of the negatively charged group attached to the steroid C3 position is important for both the neuroprotection afforded by pregnane steroids and the exacerbation of NMDA-induced neuronal death by pregn-5-enes. Dicarboxylic acid hemiesters of various lengths can substitute for the sulfate group of the positive modulator pregnenolone sulfate and the negative modulator pregnanolone sulfate. This result suggests that precise coordination with the oxygen atoms of the sulfate group is not critical for modulation and that the steroid recognition sites can accommodate bulky substituents at C3. The capacity of charged steroids to enhance or protect against NMDA-induced death of hippocampal neurons is strongly correlated with modulation of NMDA-induced Ca2+ accumulation, indicating that direct enhancement or inhibition of NMDA receptor function is responsible for the proexcitotoxic or neuroprotective effects of these steroids.

关键词：钙/代谢细胞死亡/药物作用海马/药物作用分子构象 N-甲基天冬氨酸/毒性大鼠 Sprague-Dawley 受体 N-甲基-D-天冬氨酸/药物作用受体 N-甲基-D-天冬氨酸/生理学甾类/药理学构效关系动物大鼠

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Lycopene interferes with cell cycle progression and insulin-like growth factor I signaling in mammary cancer cells

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NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL 2000年第1期36卷 101-111页

作者： Karas, M Amir, H Fishman, D Danilenko, M Segal, S Nahum, A Koifmann, A Giat, Y Levy, J Sharoni, Y Ben Gurion Univ Negev Fac Hlth Sci Dept Clin Biochem IL-84105 Beer Sheva Israel Soroka Med Ctr Beer Sheva Israel Ben Gurion Univ Negev Fac Hlth Sci Dept Immunol & Microbiol IL-84105 Beer Sheva Israel

Recent studies have shown that high insulin-like growth factor I (IGF-I) blood level is a risk factor in breast and prostate cancer. The aim of this study was to determine whether the mitogenic activity of IGF-I in mammary cancer cells can be reduced by the dietary carotenoid lycopene. The anticancer activity of lycopene, the major tomato carotenoid, has been suggested by in vitro, in vivo, and epidemiological studies. Growth stimulation of MCF7 mammary cancer cells by IGF-I was markedly reduced by physiological concentrations of lycopene. The inhibitory effects of lycopene on MCF7 cell growth were not accompanied by apoptotic or necrotic cell death, as determined by annexin V binding to plasma membrane and propidium iodide staining of nuclei in unfixed cells. Lycopene treatment markedly reduced the IGF-I stimulation of tyrosine phosphorylation of insulin receptor substrate I and binding capacity of the AP-1 transcription complex. These effects were not associated with changes in the number or affinity of IGF-I receptors, but with an increase in membrane-associated IGF-binding proteins, which were previously shown in different cancer cells to negatively regulate IGF-I receptor activation. The inhibitory effect of lycopene on IGF signaling was associated with suppression of IGF-stimulated cell cycle progression of serum-starved, synchronized cells. Moreover, in cells synchronized by mimosine treatment, lycopene delayed cell cycle progression after release from the mimosine block. Collectively, the above data suggest that the inhibitory effects of lycopene on MCF7 cell growth are not due to the toxicity of the carotenoid but, rather, to interference in IGF-I receptor signaling and cell cycle progression.

关键词：抗致癌药/药理学乳腺肿瘤/代谢乳腺肿瘤/病理学类胡萝卜素类/药理学细胞周期/药物作用细胞死亡/药物作用细胞分裂着色剂 DNA/分析 DNA/生物合成胰岛素样生长因子Ⅰ/代谢胰岛素样生长因子Ⅰ/药理学普罗匹定信号传导/药物作用肿瘤细胞培养的人类

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Effect of Ca²⁺-dependent cell death on the release of herpes simplex virus

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ARCHIVES OF VIROLOGY 2003年第2期148卷 221-235页

作者： Yura, Y Matsumoto, R Sumi, T Kusaka, J Osaka Univ Grad Sch Dent Dept Oral & Maxillofacial Surg Suita Osaka 5650871 Japan Univ Tokushima Sch Dent Dept Oral & Maxillofacial Surg Tokushima 770 Japan

The effect of a variety of cell death-inducing reagents on the release of herpes simplex virus type 1 (HSV-1) was examined. lonomycin was found to increase the release of HSV-1, whereas no significant increase was observed by the treatment with TNF-alpha, anti-Fas antibody, C2-ceramide, sphingosine, H-7, tyrphostin and camptothecin. lonomycin induced an immediate early peak and a subsequent long-lasting elevation of intracellular Ca2+ concentration ([Ca2+]i). In the absence of extracellular Ca, ionomycin neither elevated [Ca]i nor increased the release of HSV-1 from the infected cells, indicating that Ca2+ influx play an important role in the release of HSV-1. Studies with trypan blue and annexin V staining revealed that the ionomycin-induced alteration of [Ca2+]i was accompanied by cell death of the infected cells. Disintegration of cell membrane, cytoplasmic vacuole formation and the leakage of virus particles from the cell surface were observed by electron microscopy. These results indicate that Ca2+- dependent cell death showing necrotic alteration is responsible for the enhanced release of HSV-1. The data also give some initial insights into the functional importance of cell death during the late stages of HSV-1 infection.

关键词：钙/代谢钙/药理学半胱氨酸天冬氨酸蛋白酶/拮抗剂和抑制剂半胱氨酸天冬氨酸蛋白酶/代谢细胞死亡/药物作用细胞系细胞存活/药物作用酶抑制剂/药理学疱疹病毒1型人/药物作用疱疹病毒1型人/生理学离子霉素/药理学毒胡萝卜内酯/药理学时间因素人类

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Microvessels from Alzheimer's disease brains kill neurons in vitro

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AMERICAN JOURNAL OF PATHOLOGY 1999年第2期154卷 337-342页

作者： Grammas, P Moore, P Weigel, PH Univ Oklahoma Hlth Sci Ctr Dept Pathol Oklahoma City OK 73104 USA Univ Oklahoma Hlth Sci Ctr Dept Biochem & Mol Biol Oklahoma City OK 73104 USA Univ Oklahoma Hlth Sci Ctr Oklahoma Ctr Neurosci Oklahoma City OK 73104 USA

Understanding the pathogenesis of Alzheimer's disease is of widespread interest because it is an increasingly prevalent disorder that is progressive, fatal, and currently untreatable. The dementia of Alzheimer's disease is caused by neuronal cell death, We demonstrate for the first time that blood vessels isolated from the brains of Alzheimer's disease patients can directly kill neurons in vitro. Either direct co-culture of Alzheimer's disease microvessels with neurons or incubation of cultured neurons with conditioned medium from microvessels results in neuronal cell death, in contrast, vessels from elderly nondemented donors are significantly (P < 0.001) less lethal and brain vessels from younger donors are not neurotoxic. Neuronal killing by either direct coculture with Alzheimer's disease microvessels or conditioned medium is dose- and time-dependent. Neuronal death can occur by either apoptotic or necrotic mechanisms. The microvessel factor is neurospecific, killing primary cortical neurons, cerebellar granule neurons, and differentiated PC-12 cells, but not non-neuronal cell types or undifferentiated PC-12 cells, Appearance of the neurotoxic factor is decreased by blocking microvessel protein synthesis with cycloheximide, The neurotoxic factor is soluble and likely a protein, because its activity is heat labile and trypsin sensitive. These findings implicate a novel mechanism of vascular-mediated neuronal cell death in Alzheimer's disease.

关键词：阿尔茨海默病/病理学脑/血液供给脑/病理学毛细血管/化学毛细血管/生理学细胞死亡/药物作用共同培养技术培养基条件性/药理学放线菌酮/药理学神经变性神经元/细胞学神经元/药物作用 PC12细胞/药物作用 PC12细胞/病理学动物人类大鼠

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Hydrogen peroxide from the oxidative burst is neither necessary nor sufficient for hypersensitive cell death induction, phenylalanine ammonia lyase stimulation, salicylic acid accumulation, or scopoletin consumption in cultured tobacco cells treated with elicitin

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PLANT PHYSIOLOGY 1999年第1期121卷 163-171页

作者： Dorey, S Kopp, M Geoffroy, P Fritig, B Kauffmann, S Univ Strasbourg 1 CNRS Inst Biol Mol Plantes F-67084 Strasbourg France

H2O2 from the oxidative burst, cell death, and defense responses such as the production of phenylalanine ammonia lyase (PAL), salicylic acid (SA), and scopoletin were analyzed in cultured tobacco (Nicotiana tabacum) cells treated with three proteinaceous elicitors: two elicitins (alpha-megaspermin and beta-megaspermin) and one glycoprotein. These three proteins have been isolated from Phytophthora megasperma H20 and have been previously shown to be equally efficient in inducing a hypersensitive response (HR) upon infiltration into tobacco leaves. However, in cultured tobacco cells these elicitors exhibited strikingly different biological activities. beta-Megaspermin was the only elicitor that caused cell death and induced a strong, biphasic H2O2 burst. Both elicitins stimulated PAL activity similarly and strongly, while the glycoprotein caused only a slight increase. Only elicitins induced SA accumulation and scopoletin consumption, and beta-megaspermin was more efficient. To assess the role of H2O2 in HR cell death and defense response expression in elicitin-treated cells, a gain and loss of function strategy was used. Our results indicated that H2O2 was neither necessary nor sufficient for HR cell death, PAL activation, or SA accumulation, and that extracellular H2O2 was not a direct cause of intracellular scopoletin consumption.

关键词：藻蛋白质类/药理学细胞死亡/药物作用细胞培养的酶激活/药物作用糖蛋白类/药理学过氧化氢/代谢苯丙氨酸氨裂合酶/代谢疫霉属植物疾病/化学诱导植物生长调节物/药理学植物叶/细胞学植物叶/药物作用植物叶/酶学植物叶/代谢植物有毒呼吸爆发/药物作用水杨酸/代谢东莨菪亭/代谢烟草/细胞学烟草/药物作用烟草/酶学烟草/代谢

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Effects of excess vitamin A on development of cranial neural crest-derived structures: A neonatal and embryologic study

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TERATOLOGY 2000年第4期62卷 214-226页

作者： Mulder, GB Manley, N Grant, J Schmidt, K Zeng, WP Eckhoff, C Maggio-Price, L Univ Washington Sch Med Dept Comparat Med Seattle WA 98195 USA Univ Calif Irvine Univ Lab Anim Resources Irvine CA 92697 USA Med Coll Georgia Dept Pediat Inst Mol Med & Genet Augusta GA 30912 USA Childrens Hosp Alabama Birmingham AL 35233 USA Univ Washington Sch Med Dept Pediat Seattle WA 98195 USA

Background: Vitamin A and its metabolites have been shown to be teratogenic in animals and humans producing defects of neural crest derived structures that include abnormalities of the craniofacial skeleton, heart, and thymus. Our prior studies with retinoic acid have established that gestational day (gd) 9 is a sensitive embryonic age in the mouse for inducing craniofacial and thymic defects. Methods: We exposed pregnant mice to variable doses of vitamin A (retinyl acetate) on gd 9 and embryos were evaluated for changes in developing pharyngeal arch and pouch morphology, neural crest cell migration and marker gene expression. Additionally, we investigated whether a single organ system was more sensitive to low doses of vitamin A and could potentially be used as an indicator of vitamin A exposure during early gestation. Results: High (100 mg/kg) and moderate (50 and 25 mg/kg) doses of vitamin A resulted in significant craniofacial, cardiac outflow tract and thymic abnormalities. Low doses of vitamin A(10 mg/kg) produced craniofacial and thymic abnormalities that were mild and of low penetrance. Exposed embryos showed morphologic changes in the 2nd and 3rd pharyngeal arches and pouches, changes in neural crest migration, abnormalities in cranial ganglia, and altered expression of Hoxa3. Conclusions: These animal studies, along with recent epidemiologic reports on human teratogenicity with vitamin A, raise concerns about the potential for induction of defects (perhaps subtle) in offspring of women ingesting even moderate to low amounts of supplemental Vitamin A during the early gestational period. (C) 2000 Wiley-Liss, Inc.

关键词：畸形药物性/病因学畸形药物性/代谢畸形药物性/病理学畸形多发性/化学诱导畸形多发性/代谢畸形多发性/病理学鳃区/畸形细胞死亡/药物作用细胞运动/药物作用颅神经/畸形颅面骨畸形 DNA结合蛋白质类/代谢胚胎和胎儿发育/药物作用流式细胞术心脏缺损先天性/化学诱导同源盒结构域蛋白质类/代谢免疫组织化学原位缺口末端标记小鼠近交C57BL 神经嵴/畸形神经嵴/药物作用胸腺/畸形维生素A/毒性动物女(雌)性人类小鼠妊娠

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Melatoninergic neuroprotection of the murine periventricular white matter against neonatal excitotoxic challenge

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ANNALS OF NEUROLOGY 2002年第1期51卷 82-92页

作者： Husson, I Mesplès, B Bac, P Vamecq, J Evrard, P Gressens, P Hop Robert Debre Serv Neuropediat F-75019 Paris France Hop Robert Debre INSERM E9935 F-75019 Paris France UFR Pharm Neuropharmacol Lab Chatenay Malabry France

Periventricular leukomalacia is one of the main causes of cerebral palsy. Perinatal white matter lesions associated with cerebral palsy appears to involve glutamate excitotoxicity and excess free radical production. When injected intracerebrally into newborn mice, the glutamatergic analog ibotenate induces white matter cysts mimicking human periventricular leukomalacia. Melatonin acts on specific receptors. It also exhibits intrinsic free radical scavenging properties. The goal of the present study is to determine whether melatonin can protect against excitotoxic lesions induced by ibotenate in newborn mice. Mice that received intraperitoneal melatonin had an 82% reduction in size of ibotenate-induced white matter cysts when compared with controls. Although melatonin did not prevent the initial appearance of white matter lesions, it did promote secondary lesion repair. Axonal markers supported the hypothesis that melatonin induced axonal regrowth or sprouting. The protective effects of melatonin were suppressed by coadministration of luzindole, a melatonin receptor antagonist. Forskolin, an adenylate cyclase activator, prevented the protective effects of melatonin;inhibitors of protein kinase C and mitogen-associated protein kinase had no detectable effect. Melatonin and derivatives that block cAMP production through activation of melatonin receptors could represent new avenues for treating human periventricular leukomalacia.

关键词：动物新生抗氧化剂/药理学细胞死亡/药物作用脑性瘫痪/化学诱导脑性瘫痪/药物疗法脑性瘫痪/死亡率胱氨酸/类似物和衍生物胱氨酸/药理学去神经支配疾病模型动物兴奋性氨基酸激动剂自由基清除剂/药理学低温人工鹅膏蕈氨酸白质软化病脑室周围/化学诱导白质软化病脑室周围/药物疗法白质软化病脑室周围/死亡率褪黑激素/药理学小鼠近交C57BL 小鼠转基因新皮质/生理学神经保护药/药理学神经毒素类 RNA 信使/分析受体细胞表面/拮抗剂和抑制剂受体细胞表面/遗传学受体胞质和核/拮抗剂和抑制剂受体胞质和核/遗传学受体褪黑激素四氢萘类/药理学色胺类/药理学动物人类婴儿新生小鼠

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Jasmonic acid signaling modulates ozone-induced hypersensitive cell death

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PLANT CELL 2000年第9期12卷 1633-1646页

作者： Rao, MV Lee, H Creelman, RA Mullet, JE Davis, KR Paradigm Genet Inc Res Triangle Pk NC 27709 USA Texas A&M Univ Dept Biochem & Biophys Crop Biotechnol Ctr College Stn TX 77843 USA Rutgers State Univ Cook Coll Ctr Biotechnol New Brunswick NJ 08901 USA Ohio State Univ Ctr Plant Biotechnol Columbus OH 43210 USA

Recent studies suggest that cross-talk between salicylic acid (SA)-, jasmonic acid (JA)-, and ethylene-dependent signaling pathways regulates plant responses to both abiotic and biotic stress factors. Earlier studies demonstrated that ozone (O-3) exposure activates a hypersensitive response (HR)-like cell death pathway in the Arabidopsis ecotype Cvi-0. We now have confirmed the role of SA and JA signaling in influencing O-3-induced cell death. Expression of salicylate hydroxylase (NahG) in Cvi-0 reduced O-3-induced cell death. Methyl jasmonate (Me-JA) pretreatment of Cvi-O decreased O-3-induced H2O2 content and SA concentrations and completely abolished O-3-induced cell death. Cvi-0 synthesized as much JA as did Col-0 in response to O-3 exposure but exhibited much less sensitivity to exogenous Me-JA. Analyses of the responses to O-3 Of the JA-signaling mutants jar1 and fad3/7/8 also demonstrated an antagonistic relationship between JA- and SA-signaling pathways in controlling the magnitude of O-3-induced HR-like cell death.

关键词：乙酸盐类/药理学拟南芥属/细胞学拟南芥属/药物作用拟南芥属/代谢细胞死亡/药物作用环戊烷类/药理学剂量效应关系药物基因表达调控植物/药物作用过氧化氢/代谢混合功能氧化酶类/遗传学突变氧化脂类臭氧/毒性植物蛋白质类/遗传学植物基因修饰 RNA 植物/药物作用 RNA 植物/遗传学 RNA 植物/代谢活性氧/代谢水杨酸/代谢信号传导

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Neuronal death enhanced by N-methyl-D-aspartate antagonists

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第23期97卷 12885-12890页

作者： Ikonomidou, C Stefovska, V Turski, L Humboldt Univ Charite Virchow Clin Childrens Hosp Dept Pediat Neurol D-13353 Berlin Germany UCL Eisai London Res Labs London WC1E 6BT England

Glutamate promotes neuronal survival during brain development and destroys neurons after injuries in the mature brain. Glutamate antagonists are in human clinical trials aiming to demonstrate limitation of neuronal injury after head trauma, which consists of both rapid and slowly progressing neurodegeneration. Furthermore, glutamate antagonists are considered for neuroprotection in chronic neurodegenerative disorders with slowly progressing cell death only. Therefore, humans suffering from Huntington's disease. characterized by slowly progressing neurodegeneration of the basal ganglia. are subjected to trials with glutamate antagonists. Here we demonstrate that progressive neurodegeneration in the basal ganglia induced by the mitochondrial toxin 3-nitro-propionate or in the hippocampus by traumatic brain injury is enhanced by N-methyl-D-aspartate antagonists but ameliorated by alpha -amino-3-hydroxy-5-methyl-4-isoxazole-propionate antagonists. These observations reveal that N-methyl-D-aspartate antagonists may increase neurodestruction in mature brain undergoing slowly progressing neurodegeneration. whereas blockade of the action of glutamate at alpha -amino-3-hydroxy-5-methyl-4-isoxazole-propionate receptors may be neuroprotective.

关键词：脑损伤/病理学细胞死亡/药物作用地卓西平马来酸盐/药理学兴奋性氨基酸激动剂/药理学兴奋性氨基酸拮抗剂/药理学美金刚/药理学 N-甲基天冬氨酸/拮抗剂和抑制剂神经元/药物作用神经元/病理学神经保护药/药理学神经毒素类/药理学硝基化合物哌嗪类/药理学丙酸盐类/药理学喹恶啉类/药理学大鼠 Wistar 创伤和损伤 α-氨基-3-羟基-5-甲基-4-异唑丙酸/拮抗剂和抑制剂动物大鼠

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