Effect of oxidative stress on excitatory amino acid release by cerebral cortical synaptosomes

Gilman, Sara C.; Bonner, Meta J.; Pellmar, Terry C.

doi:10.1016/0891-5849(93)90172-q

Cited by 35 publications

(17 citation statements)

References 31 publications

(4 reference statements)

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“…Actin MF also plays a role in vesicle release and endocytosis, by maintaining vesicles in the active zone (Halpain, 2003). In fact, oxidative stress decreases vesicular release of neurotransmitters in synaptosomes (Gilman et al, 1993) and, although both proteins have been identified as prone to iron-dependent oxidation and subsequent proteasomal degradation , it is still unknown whether oxidation of actin and tropomyosins play a role in this deleterious effect of reactive species on neurotransmitter release.…”

Section: Discussionmentioning

confidence: 99%

Acrolein induces selective protein carbonylation in synaptosomes

et al. 2007

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Acrolein, the most reactive of the α,β-unsaturated aldehydes, is endogenously produced by lipid peroxidation, and has been found increased in the brain of patients with Alzheimer's disease. Although it is known that acrolein increases total protein carbonylation and impairs the function of selected proteins, no study has addressed which proteins are selectively carbonylated by this aldehyde. In this study we investigated the effect of increasing concentrations of acrolein (0, 0.005, 0.05, 0.5, 5, 50 μM) on protein carbonylation in gerbil synaptosomes. In addition, we applied proteomics to identify synaptosomal proteins that were selectively carbonylated by 0.5 μM acrolein. Acrolein increased total protein carbonylation in a dose-dependent manner. Proteomic analysis (2-D electrophoresis followed by mass spectrometry) revealed that tropomyosin-3-gamma isoform 2, tropomyosin-5, β-actin, mitochondrial Tu translation elongation factor (EFTu mt ) and voltagedependent anion channel (VDAC) were significantly carbonylated by acrolein. Consistent with the proteomics studies that have identified specifically oxidized proteins in Alzheimer's Disease (AD) brain, the proteins identified in this study are involved in a wide variety of cellular functions including energy metabolism, neurotransmission, protein synthesis, and cytoskeletal integrity. Our results suggest that acrolein may significantly contribute for oxidative damage in AD brain.Acrolein (2-propen-1-al), the most reactive of the α,β-unsaturated aldehydes (Esterbauer et al., 1991), is a toxic compound found in automobile exhaust gases, overheated cooking oils and a metabolite of cyclophosphamide and allyl alcohol (Halliwell and Gutteridge, 1999). Acrolein can also be endogenously produced as a product of lipid peroxidation (Adams and Klaidman, 1993,Uchida, 1999) and from polyamine metabolism (Takano et al., 2005 Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 July 13. Published in final edited form as:Neuroscience. 2007 July 13; 147(3): 674-679. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript . As a consequence, the identification of acrolein adducts has been proposed as a biologic marker for oxidative stress (Kehrer and Biswal, 2000). Accordingly, acrolein levels have been found increased in pathological conditions associated with oxidative stress, such as spinal cord injury (Luo et al., 2005), diabetic nephropathy (Suzuki and Miyata, 1999) and Alzheimer's Disease (AD) (Markesbery and Lovell, 1998,Cal...

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Section: Discussionmentioning

confidence: 99%

Acrolein induces selective protein carbonylation in synaptosomes

et al. 2007

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“…It is well known that the increase of reactive oxygen species (ROS) may lead to a higher blood-brain barrier permeability and thus inhibit mitochondrial respiration and increase protein oxidation (Gilman et al, 1993;Rovere et al, 1995), impairing synaptic interactions. The isolated use of nandrolone decanoate also increased lipid peroxidation.…”

Section: G1mentioning

confidence: 99%

Lipid peroxidation in rats treated with vincristine sulphate and nandrolone decanoate

Martins

Lopes

Mazzanti

et al. 2011

Arq. Bras. Med. Vet. Zootec.

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Brain and serum lipid peroxidation was studied in rats treated with vincristine sulphate and different doses of nandrolone decanoate. Thirty rats were distributed into six groups (n=5). The treatments were applied once a week for two weeks. Sample collection was performed in the third week. Treatments during the first week were: G1 (control) -physiologic solution, G2-vincristine sulphate (4mg/m 2 ), G3-physiologic solution, G4-physiologic solution, G5-vincristine sulphate (4mg/m 2 ), and G6-vincristine sulphate (4mg/m 2 ). In the second week, they were: G1 (control) -physiologic solution, G2-physiologic solution, G3-nandrolone decanoate (1.8mg/kg -1 ), G4-nandrolone decanoate (10mg/kg -1 ), G5-nandrolone decanoate (1.8mg/kg -1 ), and G6-nandrolone decanoate (10mg/kg -1 ). Lipid peroxidation increased with the isolated use of vincristine and nandrolone decanoate, and with vincristine associated to the highest dose of the ester as well. These results suggest that vincristine sulphate and nandrolone decanoate increase free radical production. Therapeutic dose of nandrolone decanoate when associated with vincristine sulphate proved to be beneficial, as it was able to protect the organism from damaging processes involved in free radical production.Keywords: rat, anabolic androgenic steroid, chemotherapeutic, free radicals, brain, blood serum RESUMO Este estudo teve por objetivo detectar a peroxidação lipídica presente no cérebro e no soro de ratos tratados com sulfato de vincristina e diferentes doses de decanoato de nandrolona. Trinta ratos foram distribuídos em seis grupos (n=5). Os tratamentos foram aplicados uma vez por semana, durante duas semanas, e a coleta de amostras foi realizada na terceira semana. Na primeira semana, os tratamentos consistiram de: G1(controle) -solução fisiológica; G2 -sulfato de vincristina (4mg/m 2 ); G3 -solução fisiológica; G4 -solução fisiológica; G5 -sulfato de vincristina (4mg/m 2 ) e G6 -sulfato de vincristina (4mg/m 2 ). Na segunda semana: G1(controle)-

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“…Fe2+ in the presence of a peroxide. We assayed this reaction with respect to the effects of iron or copper ions, which are under increasing discussion as initiators and/or cofactors of the de velopments of neurodegenerative (Youdim and Lavie, 1994) and atherosclerotic diseases (Meyer et al, 1992;Kögl et al, 1994;Lupo et al, 1994), where the sulphur containing amino acid, methio nine, seems to be in the focus of such oxidative destructions (Preibisch and Elstner, 1994;Gilman et al, 1993).…”

Section: Resultsmentioning

confidence: 99%

Homocysteine-Induced Oxidative Damage: Mechanisms and Possible Roles in Neurodegenerative and Atherogenic Processes

Schlussel

Preibisch

Pütter

et al. 1995

Zeitschrift Für Naturforschung C

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Increased blood plasma concentrations of the sulphur amino acid homocysteine ("homocysteinemia") have been brought into context with neurodegenerative and arteriosclerotic symptoms and diseases.We recently reported on biochemical model reactions on the prooxidative activity of hom o cysteine including the desactivation of N a+/K +-ATPases and hemolysis of erythrocytes (Preibisch et al., 1993). In this communication we extend our model reactions including the oxida tion of methionine, metabolization of pyridoxalphosphate and dihydroxyphenylalanine, desactivations of transaminases and peroxidation of low density lipoprotein.

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Effect of oxidative stress on excitatory amino acid release by cerebral cortical synaptosomes

Cited by 35 publications

References 31 publications

Acrolein induces selective protein carbonylation in synaptosomes

Acrolein induces selective protein carbonylation in synaptosomes

Lipid peroxidation in rats treated with vincristine sulphate and nandrolone decanoate

Homocysteine-Induced Oxidative Damage: Mechanisms and Possible Roles in Neurodegenerative and Atherogenic Processes

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