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Nitric Oxide Synthase Inhibition Prevents Acute Quinolinate-Induced Striatal Neurotoxicity
Abstract
Quinolinic acid (QUIN) is an endogenous excitotoxin acting on N-methyl-D-aspartate (NMDA) receptors, that leads to neurotoxic damage resembling the alterations observed in Huntington's disease. Two major end-points of QUIN induced neurotoxicity are both circling behavior (CB) and lipid peroxidation (LP). Recently, nitric oxide (NO) has been implicated as a mediator of cell injury in some neurological disorders, thus, NO as a free radical might be involved in QUIN-induced neurotoxicity and oxidative stress. In the present study we evaluated the possible role of NO on QUIN-induced neurotoxicity, by measuring nitric oxide synthase activity (NOS), before and after QUIN-induced damage and by evaluating the effect of NOS inhibition on acute QUIN-induced CB and LP. Rats were striatally microinjected with QUIN (240 nmol/microl). QUIN administration increased NOS activity by 327% as compared to control values and this enhancement was inhibited by i.v. pretreatment with a NOS inhibitor the N(G)-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg). QUIN-induced CB was also attenuated by pretreatment of rats with 1, 5, 10 and 15 mg/kg of L-NAME by -37, -55, -62 and -74% vs QUIN respectively. Similarly, L-NAME also reduced by 32% the QUIN-induced LP. These findings suggest that enhanced NOS activity may participate in QUIN-induced neurotoxicity and oxidative stress.
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“Neurotoxicity in neurons is triggered by the overstimulation of NMDA receptors, leading to disruptions in intracellular Ca2+ homeostasis and free radical formation [53,54].”
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“Activation of nNOS also has several implications in neuroinflammation: (1) NMDA receptor-mediated excitotoxicity is reduced in response to NOS inhibition in cultured rat cortical neurons (Dawson et al. 1991); (2) nNOS knockout mice report a significant reduction in death due to NMDA receptor-mediated excitotoxicity (A…”
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“transcriptionally (and robustly: by 327%) induce NOS activity in in vivo and in vitro experiments (Melillo et al. 1994; Perez-Severiano et al. 1998).”
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“kines and kynurenine metabolite QA [56–58].”
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“Interestingly, it has also been reported that the use of nitric oxide synthase inhibitors, such as Nx-nitro-L-arginine methyl ester (Pérez-Severiano et al. 1998) and Nx-nitro-L-arginine (Santamarı́a et al.”
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“…bidirectional (Schmidt et al. 1995), the use of some NOS inhibitors, such as the general inhibitors L-NARG (Santamaría et al. 1999) and L-NAME (Pérez-Severiano et al. 1998), or the neuronal NOS inhibitor L-MIN (Bazzett et al. 1997), result in some protective actions against QUIN-induced…”
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“…1983; Foster and Schwarcz, 1989; Winn et al., 1991; Behan et al., 1999; Rios and Santamaria, 1991; Santamaria and Rios, 1993; Stipek et al., 1997; Perez-Severiano et al., 1998, 2004; Stone et al., 2000; Rodriguez-Martinez et al., 2000; Cabrera et al., 2000; Santamaria et al., 2001, 2003;…”
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“NO has been directly implicated in the pattern of neurotoxicity produced by QA, because L-NAME is able to prevent QA-induced circling behaviour, lipid peroxidation and NOS activation in a Ca2+-dependent manner in vivo (Perez-Severiano et al. 1998) and in vitro (Santamaria et al. 1999).”
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Self-citationRubio-Osornio, M., Gorostieta-Salas, E., Montes, S., Pérez-Severiano, F., Rubio, C., Gómez, C., Ríos, C., & Guevara, J. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2015/276039 · Cited by 10
“We hypothesize that the administration of EC in rats is able to decrease the effect of free radicals, in response to oxidative stress associated with the microinjection of MPP+ in the rat striatum.”
BackgroundSelf-citationNitric oxide synthase inhibition prevents acute QA-induced neurotoxicity
Ivana, D., Marina, D., Milica, N., & Zivorad, M. (2002) · Acta veterinaria · doi:10.2298/avb0203079v · Cited by 7
Guevara, B., Céspedes, G., & Cubeddu, L. (2002) · Cellular and molecular neurobiology · doi:10.1023/a:1021877512519 · Cited by 6
“Both neuroprotective and neurotoxic actions have been described for nitric oxide (Choi, 1992; Connop et al., 1996; Fujisawa et al., 1993; Loschmannn et al., 1995; Perez-Severiano et al., 1998 ).”
InfluentialAzotni oksid, neurodegeneracija i Parkinsonova bolest
Dzoljic, E., Nešić, I., Stojanović, M., Divac, N., Todorović, Z., Vuckovic, M., Kostic, S., & Prostran, S. M. (2005) · Vojnosanitetski pregled · doi:10.2298/vsp0510751d · Cited by 5
“Transgeni knock-out miševi kojima nedostaje gen za nNOS, pokazali su manje izražena oštećenja kod PB, izazvane ne samo MPTP već i metamfetaminom (39, 71).”
BackgroundNitric oxide synthase inhibition and glutamate binding in quinolinate-lesioned rat hippocampus.
Lisý, V., & Št̆astný, F. (2002) · Physiological Research · doi:10.33549/physiolres.930210 · Cited by 5
Fongsaran, C., Dineley, K. T., Paessler, S., & Cisneros, I. E. (2024) · Pathogens · doi:10.3390/pathogens13050397 · Cited by 3
Bostanci, M., Bağırıcı, F., & Baş, O. (2008) · Toxicology Mechanisms and Methods · doi:10.1080/15376510801891369 · Cited by 2
“L-NAME attenuated quinolinateinduced striatal neurotoxicity in rats (Perez-Severiano et al. 1998).”
BackgroundOxidative Stress and Huntington’s Disease
Turner, C., & Schapira, A. H. V. (2003) · Oxidative stress and disease · doi:10.1201/9780203912874.ch20
Low Nitric Oxide and High C-Reactive Protein in Depression: Not a Paradox!
Oxenkrug, G. (2017) · Journal of Clinical Psychiatry · doi:10.4088/jcp.17lr11532
“Hence, PTPS becomes the ratelimiting enzyme with consequent accumulation of BH2 and its stable metabolite, neopterin.3 Therefore, the enhanced production of neopterin occurs at the expense of BH4 formation.4 Downstream kynurenine metabolites are able to activate NOS, thus increasing demand for BH4.”
BackgroundKynurenine Pathway and Related Neurodegenerative Disorders
Bedel, H. A., Coşkun, A. S., & Usta, C. (2018) · Turkiye Klinikleri Journal of Neurology · doi:10.5336/neuro.2018-60154
Vasiljević, D., Jovanović, D. M., Čolić, J., Mihajlović, R., Djukic, M., Ninkovic, M., & Maličević, Ž. (2004) · doi:10.2298/jmh0401011v
“NOS inhibitors were proposed as the candidates for the treatment of neurodegenerative disease (20).”
BackgroundMaksimović, D., Jovanović, D. M., Čolić, J., Micic, D., Mihajlović, R., & Selaković, M. (2002) · doi:10.2298/jmh0203269m
Metadata
- Authors
- Pérez-Severiano, F., Escalante, B., & Ríos, C.
- Affiliations
- Instituto Politécnico Nacional (MX)
- Venue
- Neurochemical Research
- Published
- 1998-10
- Volume
- 23
- Issue
- 10
- Pages
- 1297-1302
- ISSN
- 0364-3190 (ISSN-L)
- 1573-6903
- OpenAlex
- W2113919453
- Cited by
- 68
- References
- 0
- Citations by year
- 2024: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 4 · 2013: 3
- FWCI
- 1.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Neurochemical Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Consejo Nacional de Ciencia y Tecnología
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- quinolinic acid, nitric oxide synthase, striatal neurotoxicity, NMDA receptor excitotoxicity, circling behavior, lipid peroxidation, oxidative stress, L-NAME, Huntington's disease model
- MeSH terms
- Animals, Corpus Striatum, Enzyme Inhibitors, Male, Motor Activity, Rats, Wistar, Quinolinic Acid, Nitric Oxide Synthase, NG-Nitroarginine Methyl Ester, Rats
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