Bibliografías temáticas / 3-Nitropropionic Acid (3-NPA)

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Literatura académica sobre el tema "3-Nitropropionic Acid (3-NPA)"

Autor: Grafiati

Publicado: 7 de junio de 2025

Última modificación: 2 de agosto de 2025

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Artículos de revistas sobre el tema "3-Nitropropionic Acid (3-NPA)"

Feng, Meng-Lin, Zheng-Hui Li, and Bao-Bao Shi. "Progress on 3-Nitropropionic Acid Derivatives." Biomolecules 15, no. 8 (2025): 1066. https://doi.org/10.3390/biom15081066.

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3-Nitropropionic acid (3-NPA) is a deadly neurotoxic nitroalkane found in numerous fungi and leguminous plants. 3-NPA, known as an antimetabolite of succinate, irreversibly inhibits succinate dehydrogenase and disrupts mitochondrial oxidative phosphorylation. Its utility in modeling Huntington’s disease (HD) and oxidative stress has garnered significant research interest. Derivatives of 3-NPA, formed through esterification, have a wide range of biological activities including neurotoxic, antiviral, insecticidal, antimicrobial and antioxidant properties. This review systematically summarizes th

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Zhao, Yifang, Heng Zeng, Kun Wu, et al. "A pH-regulated ratiometric luminescence Eu-MOF for rapid detection of toxic mycotoxin in moldy sugarcane." Journal of Materials Chemistry C 8, no. 13 (2020): 4385–91. http://dx.doi.org/10.1039/d0tc00104j.

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Pass, Michael A., Carol H. Carlisle, and Kenneth R. Reuhl. "3‐Nitropropionic acid toxicity in cultured murine embryonal carcinoma cells." Natural Toxins 2, no. 6 (1994): 386–94. http://dx.doi.org/10.1002/nt.2620020608.

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AbstractThe morphologic and histochemical effects of 3‐nitropropionic acid (NPA) were examined in cultured murine embryonal carcinoma cells. NPA caused a dose‐dependent inhibition of cell proliferation of cultured murine embryonal carcinoma cells at concentrations above 1.05 mM and was lethal at 4.2 mM. Morphologic changes included gross swelling of the cells, swelling of mitochondria and accumulation of organellar debris within the cytoplasm. NPA inhibited the activity of succinate dehydrogenase but not of malate, isocitrate or glucose‐6‐phosphate dehydrogenases, resulting in a decrease in in

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Ockaili, Ramzi A., Peeyush Bhargava, and Rakesh C. Kukreja. "Chemical preconditioning with 3-nitropropionic acid in hearts: role of mitochondrial KATP channel." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (2001): H2406—H2411. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2406.

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We investigated the cardioprotective effect of 3-nitropropionic acid (3-NPA), an inhibitior of mitochondrial succinate dehydrogenase, and we wanted to show whether this protection is mediated by of opening mitochondrial ATP-sensitive potassium (KATP) channels. Adult rabbits were treated with either 3-NPA (3 mg/kg iv) or saline ( n = 6 rabbits/group). After 30 min (for early phase) or 24 h (for late phase) of the treatment, the animals were subjected to 30 min of ischemia and 3 h of reperfusion (ischemia-reperfusion). 5-Hydroxydecanoate (5-HD, 5 mg/kg iv),the mitochondrial KATP channel blocker,

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Ludolph, A. C., F. He, P. S. Spencer, J. Hammerstad, and M. Sabri. "3-Nitropropionic Acid - Exogenous Animal Neurotoxin and Possible Human Striatal Toxin." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, no. 4 (1991): 492–98. http://dx.doi.org/10.1017/s0317167100032212.

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ABSTRACT:3-Nitropropionic acid (3-NPA) — a suicide inhibitor of succinate dehydrogenase — is a widely distributed plant and fungal neurotoxin known to induce damage to basal ganglia, hippocampus, spinal tracts and peripheral nerves in animals. Recent reports from Northern China indicate that 3-NPA is also likely to be responsible for the development of putaminal necrosis with delayed dystonia in children after ingestion of mildewed sugar cane. This article discusses the role of 3-NPA in the causation of the disease in China, its neurotoxic effects in animals and the potential role for this com

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Calderón Guzmán, David, Norma Osnaya Brizuela, Maribel Ortíz Herrera, et al. "Effect of cerebrolysin on dopaminergic neurodegeneration of rat with oxidative stress induced by 3-nitropropionic acid." Acta Pharmaceutica 66, no. 3 (2016): 443–48. http://dx.doi.org/10.1515/acph-2016-0027.

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Abstract The study tested the hypothesis that cerebrolysin protects the brain from free radicals in rats treated with 3-nitropropionic acid (3-NPA). To address this hypothesis, the levels of dopamine (DA) and some oxidative stress biomarkers were measured after administration of 3-NPA. Young male Fischer rats were treated for three days with cerebrolysin, 3-NPA or both substances. Their brains were extracted, and DA, lipid peroxidation (LP), glutathione (GSH), calcium, and H2O2 were measured using validated methods. In the cortex, hemispheres and cerebellum/medulla oblongata of the group treat

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SCALLET, A. C., P. L. NONY, R. L. ROUNTREE, and Z. K. BINIENDA. "Biomarkers of 3-Nitropropionic Acid (3-NPA)-Induced Mitochondrial Dysfunction as Indicators of Neuroprotection." Annals of the New York Academy of Sciences 939, no. 1 (2006): 381–92. http://dx.doi.org/10.1111/j.1749-6632.2001.tb03647.x.

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Lopez-Sanchez, Carmen, Virginio Garcia-Martinez, Joana Poejo, Virginio Garcia-Lopez, Jairo Salazar, and Carlos Gutierrez-Merino. "Early Reactive A1 Astrocytes Induction by the Neurotoxin 3-Nitropropionic Acid in Rat Brain." International Journal of Molecular Sciences 21, no. 10 (2020): 3609. http://dx.doi.org/10.3390/ijms21103609.

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3-Nitropropionic acid (NPA) administration to rodents produces degeneration of the striatum, accompanied by neurological disturbances that mimic Huntington’s disease (HD) motor neurological dysfunctions. It has been shown that inflammation mediates NPA-induced brain degeneration, and activated microglia secreting cytokines interleukin-1α (IL-1α) and tumor necrosis factor α (TNFα) can induce a specific type of reactive neurotoxic astrocytes, named A1, which have been detected in post-mortem brain samples of Huntington’s, Alzheimer’s, and Parkinson’s diseases. In this work we used an experimenta

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Chomcheon, Porntep, Suthep Wiyakrutta, Nongluksna Sriubolmas, Nattaya Ngamrojanavanich, Duangnate Isarangkul, and Prasat Kittakoop. "3-Nitropropionic Acid (3-NPA), a Potent Antimycobacterial Agent from Endophytic Fungi: Is 3-NPA in Some Plants Produced by Endophytes?" Journal of Natural Products 68, no. 7 (2005): 1103–5. http://dx.doi.org/10.1021/np050036a.

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Shinomol, George K., M. M. Srinivas Bharath, and Muralidhara. "Pretreatment withBacopa monnieriextract offsets 3-nitropropionic acid induced mitochondrial oxidative stress and dysfunctions in the striatum of prepubertal mouse brain." Canadian Journal of Physiology and Pharmacology 90, no. 5 (2012): 595–606. http://dx.doi.org/10.1139/y2012-030.

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The present investigation was designed to determine the efficacy of Bacopa monnieri (Brahmi; BM) to offset 3-nitropropionic acid (3-NPA) induced oxidative stress and mitochondrial dysfunction in dopaminergic (N27) cells and prepubertal mouse brain. Pretreatment of N27 cells with BM ethanolic extract (BME) significantly attenuated 3-NPA-induced cytotoxicity. Further, we determined the degree of oxidative stress induction, redox status, enzymic antioxidants, and protein oxidation in the striatal mitochondria of mice given BME prophylaxis followed by 3-NPA challenge. While 3-NPA-induced marked ox

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Tesis sobre el tema "3-Nitropropionic Acid (3-NPA)"

Moreira, Amanda Lopez. "Efeitos do ácido 3-nitropropiônico (3-NP) na inervação extrínseca do coração de camundongos - modelo experimental para a doença de Huntington." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-23082017-113206/.

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A doença de Huntington (DH) é um distúrbio neurodegenerativo hereditário e autossômico dominante e tem como características alterações motoras e mentais progressivas. Recentemente, além das alterações verificadas no sistema nervoso central, também têm sido descritas alterações em órgãos periféricos, tais como osteoporose, atrofia muscular, problemas intestinais, alterações cardíacas e, sobretudo, alterações no sistema nervoso autônomo. São evidentes as alterações autonômicas do coração nos portadores da DH, as quais, são, sobretudo, um risco potencial, tornando os pacientes suscetíveis a probl

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Lee, Hsin-Jung, and 李欣蓉. "Toxic effects of 3-nitropropionic acid(3-NP) on hypothalamic neurons in rats." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/4qgc35.

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碩士 慈濟大學 神經科學研究所 93 3-Nitropropionic acid (3-NP) is an irreversible succinate dehydrogenase inhibitor and the administration of 3-NP caused neuropathological deficits is similar to these found in Huntington’s disease (HD), including behavioral alteration and cortico-striatal degeneration. HD patients were found the degeneration of the hypothalamic neurons and showed the loss of body weight. The aim in this study is to investigate the change of body weight and food intake after administering 3-NP in adult male Spraque-Dawley rats. The body weight and food intake were significantly de

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Hui-Chu, Tsung, and 鍾惠菊. "The protection of estradiol against 3-nitropropionic acid (3-NP) -induced toxicity in striatal primary cell culture." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/95860843423505477398.

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碩士 國防醫學院 生物及解剖學研究所 89 In recent years, ingestion of mildewed sugarcane caused Huntington's disease (HD) like syndrome in Southern China. It prompted further investigation and the corresponding results showed that was due to the toxicity of 3-nitroprpionic acid (3-NP) produced by Arthrinum in mildewed sugarcane. Metabolic compromise with systemic 3-NP resulted in the degeneration of striatal cell, mimicking the pathology of HD. In vivo study had shown that estradiol （E2） was able to attenuate HD like syndrome, which induced by 3-NP. However, there was no direct evidence to indic

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