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

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Publicado: 7 de junio de 2025
Última modificación: 2 de agosto de 2025

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1

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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2

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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4

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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5

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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7

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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8

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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9

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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10

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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11

Luchowska, Elzbieta, Piotr Luchowski, Marian Wielosz, Waldemar Turski, and Ewa Urbanska. "FK506 attenuates 1-methyl-4-phenylpyridinium- and 3-nitropropionic acid-evoked inhibition of kynurenic acid synthesis in rat cortical slices." Acta Neurobiologiae Experimentalis 63, no. 2 (2003): 101–8. http://dx.doi.org/10.55782/ane-2003-1459.

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Kynurenic acid (KYNA), the only known endogenous glutamate antagonist, is produced in the brain by kynurenine aminotransferases (KATs) I and II. Mitochondrial toxins, 1-methyl-4-phenylpyridinium (MPP+) and 3-nitropropionic acid (3-NPA), were previously shown to reduce KYNA synthesis via interference with KAT I and II. Data presented here demonstrate that immunophilin ligand, FK506 (10-130 µM), but not CsA (1-50 µM), or ryanodine receptor blocker, dantrolene (1-100 µM), enhances the formation of KYNA in cortical slices. FK506, but not CsA or dantrolene, abolished the inhibition of KYNA synthesi
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12

Wei, Quanwei, Guoyun Wu, Jun Xing, Dagan Mao, Reinhold J. Hutz, and Fangxiong Shi. "Roles of poly (ADP-ribose) polymerase 1 activation and cleavage in induction of multi-oocyte ovarian follicles in the mouse by 3-nitropropionic acid." Reproduction, Fertility and Development 31, no. 5 (2019): 1017. http://dx.doi.org/10.1071/rd18406.

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3-nitropropionic acid (3-NPA) is known to be a mitochondrial toxin produced by plants and fungi, which may produce DNA damage in cells. However, studies of its reproductive toxicology are lacking. We know that poly(ADP-ribose) polymerase (PARP) plays an important role in a large variety of physiological processes and is involved in DNA repair pathways. The present study was therefore aimed at exploring the involvement of PARP-1 activation and cleavage after 3-NPA stimulation in female mice. We observed an increased number of atretic follicles and multi-oocyte follicles (MOFs) after treatment w
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13

Ochoa-García, Pedro Antonio, Robin C. Anderson, Felipe Alonso Rodríguez-Almeida, et al. "EFFECT OF NITRO COMPOUNDS ON in vitro RUMINAL METHANE, CARBON DIOXIDE, HYDROGEN AND DRY MATTER DEGRADABILITY." Chilean journal of agricultural & animal sciences 40, no. 1 (2024): 190–97. http://dx.doi.org/10.29393/chjaas40-18enpa100018.

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This study determined the in vitro effects of ethyl nitroacetate (ENA), ethyl 2-nitropropionate (E-2-NPP) and 3-nitropropionic acid (NPA) on ruminal production of CH4, H2, volatile fatty acids (VFAs) and in vitro dry matter disappearance of ground alfalfa. In vitro incubations were carried out over 24-h succeeding days (3 batches). Total gas and methane production decreased with all nitro compounds (P 0.05) in all the batches. Total production of VFAs was reduced by ENA and E-2-NPP (P 0.05), but not by NPA. DM disappearance was similar between treatments but decreased across batches. Further s
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14

Binienda, Zbigniew, Ashraf Virmani, Beata Przybyla-Zawislak, and Larry Schmued. "Neuroprotective effect of l-carnitine in the 3-nitropropionic acid (3-NPA)-evoked neurotoxicity in rats." Neuroscience Letters 367, no. 2 (2004): 264–67. http://dx.doi.org/10.1016/j.neulet.2004.05.031.

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Alharbi, Khalid Saad. "Europinidin Mitigates 3-NPA-Induced Huntington’s Disease Symptoms in Rats: A Comprehensive Analysis of Oxidative Stress, Mitochondrial Enzyme Complex Activity, Pro-Inflammatory Markers and Neurotransmitter Alterations." Biomedicines 12, no. 3 (2024): 625. http://dx.doi.org/10.3390/biomedicines12030625.

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Huntington’s disease (HD) is a neurodegenerative disease that causes progressive motor and cognitive dysfunction. There is no cure for HD, and current therapeutics can only manage the signs and symptoms as well as slowing disease progression. This investigation examines the possible therapeutic advantages of europinidin in 3-nitropropionic acid (3-NPA) injected HD in rats. Wistar rats were randomly assigned to five groups (n = 6): normal control, 3-NPA (10 mg/kg, i.p.), 3-NPA + europinidin-10 (10 mg/kg, p.o.), 3-NPA + europinidin-20 (20 mg/kg, p.o.), and europinidin alone (20 mg/kg, p.o.) for
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16

Mahdi, Wael A., Shareefa A. AlGhamdi, Amira M. Alghamdi, et al. "Neuroprotectant Effects of Hibiscetin in 3-Nitropropionic Acid-Induced Huntington’s Disease via Subsiding Oxidative Stress and Modulating Monoamine Neurotransmitters in Rats Brain." Molecules 28, no. 3 (2023): 1402. http://dx.doi.org/10.3390/molecules28031402.

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Background: Previously reported data suggest that hibiscetin, isolated from roselle, contains delphinidin-3-sambubioside and cyanidin-3-sambubioside including anthocyanidins and has a broad range of physiological effects. In this study, we aim to analyze the effect of hibiscetin neuroprotective ability in rats against 3-nitropropionic acid (3-NPA)-induced Huntington’s disease (HD). Methods: To investigate possible toxicities in animals, oral acute toxicity studies of hibiscetin were undertaken, and results revealed the safety of hibiscetin in animals with a maximum tolerated dose. Wistar rats
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17

Johnson, John R., Bonnie L. Robinson, Syed F. Ali, and Zbigniew Binienda. "Dopamine toxicity following long term exposure to low doses of 3-nitropropionic acid (3-NPA) in rats." Toxicology Letters 116, no. 1-2 (2000): 113–18. http://dx.doi.org/10.1016/s0378-4274(00)00214-9.

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18

Pei, Geng, and Ted Ebendal. "Specific lesions in the extrapyramidal system of the rat brain induced by 3-nitropropionic acid (3-NPA)." Experimental Neurology 132, no. 1 (1995): 105–15. http://dx.doi.org/10.1016/0014-4886(95)90064-0.

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19

Brambrink, Ansgar M., Armin Schneider, Holger Noga, et al. "Tolerance-Inducing Dose of 3-Nitropropionic Acid Modulates bcl-2 and bax Balance in the Rat Brain: A Potential Mechanism of Chemical Preconditioning." Journal of Cerebral Blood Flow & Metabolism 20, no. 10 (2000): 1425–36. http://dx.doi.org/10.1097/00004647-200010000-00004.

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Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax, two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia–reperfusion, and to the c
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20

Jambi, Ebtihaj J., Abdulaziz Alamri, Muhammad Afzal та ін. "6-shogaol against 3-Nitropropionic acid-induced Huntington’s disease in rodents: Based on molecular docking/targeting pro-inflammatory cytokines/NF-κB-BDNF-Nrf2 pathway". PLOS ONE 19, № 7 (2024): e0305358. http://dx.doi.org/10.1371/journal.pone.0305358.

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Background Huntington’s disease (HD) is an extremely harmful autosomal inherited neurodegenerative disease. Motor dysfunction, mental disorder, and cognitive deficits are the characteristic features of this disease. The current study examined whether 6-shogaol has a protective effect against 3-Nitropropionic Acid (3-NPA)-induced HD in rats. Methods A total of thirty male Wistar rats received 6-shogaol (10 and 20 mg/kg, per oral) an hour before injection of 3-NPA (10 mg/kg i.p.) for 15 days. Behavioral tests were performed, including narrow beam walk, rotarod test, and grip strength test. Bioch
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21

BINIENDA, ZBIGNIEW, JOHN R. JOHNSON, ALEXANDER A. TYLER-HASHEMI, et al. "Protective Effect of l-Carnitine in the Neurotoxicity Induced by the Mitochondrial Inhibitor 3-Nitropropionic Acid (3-NPA)." Annals of the New York Academy of Sciences 890, no. 1 NEUROPROTECTI (1999): 173–78. http://dx.doi.org/10.1111/j.1749-6632.1999.tb07992.x.

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Fukuda, Atsuo, Shripad Deshpande, Yasunobu Shimano, Kanji Muramatsu, Akihito Okabe, and Hitoo Nishino. "Differential vulnerability to cellular Ca accumulation promoted by 3-nitropropionic acid (3-NPA) in cultured neurons and astrocytes." Neuroscience Research 28 (January 1997): S151. http://dx.doi.org/10.1016/s0168-0102(97)90405-3.

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Gonchar, Olga O., Andriy V. Maznychenko, Olena M. Klyuchko, et al. "C60 Fullerene Reduces 3-Nitropropionic Acid-Induced Oxidative Stress Disorders and Mitochondrial Dysfunction in Rats by Modulation of p53, Bcl-2 and Nrf2 Targeted Proteins." International Journal of Molecular Sciences 22, no. 11 (2021): 5444. http://dx.doi.org/10.3390/ijms22115444.

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C60 fullerene as a potent free radical scavenger and antioxidant could be a beneficial means for neurodegenerative disease prevention or cure. The aim of the study was to define the effects of C60 administration on mitochondrial dysfunction and oxidative stress disorders in a 3-nitropropionic acid (3-NPA)-induced rat model of Huntington’s disease. Animals received 3-NPA (30 mg/kg i.p.) once a day for 3 consecutive days. C60 was applied at a dose of 0.5 mg/kg of body weight, i.p. daily over 5 days before (C60 pre-treatment) and after 3-NPA exposure (C60 post-treatment). Oxidative stress biomark
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24

Shimano, Yasunobu, Michiko Kumazaki, Terumi Sakurai, and Hitoo Nishino. "Systemic administration of 3-nitropropionic acid (3-NPA) made damages in the striatum and produced reduction of muscle tonus." Neuroscience Research Supplements 19 (January 1994): S147. http://dx.doi.org/10.1016/0921-8696(94)92681-6.

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Bin-Jumah, May Nasser, Sadaf Jamal Gilani, Abdulaziz F. Alabbasi, et al. "Protective Effect of Fustin against Huntington’s Disease in 3-Nitropropionic Treated Rats via Downregulation of Oxidative Stress and Alteration in Neurotransmitters and Brain-Derived Neurotrophic Factor Activity." Biomedicines 10, no. 12 (2022): 3021. http://dx.doi.org/10.3390/biomedicines10123021.

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Researchers have revealed that Rhus verniciflua heartwood, which contains fustin as an important component, possesses antioxidant-mediated, anti-mutagenic, and anti-rheumatoid arthritis characteristics. Additionally, out of the numerous plant-derived secondary metabolites, there are various research papers concentrating on flavonoids for potential advantages in neurological illnesses. The current study aims to assess the neuroprotective potential of fustin in rodents over 3-nitropropionic acid (3-NPA)-induced Huntington’s disease (HD)-like consequences. The efficacy of fustin 50 and 100 mg/kg
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Jang, Minhee, Jong Hee Choi, Dae Sik Jang, and Ik-Hyun Cho. "Micrandilactone C, a Nortriterpenoid Isolated from Roots of Schisandra chinensis, Ameliorates Huntington’s Disease by Inhibiting Microglial STAT3 Pathways." Cells 12, no. 5 (2023): 786. http://dx.doi.org/10.3390/cells12050786.

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Huntington’s disease (HD) is a neurodegenerative disease that affects the motor control system of the brain. Its pathological mechanism and therapeutic strategies have not been fully elucidated yet. The neuroprotective value of micrandilactone C (MC), a new schiartane nortriterpenoid isolated from the roots of Schisandra chinensis, is not well-known either. Here, the neuroprotective effects of MC were demonstrated in 3-nitropropionic acid (3-NPA)-treated animal and cell culture models of HD. MC mitigated neurological scores and lethality following 3-NPA treatment, which is associated with decr
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Bracko, Oliver, Valentina Di Pietro, Giacomo Lazzarino, et al. "3-Nitropropionic Acid-Induced Ischemia Tolerance in the Rat Brain is Mediated by Reduced Metabolic Activity and Cerebral Blood Flow." Journal of Cerebral Blood Flow & Metabolism 34, no. 9 (2014): 1522–30. http://dx.doi.org/10.1038/jcbfm.2014.112.

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Tissue tolerance to ischemia can be achieved by noxious stimuli that are below a threshold to cause irreversible damage (‘preconditioning’). Understanding the mechanisms underlying preconditioning may lead to the identification of novel therapeutic targets for diseases such as stroke. We here used the oxidative chain inhibitor 3-nitropropionic acid (NPA) to induce ischemia tolerance in a rat middle cerebral artery occlusion (MCAO) stroke model. Cerebral blood flow (CBF) and structural integrity were characterized by longitudinal magnetic resonance imaging (MRI) in combination with behavioral,
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K.M., Denny Joseph, and Muralidhara. "Neuroprotective efficacy of a combination of fish oil and ferulic acid against 3-nitropropionic acid-induced oxidative stress and neurotoxicity in rats: behavioural and biochemical evidence." Applied Physiology, Nutrition, and Metabolism 39, no. 4 (2014): 487–96. http://dx.doi.org/10.1139/apnm-2013-0262.

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The beneficial effects of fish oil (FO) supplements on the central nervous system have been adequately demonstrated. However, FO supplementation at higher doses for longer duration is likely to cause oxidative stress in vivo. To overcome this, attempts have been made to enrich FO with known antioxidants/phytochemicals. In the present study, we examined the hypothesis that a combination of FO with ferulic acid (FA), a naturally occurring phenolic compound, is likely to provide higher degree of neuroprotection. This was examined by employing 3-nitropropionic acid (NPA), a well-known neurotoxin u
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A., Fukuda, Deshpande S., Fujimoto I., et al. "1310 Differential susceptibility to intracellular Ca2+ ([Ca2+]1) increases promoted by 3-nitropropionic acid (3-NPA) in cultured neurons and astrocytes." Neuroscience Research 25 (January 1996): S143. http://dx.doi.org/10.1016/0168-0102(96)88959-0.

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Nakajima, Keiya, Shripad B. Deshpande, and Hitoo Nishino. "3-Nitropropionic acid (3-NPA)-induced toxicity of endothelial cells in vitro is mediated by nitric oxide dependent and independent mechanisms." Neuroscience Research 31 (January 1998): S346. http://dx.doi.org/10.1016/s0168-0102(98)82513-3.

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Khudoerkov, Rudolf M., Vladimir N. Salkov, and Dmitry N. Voronkov. "Methods of immunohistochemistry and computerized morphometry as promising tools in the study of pathogenic patterns of neurodegenerative processes." Annals of Clinical and Experimental Neurology 12, no. 5S (2018): 55–59. https://doi.org/10.25692/acen.2018.5.7.

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Modern methods of immunohistochemistry and computer morphometry provide powerful possibilities for the study of pathogenetic patterns of neurodegeneration process occurring in physiological aging of men and women, as well as in experimental animals on modeling of Parkinsons and Huntington's diseases. Threedimensional reconstruction of the substantia nigra pars compacta of the human and rat brains revealed both common features in their organization (heterogeneity of structures) and differences in quantitative morphochemical parameters determining their species-specific characteristics. On model
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Afzal, Muhammad, Nadeem Sayyed, Khalid Saad Alharbi, et al. "Anti-Huntington’s Effect of Rosiridin via Oxidative Stress/AchE Inhibition and Modulation of Succinate Dehydrogenase, Nitrite, and BDNF Levels against 3-Nitropropionic Acid in Rodents." Biomolecules 12, no. 8 (2022): 1023. http://dx.doi.org/10.3390/biom12081023.

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Background: Rosiridin is a compound extracted from Rhodiola sachalinensis; water extracts of Rhodiola root elicit positive effects on the human central nervous system and improve brain function. They are also thought to be beneficial to one’s health, in addition to being antioxidants. The present study aims to evaluate the anti-Huntington’s effect of rosiridin against 3-nitropropionic acid (3-NPA)-induced Huntington’s disease (HD)-like effects in rats. Materials and Methods: The acute toxicity in rats was elucidated to track the conceivable toxicities in the rats. The effectiveness of rosiridi
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Guo, Wei, Weiwei Wang, Ying Zhang, and Mi Zhou. "Effect of 3-Nitropropionic Acid at Different Doses on In Vitro Rumen Fermentation, Digestibility, and Methane Emissions of Grazing Yak and Cattle." Animals 14, no. 12 (2024): 1804. http://dx.doi.org/10.3390/ani14121804.

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3-nitropropionic acid (3NPA) has been proposed as an useful modifier to mitigate ruminal enteric methane emissions. However, few studies investigated the effects of 3NPA on ruminal fermentation characteristics of grazing ruminants in vitro. Rumen fluid from grazing yak and cattle were collected and incubated with additions of 0, 8, and 16 mM 3NPA. The total gas production, CH4 production, and dry matter digestibility significantly decreased with increasing 3NPA doses in both ruminant species (p < 0.05) and methane production decreased to almost 100% in cattle at 8 mM NPA but not yak, while
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Anitha, Devi U., G. Renuka, Venkateshwarlu, and T. *Ugandhar. ""SPOILED COCONUT WATER-INDUCED NEUROTOXICITY: NOVEL INSIGHTS INTO FUNGAL CONTAMINATION, 3-NPA POISONING, PREVENTION, AND PLANT-BASED THERAPIES"." World Journal of Pharmaceutical Science and Research 4, no. 2 (2025): 1071–83. https://doi.org/10.5281/zenodo.15364989.

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Coconut water is a widely consumed natural beverage, prized for its hydration and health benefits. However, recent clinical evidence highlights a rare but life-threatening risk associated with its improper storage. This review centres on a fatal case involving a 69-year-old man in Denmark who developed acute neurotoxic symptoms such as nausea, vomiting, profuse sweating, and brain swelling after consuming coconut water left unrefrigerated for one month. Laboratory analysis confirmed contamination by the fungus <em>Arthrinium saccharicola</em>, which produces 3-nitropropionic acid (3-NPA), a mi
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Vercammen, Ken, Qing Wei, Daniel Charlier, et al. "Pseudomonas aeruginosa LysR PA4203 Regulator NmoR Acts as a Repressor of the PA4202nmoAGene, Encoding a Nitronate Monooxygenase." Journal of Bacteriology 197, no. 6 (2014): 1026–39. http://dx.doi.org/10.1128/jb.01991-14.

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The PA4203 gene encodes a LysR regulator and lies between theppgLgene (PA4204), which encodes a periplasmic gluconolactonase, and, in the opposite orientation, the PA4202 (nmoA) gene, coding for a nitronate monooxygenase, andddlA(PA4201), encoding ad-alanine alanine ligase. The intergenic regions between PA4203 andppgLand between PA4203 andnmoAare very short (79 and 107 nucleotides, respectively). Here we show that PA4203 (nmoR) represses its own transcription and the expression ofnmoA. A chromatin immunoprecipitation analysis showed the presence of a single NmoR binding site betweennmoAandnmo
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Pei, Xingyao, Wenjuan Zhang, Haiyang Jiang, et al. "Food-Origin Mycotoxin-Induced Neurotoxicity: Intend to Break the Rules of Neuroglia Cells." Oxidative Medicine and Cellular Longevity 2021 (September 28, 2021): 1–14. http://dx.doi.org/10.1155/2021/9967334.

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Mycotoxins are key risk factors in human food and animal feed. Most of food-origin mycotoxins could easily enter the organism and evoke systemic toxic effects, such as aflatoxin B1 (AFB1), ochratoxin A (OTA), T-2 toxin, deoxynivalenol (DON), zearalenone (ZEN), fumonisin B1 (FB1), and 3-nitropropionic acid (3-NPA). For the last decade, the researches have provided much evidences in vivo and in vitro that the brain is an important target organ on mycotoxin-mediated neurotoxic phenomenon and neurodegenerative diseases. As is known to all, glial cells are the best regulator and defender of neurons
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Ringsborg Westphal, K., N. Vittrup Andersen, B. Uttrup Dideriksen, A. Filtenborg Gunggaard, M. A. Duus, and T. E. Sondergaard. "Deadly nuts – detection of 3-nitropropionic acid in coconuts." World Mycotoxin Journal, November 30, 2023, 1–5. http://dx.doi.org/10.1163/18750796-20232879.

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Abstract The secondary metabolite 3-nitropropionic acid (3-NPA) is produced by certain fungi. The metabolite is a potent toxin which inhibits the citric acid cycle. A medical case from 2021 described a 69-year-old Danish man who ingested 3-nitropropionic acid contaminated coconut water. The man died 26 hours after ingestion. Subsequent analysis identified Apiospora saccharicola as the fungi responsible for synthesising 3-NPA in the coconut. The metabolic pathway for 3-NPA is unknown but is thought to be activated by adverse growth conditions. This study aimed to confirm that Apiospora can prod
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38

Kang, Bo, Xinxing Wang, Qilin Xu, Yongsheng Wu, Xiaohui Si, and Dongmei Jiang. "Effect of 3-nitropropionic acid inducing oxidative stress and apoptosis of granulosa cells in geese." Bioscience Reports 38, no. 5 (2018). http://dx.doi.org/10.1042/bsr20180274.

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The mechanism of action by which oxidative stress induces granulosa cell apoptosis, which plays a vital role in initiating follicular atresia, is not well understood. In the present study, the effect of 3-nitropropionic acid (3-NPA) on oxidative stress and apoptosis in granulosa cells in geese was investigated. Our results showed that treatment with 3-NPA at 5.0 mmol/l for 24 h increased intracellular reactive oxygen species (ROS) production by 25.4% and decreased granulosa cell viability by 45.5% (P&lt;0.05). Catalase and glutathione peroxidase gene expression levels in granulosa cells treate
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Jiang, Wenyan, Xuelian Liang, Huiling Li, et al. "Inhibitory effect of tannic acid on the growth of Apiospora arundinis and 3-Nitropropionic acid production." Journal of Applied Microbiology, November 13, 2023. http://dx.doi.org/10.1093/jambio/lxad264.

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Abstract Aims This study aimed to investigate the inhibitory effect of tannic acid (TA) on the growth of Apiospora arundinis and 3-Nitropropionic acid (3-NPA) production. Methods and results To investigate the antifungal mechanism, the effects of TA on the hypha growth, electrical conductivity, hypha morphology, defence-related enzymes and 3-NPA production of A. arundinis were studied. TA concentrations of 640 and 1280 μg⋅mL−1 exhibited strong antifungal activity against A. arundinis. The results of SEM and TEM showed that the hypha of the A. arundinis was severely deformed after TA treatment,
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Ranganayaki, Sathyanarayanan, Neema Jamshidi, Mohamad Aiyaz, et al. "Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-020-79339-2.

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AbstractMitochondrial dysfunction and neurodegeneration underlie movement disorders such as Parkinson’s disease, Huntington’s disease and Manganism among others. As a corollary, inhibition of mitochondrial complex I (CI) and complex II (CII) by toxins 1-methyl-4-phenylpyridinium (MPP+) and 3-nitropropionic acid (3-NPA) respectively, induced degenerative changes noted in such neurodegenerative diseases. We aimed to unravel the down-stream pathways associated with CII inhibition and compared with CI inhibition and the Manganese (Mn) neurotoxicity. Genome-wide transcriptomics of N27 neuronal cell
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41

Alenezi, Sattam Khulaif. "Barbigerone attenuates 3-nitropropionic acid-induced Huntington’s disease-like neuropathology in rats via antioxidant, anti-inflammatory, and neuroprotective mechanisms." Scientific Reports 15, no. 1 (2025). https://doi.org/10.1038/s41598-025-07181-5.

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Abstract Huntington’s Disease (HD), a neurodegenerative disease characterized by motor and cognitive impairments, arises from genetic mutations causing protein aggregation within the brain. The 3-Nitropropionic acid (3-NPA) rat model mimics key features of HD. This study explored the therapeutic efficacy of barbigerone, a compound with antioxidant and anti-inflammatory properties, in ameliorating 3-NPA-induced neurodegeneration and cognitive deficits in rats. Male Wistar rats were randomized into four groups: a normal control group, a 3-NPA control group, and two groups treated with different
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42

Jiang, Dongmei, Qian Sun, Yilong Jiang, et al. "Effects of exogenous spermidine on autophagy and antioxidant capacity in ovaries and granulosa cells of Sichuan white geese." Journal of Animal Science, September 12, 2023. http://dx.doi.org/10.1093/jas/skad301.

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Abstract Autophagy can inhibit ovarian senescence induced by oxidative stress and regulate follicle development and atresia, but its mechanism is still unclear. Exogenous spermidine can induce autophagy and scavenge reactive oxygen species (ROS). In this experiment, oxidative stress in Sichuan white geese ovaries and follicular granulosa cells (GCs) were caused by 3-nitropropionic acid (3-NPA) and spermidine was added to explore the effect of exogenous spermidine inducing autophagy and inhibiting oxidative stress in vivo and in vitro. Research results showed that putrescine, spermidine and spe
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Kaur, Prabhjot, Shivani Attri, Davinder Singh, et al. "Neuromodulatory effect of 4-(methylthio)butyl isothiocyanate against 3-nitropropionic acid induced oxidative impairments in human dopaminergic SH-SY5Y cells via BDNF/CREB/TrkB pathway." Scientific Reports 13, no. 1 (2023). http://dx.doi.org/10.1038/s41598-023-31716-3.

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AbstractMitochondrial impairment, energetic crisis and elevated oxidative stress have been demonstrated to play a pivotal role in the pathological processes of Huntington’s disease (HD). 3-Nitropropionic acid (3-NPA) is a natural neurotoxin that mimics the neurological dysfunctions, mitochondrial impairments and oxidative imbalance of HD. The current investigation was undertaken to demonstrate the neuroprotective effect of 4-(methylthio)butyl isothiocyanate (4-MTBITC) against the 3-NPA induced neurotoxicity in human dopaminergic SH-SY5Y cells. The experimental evidence of oxidative DNA damage
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44

Yan, Shoulei, Huixia Wang, Yassin Haran, et al. "Purification and Clean-up of 3-NPA from Sugarcane by using Molecularly Imprinted Polymer Solid Phase Extraction Coupled with HPLC-siftdesk." SDRP Journal of Food Science & Technology, 2022, 406–16. http://dx.doi.org/10.25177/jfst.6.3.ra.10777.

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The agricultural product is in constant need of improved analytical techniques that can be used to control the manufacturing process and the food safety of the products. A new selective material based on molecularly imprinted polymers (MIPs) were prepared by bulk polymerization methods and used as solid-phase extraction (SPE) sorbent for sample enhancement of 3-nitropropanic acid (3-NPA) in sugarcane samples prior to high-performance liquid chromatography (HPLC). The objective of this work was to devolved techniques for the extraction, purification, clean up, and preconcentration of 3-NPA from
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45

Jo, Hyo-Sung, Youn-Woo Lee, So-Ri Son, et al. "A supercritical oil extract of Schisandra chinensis seeds ameliorates Huntington’s disease-like symptoms and neuropathology: the potential role of anti-oxidant and anti-inflammatory effects." Frontiers in Pharmacology 15 (December 23, 2024). https://doi.org/10.3389/fphar.2024.1471024.

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BackgroundHuntington disease (HD), a neurodegenerative autosomal dominant disorder, is characterized by involuntary choreatic movements with cognitive and behavioral disturbances. Up to now, no therapeutic strategies are available to completely ameliorate the progression of HD. Schisandra chinensis has various pharmacologic effects such as antioxidant and anti-inflammatory activities. However, the neuroprotective value of seed oil of S. chinensis (SOSC) has not been elucidated yet. The purpose of this study was to determine neuroprotective effects of SOSC by supercritical fluid extraction agai
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46

He, Weiwei, Hui-Juan Guan, Teng-Da Guo, Shu-Hong Liu, Deng Pan, and Hui-Min Jia. "AuCo Nanoparticles Inserted between the Layers of Ti3C2: An Efficient Nanozyme for Aliphatic Nitro‐to‐Amine Reduction." ChemNanoMat, May 15, 2025. https://doi.org/10.1002/cnma.202500171.

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The construction of nanozyme with superior catalytic activity and stable structure is urgently needed in practical application. In this work, AuCo nanoparticles inserted between the layers of Ti3C2 (AuCo/Ti3C2) were prepared by strong electrostatic adsorption (SEA) method and thermal treatment process. The nitroreductase‐like activity of AuCo/Ti3C2 was explored with a new hydrogenation reaction of 3‐nitropropionic acid (3‐NPA) to beta‐alanine (BA) as probe. AuCo/Ti3C2 shows the highest catalytic activity with TOF value of 4.5 × 1019 molecules·g‐1·s‐1 in comparison to Au/Ti3C2 and Co/Ti3C2, att
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47

Wang, Zelong, Dongmei Jiang, Xin Wang, et al. "Spermidine improves the antioxidant capacity and morphology of intestinal tissues and regulates intestinal microorganisms in Sichuan white geese." Frontiers in Microbiology 14 (January 16, 2024). http://dx.doi.org/10.3389/fmicb.2023.1292984.

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IntroductionIntestinal health is very important to the health of livestock and poultry, and is even a major determining factor in the performance of livestock and poultry production. Spermidine is a type of polyamine that is commonly found in a variety of foods, and can resist oxidative stress, promote cell proliferation and regulate intestinal flora.MethodsIn this study, we explored the effects of spermidine on intestinal health under physiological states or oxidative stress conditions by irrigation with spermidine and intraperitoneal injection of 3-Nitropropionic acid (3-NPA) in Sichuan whit
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48

Liao, Jie, Xuelian Liang, Huiling Li, et al. "Biocontrol ability of Bacillus velezensis T9 against Apiospora arundinis causing Apiospora mold on sugarcane." Frontiers in Microbiology 14 (December 22, 2023). http://dx.doi.org/10.3389/fmicb.2023.1314887.

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Sugarcane (Saccharum officinarum L.) may be infected with Apiospora, which can produce the toxin 3-nitropropionic acid (3-NPA) during improper transportation and storage. The consumption of sugarcane that contains 3-NPA can lead to food poisoning. Therefore, this study sought to explore a novel biocontrol agent to prevent and control Apiospora mold. Bacteria were isolated from the soil of healthy sugarcane and identified as Bacillus velezensis T9 through colony morphological, physiological and biochemical characterization and molecular identification. The inhibitory effect of B. velezensis T9
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49

Huang, Yupei, Yanfan Cui, Jian Huang, et al. "Proanthocyanidins protects 3-NPA-induced ovarian function decline by activating SESTRIN2-NRF2-mediated oxidative stress in mice." Scientific Reports 14, no. 1 (2024). http://dx.doi.org/10.1038/s41598-024-76743-w.

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AbstractAbnormal apoptosis of ovarian cells caused by oxidative stress is an important cause of premature ovarian failure (POF). Previous studies revealed that proanthocyanidins (PCs) are powerful natural antioxidants that can safely prevent oxidative damage in humans. However, the protective effect and mechanism of PCs on ovarian function during the course of POF remain unknown. In this study, female mice were injected with 3-nitropropionic acid (3-NPA) to establish an ovarian oxidative stress model; at the same time, the mice were treated with PC via gavage. Thereafter, the expression of var
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50

Upadhayay, Shubham, Narhari Gangaram Yedke, Vikrant Rahi, et al. "An Overview of the Pathophysiological Mechanisms of 3-Nitropropionic Acid (3-NPA) as a Neurotoxin in a Huntington's Disease Model and Its Relevance to Drug Discovery and Development." Neurochemical Research, February 4, 2023. http://dx.doi.org/10.1007/s11064-023-03868-1.

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