Neurotoxicity Research最新文献

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Curcumin Improves Hippocampal Cell Bioenergetics, Redox and Inflammatory Markers, and Synaptic Proteins, Regulating Mitochondrial Calcium Homeostasis. 姜黄素改善海马细胞生物能量学,氧化还原和炎症标志物,以及突触蛋白,调节线粒体钙稳态。
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2025-01-08 DOI: 10.1007/s12640-024-00726-y
Claudia Jara, Angie K Torres, Han S Park-Kang, Lisette Sandoval, Claudio Retamal, Alfonso Gonzalez, Micaela Ricca, Sebastián Valenzuela, Michael P Murphy, Nibaldo C Inestrosa, Cheril Tapia-Rojas
{"title":"Curcumin Improves Hippocampal Cell Bioenergetics, Redox and Inflammatory Markers, and Synaptic Proteins, Regulating Mitochondrial Calcium Homeostasis.","authors":"Claudia Jara, Angie K Torres, Han S Park-Kang, Lisette Sandoval, Claudio Retamal, Alfonso Gonzalez, Micaela Ricca, Sebastián Valenzuela, Michael P Murphy, Nibaldo C Inestrosa, Cheril Tapia-Rojas","doi":"10.1007/s12640-024-00726-y","DOIUrl":"10.1007/s12640-024-00726-y","url":null,"abstract":"<p><p>Mitochondria produces energy through oxidative phosphorylation (OXPHOS), maintaining calcium homeostasis, survival/death cell signaling mechanisms, and redox balance. These mitochondrial functions are especially critical for neurons. The hippocampus is crucial for memory formation in the brain, which is a process with high mitochondrial function demand. Loss of hippocampal function in aging is related to neuronal damage, where mitochondrial impairment is critical. Synaptic and mitochondrial dysfunction are early events in aging; both are regulated reciprocally and contribute to age-associated memory loss together. We previously showed that prolonged treatment with Curcumin or Mitoquinone (MitoQ) improves mitochondrial functions in aged mice, exerting similar neuroprotective effects. Curcumin has been described as an anti-inflammatory and antioxidant compound, and MitoQ is a potent antioxidant directly targeting mitochondria; however, whether Curcumin exerts a direct impact on the mitochondria is unclear. In this work, we study whether Curcumin could have a mechanism similar to MitoQ targeting the mitochondria. We utilized hippocampal slices of 4-6-month-old C57BL6 mice to assess the cellular changes induced by acute Curcumin treatment ex-vivo compared to MitoQ. Our results strongly suggest that both compounds improve the synaptic structure, oxidative state, and energy production in the hippocampus. Nevertheless, Curcumin and MitoQ modify mitochondrial function differently; MitoQ improves the mitochondrial bioenergetics state, reducing ROS production and increasing ATP generation. In contrast, Curcumin reduces mitochondrial calcium levels and prevents calcium overload related to mitochondrial swelling. Thus, Curcumin is described as a new regulator of mitochondrial calcium homeostasis and could be used in pathological events involving calcium deregulation and excitotoxicity, such as aging and neurodegenerative diseases.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 1","pages":"3"},"PeriodicalIF":2.9,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143055810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Cannabigerol Mitigates Haloperidol-Induced Vacuous Chewing Movements in Mice. 大麻酚减轻小鼠氟哌啶醇诱导的真空咀嚼运动。
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-12-19 DOI: 10.1007/s12640-024-00724-0
R Ponciano, J E C Hallak, J A Crippa, F S Guimarães, Elaine Ap Del Bel
{"title":"Cannabigerol Mitigates Haloperidol-Induced Vacuous Chewing Movements in Mice.","authors":"R Ponciano, J E C Hallak, J A Crippa, F S Guimarães, Elaine Ap Del Bel","doi":"10.1007/s12640-024-00724-0","DOIUrl":"10.1007/s12640-024-00724-0","url":null,"abstract":"<p><p>Chronic use of typical antipsychotics can lead to varying motor effects depending on the timing of analysis. Acute treatment typically induces hypokinesia, resembling parkinsonism, while repeated use can result in tardive dyskinesia, a hyperkinetic syndrome marked by involuntary orofacial movements, such as vacuous chewing movements in mice. Tardive dyskinesia is particularly concerning due to its potential irreversibility and associated motor discomfort. One prevailing theory suggests that tardive dyskinesia arises from hypersensitivity of D2-type dopaminergic receptors caused by continuous blockade from typical antipsychotics like haloperidol. Additionally, increased inflammation, oxidative stress, and elevated FosB protein expression in the dorsolateral striatum are implicated in its pathophysiology. Current treatments for tardive dyskinesia often lack clear efficacy and may lead to significant side effects. Cannabigerol, a non-psychotomimetic cannabinoid with antioxidant and anti-inflammatory properties, has been investigated for its potential antidyskinetic effects. In this study, mice were treated with cannabigerol at doses of 3 and 10 mg/kg to evaluate its ability to prevent, ameliorate, or reverse haloperidol-induced vacuous chewing movements. Cannabigerol successfully reduced vacuous chewing movements without affecting normal motor activity, exacerbating haloperidol-induced hypokinesia, or inducing dyskinetic effects on its own. However, no significant reversal of the haloperidol-induced motor effects was observed under the current protocol. Furthermore, cannabigerol did not alter FosB expression or microglia morphology. These findings underscore the need for further research to explore cannabigerol's therapeutic potential and contribute to our understanding of its possible clinical applications in managing tardive dyskinesia.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 1","pages":"2"},"PeriodicalIF":2.9,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Implication of Pyrethroid Neurotoxicity for Human Health: A Lesson from Animal Models. 拟除虫菊酯神经毒性对人类健康的影响:动物模型的启示
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-12-16 DOI: 10.1007/s12640-024-00723-1
Mega Obukohwo Oyovwi, Adedeji David Atere, Paul Chimwuba, Uchechukwu Gregory Joseph
{"title":"Implication of Pyrethroid Neurotoxicity for Human Health: A Lesson from Animal Models.","authors":"Mega Obukohwo Oyovwi, Adedeji David Atere, Paul Chimwuba, Uchechukwu Gregory Joseph","doi":"10.1007/s12640-024-00723-1","DOIUrl":"10.1007/s12640-024-00723-1","url":null,"abstract":"<p><p>Pyrethroids, synthetic insecticides used in pest management, pose health risks, particularly neurotoxic effects, with studies linking exposure to a neurodegenerative disorder. This review examines the neurotoxic mechanisms of pyrethroids analyzing literature from animal model studies. It identifies critical targets for neurotoxicity, including ion channels, oxidative stress, inflammation, neuronal cell loss, and mitochondrial dysfunction. The review also discusses key therapeutic targets and signaling pathways relevant to Pyrethroids neurotoxicity management, including calcium, Wnt/β-catenin, mTOR, MAPK/Erk, PI3K/Akt, Nrf2, Nurr1, and PPARγ. Our findings demonstrate that pyrethroid exposure triggers multiple neurotoxic pathways that bear resemblance to the mechanisms underlying neurotoxicity. Oxidative stress and inflammation emerge as prominent factors that contribute to neuronal degeneration, alongside disrupted mitochondrial function. The investigation highlights the significance of ion channels as primary neurodegeneration targets while acknowledging the potential involvement of various other receptors and enzymes that may exacerbate neurological damage. Additionally, we elucidate how pyrethroids may interfere with therapeutic targets associated with neuronal dysfunction, potentially impairing treatment efficacy.Also, exposure to these chemicals can alter DNA methylation patterns and histone modifications, ultimately leading to changes in gene expression that may enhance susceptibility to neurological disorders. Pyrethroid neurotoxicity poses a significant public health risk, necessitating future research for protective strategies against pesticide-induced neurological disorders and understanding the interplay between neurodegenerative diseases, potentially leading to innovative therapeutic interventions.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"43 1","pages":"1"},"PeriodicalIF":2.9,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
No Benefit of 3% Hypertonic Saline Following Experimental Intracerebral Hemorrhage. 实验性脑出血后使用 3% 高渗盐水无益。
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-10-18 DOI: 10.1007/s12640-024-00722-2
Tiffany F C Kung, Anna C J Kalisvaart, Angely Claire C Suerte, Glen C Jickling, Frank K H van Landeghem, Frederick Colbourne
{"title":"No Benefit of 3% Hypertonic Saline Following Experimental Intracerebral Hemorrhage.","authors":"Tiffany F C Kung, Anna C J Kalisvaart, Angely Claire C Suerte, Glen C Jickling, Frank K H van Landeghem, Frederick Colbourne","doi":"10.1007/s12640-024-00722-2","DOIUrl":"10.1007/s12640-024-00722-2","url":null,"abstract":"<p><p>Intracerebral hemorrhage (ICH) is a stroke subtype with a high mortality rate (~ 40%). After ICH, the mass effect of the hematoma and edema contribute to raised intracranial pressure (ICP) and poor outcome. Endogenous compensatory mechanisms that blunt ICP elevations include redirection of venous blood and cerebrospinal fluid, along with brain tissue compliance (e.g., decreased cell volume, increased cell density); however, these limited reserves can be exhausted after severe stroke, resulting in decompensated ICP that requires careful clinical management. Management strategies can include administration of hypertonic saline (HTS), an osmotic agent that putatively attenuates edema, and thereby ICP elevations. Evidence regarding the efficacy of HTS treatment following ICH remains limited. In this study, adult male rats were given a collagenase-induced striatal ICH and a bolus of either 3% HTS or 0.9% saline vehicle at 2- and 14-hours post-stroke onset. Neurological deficits, edema, ipsilateral cell volume and density (in areas S1 and CA1), and contralateral CA1 ultrastructural morphology were assessed 24 h post-ICH. Animals had large bleeds (median 108.2 µL), extensive edema (median 83.9% brain water content in ipsilateral striatum), and evident behavioural deficits (median 5.4 neurological deficit scale score). However, HTS did not affect edema (p ≥ 0.4797), behaviour (p = 0.6479), cell volume (p ≥ 0.1079), or cell density (p ≥ 0.0983). Qualitative ultrastructural assessment of contralateral area CA1 suggested that HTS administration was associated with paradoxical cellular swelling in ICH animals. Overall, there was no benefit with administering 3% HTS after ICH.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 6","pages":"44"},"PeriodicalIF":2.9,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11489293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
How is Excitotoxicity Being Modelled in iPSC-Derived Neurons? 如何在 iPSC 衍生神经元中模拟兴奋毒性?
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-10-15 DOI: 10.1007/s12640-024-00721-3
Jan L Cheng, Anthony L Cook, Jana Talbot, Sharn Perry
{"title":"How is Excitotoxicity Being Modelled in iPSC-Derived Neurons?","authors":"Jan L Cheng, Anthony L Cook, Jana Talbot, Sharn Perry","doi":"10.1007/s12640-024-00721-3","DOIUrl":"10.1007/s12640-024-00721-3","url":null,"abstract":"<p><p>Excitotoxicity linked either to environmental causes (pesticide and cyanotoxin exposure), excitatory neurotransmitter imbalance, or to intrinsic neuronal hyperexcitability, is a pathological mechanism central to neurodegeneration in amyotrophic lateral sclerosis (ALS). Investigation of excitotoxic mechanisms using in vitro and in vivo animal models has been central to understanding ALS mechanisms of disease. In particular, advances in induced pluripotent stem cell (iPSC) technologies now provide human cell-based models that are readily amenable to environmental and network-based excitotoxic manipulations. The cell-type specific differentiation of iPSC, combined with approaches to modelling excitotoxicity that include editing of disease-associated gene variants, chemogenetics, and environmental risk-associated exposures make iPSC primed to examine gene-environment interactions and disease-associated excitotoxic mechanisms. Critical to this is knowledge of which neurotransmitter receptor subunits are expressed by iPSC-derived neuronal cultures being studied, how their activity responds to antagonists and agonists of these receptors, and how to interpret data derived from multi-parameter electrophysiological recordings. This review explores how iPSC-based studies have contributed to our understanding of ALS-linked excitotoxicity and highlights novel approaches to inducing excitotoxicity in iPSC-derived neurons to further our understanding of its pathological pathways.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 5","pages":"43"},"PeriodicalIF":2.9,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11480214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Impact of 5-Lipoxygenase Deficiency on Dopamine-Mediated Behavioral Responses. 5-脂氧合酶缺陷对多巴胺介导的行为反应的影响
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-10-04 DOI: 10.1007/s12640-024-00720-4
Ana Carolina Issy, João Francisco Pedrazzi, Glauce Crivelaro Nascimento, Lúcia Helena Faccioli, Elaine Del Bel
{"title":"Impact of 5-Lipoxygenase Deficiency on Dopamine-Mediated Behavioral Responses.","authors":"Ana Carolina Issy, João Francisco Pedrazzi, Glauce Crivelaro Nascimento, Lúcia Helena Faccioli, Elaine Del Bel","doi":"10.1007/s12640-024-00720-4","DOIUrl":"10.1007/s12640-024-00720-4","url":null,"abstract":"<p><p>The 5-lipoxygenase/leukotriene system has been implicated in both physiological and pathological states within the central nervous system. Understanding how this system interacts with the dopaminergic system could provide valuable insights into dopamine-related pathologies. This study focused on examining both motor and non-motor dopamine-related responses in 5-lipoxygenase/leukotriene-deficient mice. We used pharmacological agents such as amphetamine, apomorphine, and reserpine to challenge the dopaminergic system, evaluating their effects on prepulse inhibition reaction (PPI), general motor activity, and oral involuntary movements. Additionally, we analyzed striatal glial marker expression (GFAP and Iba-1) in reserpine-treated mice. The 5-lipoxygenase/leukotriene-deficient mice exhibited increased spontaneous locomotor activity, including both horizontal and vertical exploration, along with stereotyped behavior compared to wild-type mice. This hyperactivity was reduced by acute apomorphine treatment. Although basal PPI responses were unchanged, 5-lipoxygenase/leukotriene-deficient mice displayed a significant reduction in susceptibility to amphetamine-induced PPI disruption. Conversely, these mice were more vulnerable to reserpine-induced involuntary movements. There were no significant differences in the basal expression of striatal GFAP and Iba-1 positive cells between 5-lipoxygenase/leukotriene-deficient and wild-type mice. However, reserpine treatment significantly increased GFAP immunoreactivity in wild-type mice, an effect not observed in 5-lipoxygenase-deficient mice. Additionally, the percentage of activated microglia was significantly higher in reserpine-treated wild-type mice, an effect absents in 5-lipoxygenase/leukotriene-deficient mice. Our findings suggest that 5-lipoxygenase/leukotriene deficiency leads to a distinctive dopaminergic phenotype, indicating that leukotrienes may influence the modulation of dopamine-mediated responses.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 5","pages":"42"},"PeriodicalIF":2.9,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Pharmacology of Adenosine A1 Receptor Agonist in a Humanized Esterase Mouse Seizure Model Following Soman Intoxication. 腺苷 A1 受体激动剂在人源化酯酶小鼠苏曼中毒后癫痫模型中的药理作用。
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-09-04 DOI: 10.1007/s12640-024-00717-z
Tsung-Ming Shih, Crystal Munoz, Cindy Acon-Chen, Zora-Maya Keith
{"title":"Pharmacology of Adenosine A<sub>1</sub> Receptor Agonist in a Humanized Esterase Mouse Seizure Model Following Soman Intoxication.","authors":"Tsung-Ming Shih, Crystal Munoz, Cindy Acon-Chen, Zora-Maya Keith","doi":"10.1007/s12640-024-00717-z","DOIUrl":"10.1007/s12640-024-00717-z","url":null,"abstract":"<p><p>Recently a novel genetically modified mouse strain with serum carboxylesterase knocked-out and the human acetylcholinesterase gene knocked-in (KIKO) was created to simulate human responses to nerve agent (NA) exposure and its standard medical treatment. A<sub>1</sub> adenosine receptor (A<sub>1</sub>AR) agonist N-bicyclo-(2.2.1)-hept-2-yl-5'-chloro-5'-deoxyadenosine (ENBA) alone is a potent anticonvulsant and neuroprotectant (A/N) in both rat and KIKO mouse soman (GD) seizure models. In this study we utilized the KIKO mouse to evaluate further the basic pharmacologic A/N effects of ENBA as an adjunct to standard NA medical treatments (i.e., atropine sulfate, pralidoxime chloride [2-PAM], and midazolam). Male mice, implanted with cortical electroencephalographic (EEG) electrodes, were pretreated with asoxime (HI-6) and exposed to an epileptogenic dose of GD (33 µg/kg, s.c.) or saline (sham exposure) and then treated 15 min after seizure onset with ENBA at 15 mg/kg, i.p. (a minimum efficacy dose in suppressing NA-induced seizure) alone or as an adjunct to standard medical treatments. We collected EEG activity, seizure suppression outcomes, daily body temperature and weight, heart rate, toxic signs, neuropathology, and lethality data for up to 14 days. Without ENBA, death from NA exposure was 45%, while with ENBA, either alone or in combination with midazolam, the survival improved to 80% and 90%, respectively. Additionally, seizure was suppressed quickly and permanently, toxic signs, hypothermia, and bradycardia recovered by 48 h, and no neuropathology was evident. Our findings confirmed that ENBA is a potent A/N adjunct for delayed medical treatments of NA exposure.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 5","pages":"41"},"PeriodicalIF":2.9,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11374867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142126274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Role of Vitamin C on ATPases Activities in Monosodium Glutamate-Induced Oxidative Stress in Rat Striatum and Cerebellum. 维生素 C 对谷氨酸钠诱导的大鼠纹状体和小脑氧化应激中 ATP 酶活性的作用
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-08-30 DOI: 10.1007/s12640-024-00719-x
Olusegun L Adebayo, Vivian A Agu, Grace A Idowu, Blessing C Ezejiaku, Adeleke K Atunnise
{"title":"The Role of Vitamin C on ATPases Activities in Monosodium Glutamate-Induced Oxidative Stress in Rat Striatum and Cerebellum.","authors":"Olusegun L Adebayo, Vivian A Agu, Grace A Idowu, Blessing C Ezejiaku, Adeleke K Atunnise","doi":"10.1007/s12640-024-00719-x","DOIUrl":"10.1007/s12640-024-00719-x","url":null,"abstract":"<p><p>Monosodium glutamate (MSG) is a silent excitotoxin used as a flavour enhancer but exerts serious health hazards to consumers. MSG plays a role in neuronal function as the dominant excitatory neurotransmitter. It is transferred into the blood and ultimately increases brain glutamate levels, causing functional disruptions notably via oxidative stress. The study evaluated the toxic effect of high consumption of MSG and the modulatory role of vitamin C on ATPase activities in the striatum and cerebellum of male Wistar rats for five weeks. Rats were grouped into four (A-D): group A was fed with rat's show only; Group B was fed with diet containing 15% MSG; Group C was treated with vitamin C (200 mg/kg b.wgt orally in 0.9% saline solution) only for 3 weeks; and group D rats were fed with MSG and vitamin C. The findings show that MSG does not affect body and cerebellum weights but increases striatal weight. MSG increases the malondialdehyde (MDA) level and significantly decreases catalase (CAT) and superoxide dismutase (SOD) activities and glutathione (GSH) levels. MSG significantly impaired striatal and cerebellar ATPases activities (Na<sup>+</sup>/K<sup>+</sup>-, Ca<sup>2+</sup>-, Mg<sup>2+</sup>- and total ATPases). Vitamin C treatment abolishes MSG-induced oxidative stress and improves ATPase activities. The findings show that vitamin C has beneficial effects in improving the functions of membrane-bound ATPases against MSG toxicity in rat's striatum and cerebellum.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 5","pages":"40"},"PeriodicalIF":2.9,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142110007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Methylphenidate Exposing During Neurodevelopment Alters Amino Acid Profile, Astrocyte Marker and Glutamatergic Excitotoxicity in the Rat Striatum. 神经发育期暴露于哌醋甲酯会改变大鼠纹状体的氨基酸谱、星形胶质细胞标记和谷氨酸能兴奋毒性
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-08-27 DOI: 10.1007/s12640-024-00718-y
Felipe Schmitz, Luz Elena Durán-Carabali, Alessandra Schmitt Rieder, Josiane S Silveira, Osmar Vieira Ramires Junior, Larissa D Bobermin, André Quincozes-Santos, Vinícius S Alves, Robson Coutinho-Silva, Luiz Eduardo B Savio, Daniella M Coelho, Carmen R Vargas, Carlos Alexandre Netto, Angela T S Wyse
{"title":"Methylphenidate Exposing During Neurodevelopment Alters Amino Acid Profile, Astrocyte Marker and Glutamatergic Excitotoxicity in the Rat Striatum.","authors":"Felipe Schmitz, Luz Elena Durán-Carabali, Alessandra Schmitt Rieder, Josiane S Silveira, Osmar Vieira Ramires Junior, Larissa D Bobermin, André Quincozes-Santos, Vinícius S Alves, Robson Coutinho-Silva, Luiz Eduardo B Savio, Daniella M Coelho, Carmen R Vargas, Carlos Alexandre Netto, Angela T S Wyse","doi":"10.1007/s12640-024-00718-y","DOIUrl":"10.1007/s12640-024-00718-y","url":null,"abstract":"<p><p>There is a public health concern about the use of methylphenidate (MPH) since the higher prescription for young individuals and non-clinical purposes is addressed to the limited understanding of its neurochemical and psychiatric consequences. This study aimed to evaluate the impact of early and chronic MPH treatment on the striatum focusing on amino acid profile, glutamatergic excitotoxicity, redox status, neuroinflammation and glial cell responses. Male Wistar rats were treated with MPH (2.0 mg/kg) or saline solution from the 15th to the 44th postnatal day. Biochemical and histological analyses were conducted after the last administration. MPH altered the amino acid profile in the striatum, increasing glutamate and ornithine levels, while decreasing the levels of serine, phenylalanine, and branched-chain amino acids (leucine, valine, and isoleucine). Glutamate uptake and Na<sup>+</sup>,K<sup>+</sup>-ATPase activity were decreased in the striatum of MPH-treated rats as well as increased ATP levels, as indicator of glutamatergic excitotoxicity. Moreover, MPH caused lipid peroxidation and nitrative stress, increased TNF alpha expression, and induced high levels of astrocytes, and led to a decrease in BDNF levels. In summary, our results suggest that chronic early-age treatment with MPH induces parallel activation of damage-associated pathways in the striatum and increases its vulnerability during the juvenile period. In addition, data presented here contribute to shedding light on the mechanisms underlying MPH-induced striatal damage and its potential implications for neurodevelopmental disorders.</p>","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"42 5","pages":"39"},"PeriodicalIF":2.9,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142073360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Blunted Melatonin Circadian Rhythm in Parkinson's Disease: Express Bewilderment. 帕金森病患者褪黑激素昼夜节律失调:表达困惑。
IF 2.9 3区 医学
Neurotoxicity Research Pub Date : 2024-08-23 DOI: 10.1007/s12640-024-00716-0
Areej Turkistani, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Walaa A Negm, Mostafa M Bahaa, Mostafa E Metawee, Gaber El-Saber Batiha
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