Auswahl der wissenschaftlichen Literatur zum Thema „Tri-ortho-cresyl phosphate“
Geben Sie eine Quelle nach APA, MLA, Chicago, Harvard und anderen Zitierweisen an
Inhaltsverzeichnis
Machen Sie sich mit den Listen der aktuellen Artikel, Bücher, Dissertationen, Berichten und anderer wissenschaftlichen Quellen zum Thema "Tri-ortho-cresyl phosphate" bekannt.
Neben jedem Werk im Literaturverzeichnis ist die Option "Zur Bibliographie hinzufügen" verfügbar. Nutzen Sie sie, wird Ihre bibliographische Angabe des gewählten Werkes nach der nötigen Zitierweise (APA, MLA, Harvard, Chicago, Vancouver usw.) automatisch gestaltet.
Sie können auch den vollen Text der wissenschaftlichen Publikation im PDF-Format herunterladen und eine Online-Annotation der Arbeit lesen, wenn die relevanten Parameter in den Metadaten verfügbar sind.
Zeitschriftenartikel zum Thema "Tri-ortho-cresyl phosphate"
Hou, Wei-Yuan, Ding-Xin Long und Yi-Jun Wu. „Effect of Inhibition of Neuropathy Target Esterase in Mouse Nervous Tissues In Vitro on Phosphatidylcholine and Lysophosphatidylcholine Homeostasis“. International Journal of Toxicology 28, Nr. 5 (20.07.2009): 417–24. http://dx.doi.org/10.1177/1091581809340704.
Der volle Inhalt der QuelleLiu, Meng-Ling, Jing-Lei Wang, Jie Wei, Lin-Lin Xu, Mei Yu, Xiao-Mei Liu, Wen-Li Ruan und Jia-Xiang Chen. „Tri-ortho-cresyl phosphate induces autophagy of rat spermatogonial stem cells“. REPRODUCTION 149, Nr. 2 (Februar 2015): 163–70. http://dx.doi.org/10.1530/rep-14-0446.
Der volle Inhalt der QuelleWang, Jinglei, Wenli Ruan, Boshu Huang, Shuxin Shao, Dan Yang, Mengling Liu, Lin Zeng, Jie Wei und Jiaxiang Chen. „Tri-ortho-cresyl phosphate induces autophagy of mouse ovarian granulosa cells“. Reproduction 158, Nr. 1 (Juli 2019): 61–69. http://dx.doi.org/10.1530/rep-18-0456.
Der volle Inhalt der QuelleKnoll-Gellida, Anja, Leslie E. Dubrana, Laure M. Bourcier, Théo Mercé, Gaëlle Gruel, Magalie Soares und Patrick J. Babin. „Hyperactivity and Seizure Induced by Tricresyl Phosphate Are Isomer Specific and Not Linked to Phenyl Valerate-Neuropathy Target Esterase Activity Inhibition in Zebrafish“. Toxicological Sciences 180, Nr. 1 (23.01.2021): 160–74. http://dx.doi.org/10.1093/toxsci/kfab006.
Der volle Inhalt der QuelleSheets, Larry, Ruth S. Hassanein und Stata Norton. „Gait analysis of chicks following treatment with tri‐ortho‐cresyl phosphate in ovo“. Journal of Toxicology and Environmental Health 21, Nr. 4 (August 1987): 445–53. http://dx.doi.org/10.1080/15287398709531034.
Der volle Inhalt der QuelleSong, Fuyong, Ruirui Kou, Chaoshuang Zou, Yuan Gao, Tao Zeng und Keqin Xie. „Involvement of autophagy in tri-ortho-cresyl phosphate- induced delayed neuropathy in hens“. Neurochemistry International 64 (Januar 2014): 1–8. http://dx.doi.org/10.1016/j.neuint.2013.10.017.
Der volle Inhalt der QuelleZou, Chaoshuang, Ruirui Kou, Yuan Gao, Keqin Xie und Fuyong Song. „Activation of mitochondria-mediated apoptotic pathway in tri-ortho-cresyl phosphate-induced delayed neuropathy“. Neurochemistry International 62, Nr. 7 (Juni 2013): 965–72. http://dx.doi.org/10.1016/j.neuint.2013.03.013.
Der volle Inhalt der QuelleINUI, KOUSEI, KUNITOSHI MITSUMORI, TAKANORI HARADA und KEIZO MAITA. „Quantitative Analysis of Neuronal Damage Induced by Tri-ortho-cresyl Phosphate in Wistar Rats“. Toxicological Sciences 20, Nr. 1 (1993): 111–19. http://dx.doi.org/10.1093/toxsci/20.1.111.
Der volle Inhalt der QuelleWang, Yu, Cuiqin Zhang, Zhenyu Shen, Ruirui Kou, Keqin Xie und Fuyong Song. „Activation of PINK1-Parkin-dependent mitophagy in Tri-ortho-cresyl phosphate-treated Neuro2a cells“. Chemico-Biological Interactions 308 (August 2019): 70–79. http://dx.doi.org/10.1016/j.cbi.2019.05.025.
Der volle Inhalt der QuelleLong, Ding-Xin, Dan Hu, Pan Wang und Yi-Jun Wu. „Induction of autophagy in human neuroblastoma SH-SY5Y cells by tri-ortho-cresyl phosphate“. Molecular and Cellular Biochemistry 396, Nr. 1-2 (03.07.2014): 33–40. http://dx.doi.org/10.1007/s11010-014-2139-7.
Der volle Inhalt der QuelleDissertationen zum Thema "Tri-ortho-cresyl phosphate"
Mercé, Théo. „High-throughput zebrafish larval locomotion assays of neuronal and muscular functions : Application to organophosphorus toxicity and antid“. Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0011.
Der volle Inhalt der QuelleThe growing prevalence of chemical contaminants poses major public health concerns, necessitating efficient methodologies for toxicological risk assessment. An initial work was carried out to optimize a new approach methodology (NAM) using zebrafish pre-feeding larvae, called the electric field pulse (EFP) motor response test (EFPMRT). The method aims to perform a high-throughput screening of chemicals inducing motor capabilities and postural control defects. The robustness, reproducibility, productivity, and transferability of EFPMRT were enhanced by developing a novel software tool, DanioTracker, performing the automated analysis of endpoints linked to EFP-induced locomotor behavior. Then, using a battery of tests, the neurotoxicity induced by organophosphorus (OPs) compounds and their metabolites was assessed. Behavioral disruptions were evaluated using EFPMRT and a complementary sensory-dependent neurobehavioral test, the visual motor response test (VMRT). Contributions of acetylcholinesterase (AChE) and neuropathy target esterase (NTE) inhibition to behavioral disruptions were tested. Chlorpyrifos, parathion and tri-ortho-cresyl-phosphate disturbed integrative swimming control functions in quantitatively distinct manners and decreased the neuromuscular capacities of pre-feeding larvae. Their respective metabolites chlorpyrifos-oxon, paraoxon and cresyl-saligenin-phosphate fully inhibited AChE, thus inducing a cholinergic syndrome. Comparative study of the antidotal efficacy of an AChE reactivator, pralidoxime, in mitigating some toxic effects was performed. The antidote induced a recovery of the cholinergic syndromes associated with metabolites exposure. Strikingly, pralidoxime (2-PAM) also partially restored hyperactivities induced by parent compounds apparently independently of the activities of AChE and NTE. However, it did not restore neuromuscular dysfunctions induced by parathion or tri-ortho-cresyl phosphate. This suggests the existence of one or more unknown OP-specific multiple modes of action (MOAs) associated with parent compound but not corresponding metabolites, of which some are restorable by 2-PAM. Overall, this work offers a robust, transferable NAM that contributes to a comprehensive chemical risk assessment strategy. It also uncovers potential alternative MOA for selected OPs, suggesting the need for further research on metabolites within regulatory frameworks, and contributes to understanding and preventing neurobehavioral disorders induced by environmental exposures alone or in mixtures