Gotowa bibliografia na temat „Tri-ortho-cresyl phosphate”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Spis treści
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Tri-ortho-cresyl phosphate”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Tri-ortho-cresyl phosphate"
Hou, Wei-Yuan, Ding-Xin Long i 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.
Pełny tekst źródłaLiu, Meng-Ling, Jing-Lei Wang, Jie Wei, Lin-Lin Xu, Mei Yu, Xiao-Mei Liu, Wen-Li Ruan i Jia-Xiang Chen. "Tri-ortho-cresyl phosphate induces autophagy of rat spermatogonial stem cells". REPRODUCTION 149, nr 2 (luty 2015): 163–70. http://dx.doi.org/10.1530/rep-14-0446.
Pełny tekst źródłaWang, Jinglei, Wenli Ruan, Boshu Huang, Shuxin Shao, Dan Yang, Mengling Liu, Lin Zeng, Jie Wei i Jiaxiang Chen. "Tri-ortho-cresyl phosphate induces autophagy of mouse ovarian granulosa cells". Reproduction 158, nr 1 (lipiec 2019): 61–69. http://dx.doi.org/10.1530/rep-18-0456.
Pełny tekst źródłaKnoll-Gellida, Anja, Leslie E. Dubrana, Laure M. Bourcier, Théo Mercé, Gaëlle Gruel, Magalie Soares i 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.
Pełny tekst źródłaSheets, Larry, Ruth S. Hassanein i Stata Norton. "Gait analysis of chicks following treatment with tri‐ortho‐cresyl phosphate in ovo". Journal of Toxicology and Environmental Health 21, nr 4 (sierpień 1987): 445–53. http://dx.doi.org/10.1080/15287398709531034.
Pełny tekst źródłaSong, Fuyong, Ruirui Kou, Chaoshuang Zou, Yuan Gao, Tao Zeng i Keqin Xie. "Involvement of autophagy in tri-ortho-cresyl phosphate- induced delayed neuropathy in hens". Neurochemistry International 64 (styczeń 2014): 1–8. http://dx.doi.org/10.1016/j.neuint.2013.10.017.
Pełny tekst źródłaZou, Chaoshuang, Ruirui Kou, Yuan Gao, Keqin Xie i Fuyong Song. "Activation of mitochondria-mediated apoptotic pathway in tri-ortho-cresyl phosphate-induced delayed neuropathy". Neurochemistry International 62, nr 7 (czerwiec 2013): 965–72. http://dx.doi.org/10.1016/j.neuint.2013.03.013.
Pełny tekst źródłaINUI, KOUSEI, KUNITOSHI MITSUMORI, TAKANORI HARADA i 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.
Pełny tekst źródłaWang, Yu, Cuiqin Zhang, Zhenyu Shen, Ruirui Kou, Keqin Xie i Fuyong Song. "Activation of PINK1-Parkin-dependent mitophagy in Tri-ortho-cresyl phosphate-treated Neuro2a cells". Chemico-Biological Interactions 308 (sierpień 2019): 70–79. http://dx.doi.org/10.1016/j.cbi.2019.05.025.
Pełny tekst źródłaLong, Ding-Xin, Dan Hu, Pan Wang i 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 (3.07.2014): 33–40. http://dx.doi.org/10.1007/s11010-014-2139-7.
Pełny tekst źródłaRozprawy doktorskie na temat "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.
Pełny tekst źródłaThe 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