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Thematische Bibliographien / Tri-ortho-cresyl phosphate / Zeitschriftenartikel

Zeitschriftenartikel zum Thema „Tri-ortho-cresyl phosphate“

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Autor: Grafiati

Veröffentlicht am 7. Juli 2024

Zuletzt aktualisiert am 7. Juli 2024

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1

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.

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Neuropathy target esterase has been shown to be a lysophospholipase in mouse. The authors investigate the effect of neuropathy target esterase inhibition in mouse nervous tissues in vitro on the homeostasis of phosphatidylcholine and lysophosphatidylcholine by treating the homogenates with tri-ortho-cresyl phosphate, paraoxon, paraoxon plus mipafox, and phenylmethylsulfonyl fluoride. The activity of neuropathy target esterase is significantly inhibited by phenylmethylsulfonyl fluoride and paraoxon plus mipafox but not by paraoxon alone. Tri-ortho-cresyl phosphate slightly but significantly inhibits neuropathy target esterase activity in brain. The levels of phosphatidylcholine and lysophosphatidylcholine in all 3 nervous tissues are not obviously altered after treatment with tri-ortho-cresyl phosphate, paraoxon, or paraoxon plus mipafox. However, phosphatidylcholine and lysophosphatidylcholine levels are clearly enhanced by phenylmethylsulfonyl fluoride. It is concluded that inhibition of neuropathy target esterase in mouse nervous tissues is not enough to disrupt the homeostasis of phosphatidylcholine and lysophosphatidylcholine and that the upregulation by phenylmethylsulfonyl fluoride may be the consequence of combined inhibition of neuropathy target esterase and other phospholipases.

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2

Liu, 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.

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Tri-ortho-cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners, and flame retardants in industry and reported to have a deleterious effect on the male reproductive system in animals besides delayed neurotoxicity. Our preliminary results found that TOCP could disrupt the seminiferous epithelium in the testis and inhibit spermatogenesis, but the precise mechanism is yet to be elucidated. This study shows that TOCP inhibited viability of rat spermatogonial stem cells in a dose-dependent manner. TOCP could not lead to cell cycle arrest in the cells; the mRNA levels of p21, p27, p53, and cyclin D1 in the cells were also not affected by TOCP. Meanwhile, TOCP did not induce apoptosis of rat spermatogonial stem cells. After treatment with TOCP, however, both LC3-II and the ratio of LC3-II/LC3-I were markedly increased; autophagy proteins ATG5 and beclin 1 were also increased after treatment with TOCP, indicating that TOCP could induce autophagy in the cells. Ultrastructural observation under the transmission electron microscopy indicated that autophagic vesicles in the cytoplasm containing extensively degraded organelles such as mitochondria and endoplasmic reticulum increased significantly after the cells were treated with TOCP. In summary, we have shown that TOCP can inhibit viability of rat spermatogonial stem cells and induce autophagy of the cells, without affecting cell cycle and apoptosis.

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3

Wang, 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.

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Tri-ortho-cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners and flame-retardants in industry and reported to have male reproductive toxicology. However, it is still unknown whether TOCP affects the female reproductive system and its underlying mechanism. In the present study, we found that TOCP exposure significantly decreased ovarian coefficient, caused disintegration and depletion of the granulosa cells in the ovary tissue and significantly inhibited the level of serum estradiol (E2). TOCP markedly increased both LC3-II and the ratio of LC3-II/LC3-I as well as autophagy proteins ATG5 and Beclin1 in the ovary tissue, implying that TOCP could induce autophagy in the ovary tissue. To further investigate the potential mechanism, primary ovarian granulosa cells were isolated in vitro and treated with 0–0.5 mM TOCP for 48 h. We showed that TOCP decreased the number of viable mouse granulosa cells without affecting cell cycle and apoptosis of the cells. Intriguingly, TOCP treatment markedly increased both LC3-II and the ratio of LC3-II/LC3-I as well as ATG5 and Beclin1. Furthermore, transmission electron microscopy (TEM) showed that autophagic vesicles in the cytoplasm increased significantly in the TOCP-treated cells, indicating that TOCP could induce autophagy in the cells. Taken together, TOCP reduces the number of viable cells and induces autophagy in mouse ovarian granulosa cells without affecting cell cycle and apoptosis.

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4

Knoll-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.

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Abstract Environmental exposure to tricresyl phosphate (TCP) may lead to severe neurotoxic effects, including organophosphate (OP)-induced delayed neuropathy. TCP has three symmetric isomers, distinguished by the methyl group position on the aromatic ring system. One of these isomers, tri-ortho-cresyl phosphate (ToCP), has been reported for years as a neuropathic OP, targeting neuropathic target esterase (NTE/PNPLA6), but its mode of toxic action had not been fully elucidated. Zebrafish eleuthero-embryo and larva were used to characterize the differential action of the TCP isomers. The symmetric isomers inhibited phenyl valerate (PV)-NTE enzymatic activity in vivo with different IC50, while no effect was observed on acetylcholinesterase activity. Moreover, the locomotor behavior was also affected by tri-para-cresyl phosphate and tri-meta-cresyl phosphate, only ToCP exposure led to locomotor hyperactivity lasting several hours, associated with defects in the postural control system and an impaired phototactic response, as revealed by the visual motor response test. The electric field pulse motor response test demonstrated that a seizure-like, multiple C-bend-spaghetti phenotype may be significantly induced by ToCP only, independently of any inhibition of PV-NTE activity. Eleuthero-embryos exposed to picrotoxin, a known gamma-aminobutyric acid type-A receptor inhibitor, exhibited similar adverse outcomes to ToCP exposure. Thus, our results demonstrated that the TCP mode of toxic action was isomer specific and not initially related to modulation of PV-NTE activity. Furthermore, it was suggested that the molecular events involved were linked to an impairment of the balance between excitation and inhibition in neuronal circuits.

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5

Sheets, 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.

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6

Song, 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.

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7

Zou, 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.

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8

INUI, 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.

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9

Wang, 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.

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10

Long, 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.

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11

Inui, K. „Quantitative Analysis of Neuronal Damage Induced by Tri-ortho-cresyl Phosphate in Wistar Rats“. Fundamental and Applied Toxicology 20, Nr. 1 (Januar 1993): 111–19. http://dx.doi.org/10.1006/faat.1993.1013.

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12

Yang, Si, Shuxin Shao, Boshu Huang, Dan Yang, Lin Zeng, Yu Gan, Dingxin Long, Jiaxiang Chen und Jinglei Wang. „Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells“. Environmental Toxicology 35, Nr. 4 (02.12.2019): 478–86. http://dx.doi.org/10.1002/tox.22883.

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13

Li, Jing, und Yi-Jun Wu. „Tri-ortho-cresyl phosphate induces hepatic steatosis by mTOR activation and ER stress induction“. Ecotoxicology and Environmental Safety 271 (Februar 2024): 116010. http://dx.doi.org/10.1016/j.ecoenv.2024.116010.

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14

Xu, LL, CY Long, JL Wang, M. Yu und JX Chen. „Involvement of oxidative stress in tri-ortho–cresyl phosphate-induced liver injury in male mice“. Human & Experimental Toxicology 35, Nr. 10 (11.07.2016): 1093–101. http://dx.doi.org/10.1177/0960327115621363.

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Tri- ortho–cresyl phosphate (TOCP) has been widely used as plasticizers, plastic softeners, and flame retardants in industry and reported to have delayed neurotoxicity and reproductive toxicology in animals. However, it remains to be elusive whether TOCP induces liver injury. In this study, male mice were orally administered different concentrations of TOCP (100, 200, or 400 mg/kg/day) for 28 days. Histological examination showed that TOCP led to serious hepatocellular injury. In addition, administration of TOCP induced a marked elevation in the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in mice. The content of malondialdehyde (MDA) was increased significantly in the liver after the mice were treated with TOCP; while there was a dramatic decrease in the content of glutathione (GSH) and the activities of antioxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). TOCP inhibited viability of mouse liver cancer Hepa 1-6 cells in a dose-dependent manner. Meanwhile, TOCP significantly increased MDA content and inhibited GSH content and the activities of SOD and GSH-PX in the cells, respectively. Oxidative stress dramatically inhibited viability of Hepa 1-6 cells; while inhibition of oxidative stress by N-acetyl-l-cysteine could rescue the cell viability inhibited by TOCP to a certain extent. In summary, oxidative stress might be involved in TOCP-induced hepatocellular injury in male mice.

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15

Reinen, Jelle, Leyla Nematollahi, Alex Fidder, Nico P. E. Vermeulen, Daan Noort und Jan N. M. Commandeur. „Characterization of Human Cytochrome P450s Involved in the Bioactivation of Tri-ortho-cresyl Phosphate (ToCP)“. Chemical Research in Toxicology 28, Nr. 4 (02.03.2015): 711–21. http://dx.doi.org/10.1021/tx500490v.

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16

Zhang, Cuiqin, Kang Kang, Yisi Chen, Shulin Shan, Keqin Xie und Fuyong Song. „Atg7 Knockout Alleviated the Axonal Injury of Neuro-2a Cells Induced by Tri-Ortho-Cresyl Phosphate“. Neurotoxicity Research 39, Nr. 4 (01.03.2021): 1076–86. http://dx.doi.org/10.1007/s12640-021-00344-y.

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17

TOCCO, DONALD R., JOAN L. RANDALL, RAYMOND G. YORK und KATE M. SMITH. „Evaluation of the Teratogenic Effects of Tri-ortho-cresyl Phosphate in the Long-Evans Hooded Rat“. Toxicological Sciences 8, Nr. 3 (1987): 291–97. http://dx.doi.org/10.1093/toxsci/8.3.291.

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18

Song, Fuyong, Xiaoying Han, Tao Zeng, Cuili Zhang, Chaoshuang Zou und Keqin Xie. „Changes in beclin-1 and micro-calpain expression in tri-ortho-cresyl phosphate-induced delayed neuropathy“. Toxicology Letters 210, Nr. 3 (Mai 2012): 276–84. http://dx.doi.org/10.1016/j.toxlet.2012.02.011.

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19

Zhao, X., C. Zhang, Z. Zhu, L. Yu und K. Xie. „Time-dependent electrophysiologic changes of sciatic-tibial nerve in hens induced by tri-ortho-cresyl phosphate“. Toxicology Letters 196 (Juli 2010): S228. http://dx.doi.org/10.1016/j.toxlet.2010.03.763.

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20

Song, Fuyong, Yongjian Yan, Xiulan Zhao, Cuili Zhang und Keqin Xie. „Neurofilaments degradation as an early molecular event in tri-ortho-cresyl phosphate (TOCP) induced delayed neuropathy“. Toxicology 258, Nr. 2-3 (28.04.2009): 94–100. http://dx.doi.org/10.1016/j.tox.2009.01.011.

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21

TOCCO, D. „Evaluation of the teratogenic effects of tri-ortho-cresyl phosphate in the Long-Evans hooded rat“. Fundamental and Applied Toxicology 8, Nr. 3 (April 1987): 291–97. http://dx.doi.org/10.1016/0272-0590(87)90079-0.

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22

Nanda, Sajalendu, und Pranab Kumar Tapaswi. „Biochemical, Neuropathological and Behavioral Studies in Hens Induced by Acute Exposure of Tri-Ortho-Cresyl Phosphate“. International Journal of Neuroscience 82, Nr. 3-4 (Januar 1995): 243–54. http://dx.doi.org/10.3109/00207459508999804.

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23

Honorato de Oliveira, Georgino, Vanessa Moreira und Sheila Patricia Ribeiro Goes. „Organophosphate induced delayed neuropathy in genetically dissimilar chickens: studies with tri-ortho-cresyl phosphate (TOCP) and trichlorfon“. Toxicology Letters 136, Nr. 2 (Dezember 2002): 143–50. http://dx.doi.org/10.1016/s0378-4274(02)00295-3.

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24

Song, Fuyong, Yongjian Yan, Xiulan Zhao, Dandan Dou, Cuili Zhang und Keqin Xie. „Phenylmethylsulfonyl fluoride protects against the degradation of neurofilaments in tri-ortho-cresyl phosphate (TOCP) induced delayed neuropathy“. Toxicology 262, Nr. 3 (August 2009): 258–64. http://dx.doi.org/10.1016/j.tox.2009.06.018.

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25

Hu, Liaoliao, Tingting Peng, Jian Huang, Tie Su, Ruichen Luo, Yuehui Zheng, Zhisheng Zhong, Peiling Yu, Kun Nie und Liping Zheng. „Tri-ortho-cresyl phosphate (TOCP) induced ovarian failure in mice is related to the Hippo signaling pathway disruption“. Reproductive Toxicology 83 (Januar 2019): 21–27. http://dx.doi.org/10.1016/j.reprotox.2018.10.007.

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26

Padilla, Stephanie, und Bellina Veronesi. „The relationship between neurological damage and neurotoxic esterase inhibition in rats acutely exposed to tri-ortho-cresyl phosphate“. Toxicology and Applied Pharmacology 78, Nr. 1 (März 1985): 78–87. http://dx.doi.org/10.1016/0041-008x(85)90307-2.

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27

Jensen, K. F., D. M. Lapadula, J. Knoth Anderson, N. Haykal-Coates und M. B. Abou-Donia. „Anomalous phosphorylated neurofilament aggregations in central and peripheral axons of hens treated with tri-Ortho-cresyl phosphate (TOCP)“. Journal of Neuroscience Research 33, Nr. 3 (November 1992): 455–60. http://dx.doi.org/10.1002/jnr.490330311.

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28

Xing Xin, Tao Zeng, Dan-Dan Dou, Sheng Zhao, Jing-Yun Du, Jing-Jing Pei, Ke-Qin Xie und Xiu-Lan Zhao. „Changes of mitochondrial ultrastructures and function in central nervous tissue of hens treated with tri-ortho-cresyl phosphate (TOCP)“. Human & Experimental Toxicology 30, Nr. 8 (21.10.2010): 1062–72. http://dx.doi.org/10.1177/0960327110386815.

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Tri-ortho-cresyl phosphate (TOCP), an organophosphorus ester, is capable of producing organophosphorus ester-induced delayed neurotoxicity (OPIDN) in humans and sensitive animals. The mechanism of OPIDN has not been fully understood. The present study has been designed to evaluate the role of mitochondrial dysfunctions in the development of OPIDN. Adult hens were treated with 750 mg/kg·bw TOCP by gavage and control hens were given an equivalent volume of corn oil. On day 1, 5, 15, 21 post-dosing, respectively, hens were anesthetized by intraperitoneal injection of sodium pentobarbital and perfused with 4% paraformaldehyde. The cerebral cortex cinerea and the ventral horn of lumbar spinal cord were dissected for electron microscopy. Another batch of hens were randomly divided into three experimental groups and control group. Hens in experimental groups were, respectively, given 185, 375, 750 mg/kg·bw TOCP orally and control group received solvent. After 1, 5, 15, 21 days of administration, they were sacrificed and the cerebrum and spinal cord dissected for the determination of the mitochondrial permeability transition (MPT), membrane potential (Δψ m) and the activity of succinate dehydrogenase. Structural changes of mitochondria were observed in hens’ nervous tissues, including vacuolation and fission, which increased with time post-dosing. MPT was increased in both the cerebrum and spinal cord, with the most noticeable increase in the spinal cord. Δψm was decreased in both the cerebrum and spinal cord, although there was no significant difference in the three treated groups and control group. The activity of mitochondrial succinate dehydrogenase assayed by methyl thiazolyl tetrazolium (MTT) reduction also confirmed mitochondrial dysfunctions following development of OPIDN. The results suggested mitochondrial dysfunction might partly account for the development of OPIDN induced by TOCP.

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29

Zhao, Xiu-lan, Tian-liang Zhang, Cui-li Zhang, Xiao-ying Han, Su-fang Yu, Shan-xia Li, Ning Cui und Ke-qin Xie. „Expression changes of neurofilament subunits in the central nervous system of hens treated with tri-ortho-cresyl phosphate (TOCP)“. Toxicology 223, Nr. 1-2 (Juni 2006): 127–35. http://dx.doi.org/10.1016/j.tox.2006.03.008.

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30

Wang, Lian, Yong-Hong Liu, Yan Xu, Wen Yin und Yuan-Gui Huang. „Thirteen-year follow-up of patients with tri-ortho-cresyl phosphate poisoning in northern suburbs of Xi’an in China“. NeuroToxicology 30, Nr. 6 (November 2009): 1084–87. http://dx.doi.org/10.1016/j.neuro.2009.06.006.

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31

Yang, Bei, Xinlu Wang, Yilin Ma, Lei Yan, Yuan Ren, Dainan Yu, Bo Qiao et al. „Tri‐ortho‐cresyl phosphate (TOCP)‐induced reproductive toxicity involved in placental apoptosis, autophagy and oxidative stress in pregnant mice“. Environmental Toxicology 35, Nr. 1 (30.09.2019): 97–107. http://dx.doi.org/10.1002/tox.22846.

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32

Long, Ding-Xin, und Yi-Jun Wu. „Growth inhibition and induction of G1 phase cell cycle arrest in neuroblastoma SH-SY5Y cell by tri-ortho-cresyl phosphate“. Toxicology Letters 181, Nr. 1 (10.09.2008): 47–52. http://dx.doi.org/10.1016/j.toxlet.2008.06.871.

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33

Hausherr, Vanessa, Christoph van Thriel, Anne Krug, Marcel Leist und Nicole Schöbel. „Impairment of Glutamate Signaling in Mouse Central Nervous System Neurons In Vitro by Tri-Ortho-Cresyl Phosphate at Noncytotoxic Concentrations“. Toxicological Sciences 142, Nr. 1 (08.09.2014): 274–84. http://dx.doi.org/10.1093/toxsci/kfu174.

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Zhang, Li-Ping, Qing-Shan Wang, Xin Guo, Ying-Jian Zhu, Gui-Zhen Zhou und Ke-Qin Xie. „Time-dependent changes of lipid peroxidation and antioxidative status in nerve tissues of hens treated with tri-ortho-cresyl phosphate (TOCP)“. Toxicology 239, Nr. 1-2 (September 2007): 45–52. http://dx.doi.org/10.1016/j.tox.2007.06.091.

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Zhou, Shou-hong, Xin-ping Ouyang, Shao-wen Tian, Wei-lan Yin und Bi Hu. „RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens“. Neurochemical Research 40, Nr. 11 (09.10.2015): 2374–82. http://dx.doi.org/10.1007/s11064-015-1725-8.

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36

Tacal, Ozden, und Lawrence M. Schopfer. „Healthy F-16 pilots show no evidence of exposure to tri-ortho-cresyl phosphate through the on-board oxygen generating system“. Chemico-Biological Interactions 215 (Mai 2014): 69–74. http://dx.doi.org/10.1016/j.cbi.2014.03.004.

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Deng, Qiang, Lan Jiang, Liang Mao, Xiao‐Hua Song, Chu‐Qi He, Xiao‐Ling Li, Zhao‐Hui Zhang, Huai‐Cai Zeng, Jia‐xiang Chen und Ding‐Xin Long. „The role of protein kinase C alpha in tri‐ortho‐cresyl phosphate‐induced autophagy in human neuroblastoma SK‐N‐SH cells“. Journal of Applied Toxicology 40, Nr. 11 (06.07.2020): 1480–90. http://dx.doi.org/10.1002/jat.3999.

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38

Tosi, L., C. Righetti, L. Adami und G. Zanette. „October 1942: a strange epidemic paralysis in Saval, Verona, Italy. Revision and diagnosis 50 years later of tri-ortho-cresyl phosphate poisoning.“ Journal of Neurology, Neurosurgery & Psychiatry 57, Nr. 7 (01.07.1994): 810–13. http://dx.doi.org/10.1136/jnnp.57.7.810.

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39

Zhou, Shou-hong, Xin-ping Ouyang, Shao-wen Tian, Wei-lan Yin und Bi Hu. „Retraction Note to: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens“. Neurochemical Research 41, Nr. 11 (01.09.2016): 3160. http://dx.doi.org/10.1007/s11064-016-2049-z.

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40

Chen, Jia-Xiang, Lin-Lin Xu, Jin-Hong Mei, Xu-Bo Yu, Hai-Bin Kuang, Hong-Yu Liu, Yi-Jun Wu und Jing-Lei Wang. „Involvement of neuropathy target esterase in tri-ortho-cresyl phosphate-induced testicular spermatogenesis failure and growth inhibition of spermatogonial stem cells in mice“. Toxicology Letters 211, Nr. 1 (Mai 2012): 54–61. http://dx.doi.org/10.1016/j.toxlet.2012.03.004.

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41

Li, Jing, Qilian Qin, Yu-Xia Li, Xin-Fu Leng und Yi-Jun Wu. „Tri-ortho-cresyl phosphate exposure leads to low egg production and poor eggshell quality via disrupting follicular development and shell gland function in laying hens“. Ecotoxicology and Environmental Safety 225 (Dezember 2021): 112771. http://dx.doi.org/10.1016/j.ecoenv.2021.112771.

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42

Song, Fuyong, Chaoshuang Zou, Xiaoying Han, Tao Zeng, Cuili Zhang und Keqin Xie. „Reduction of retrograde axonal transport associated-proteins motor proteins, dynein and dynactin in the spinal cord and cerebral cortex of hens by tri-ortho-cresyl phosphate (TOCP)“. Neurochemistry International 60, Nr. 2 (Januar 2012): 99–104. http://dx.doi.org/10.1016/j.neuint.2011.12.004.

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Liu, Chang, Wenjuan Zhou, Zhaopei Li, Jun Ren, Xian Li, Shan Li, Qian Liu, Fuyong Song, Aijun Hao und Fuwu Wang. „Melatonin Protects Neural Stem Cells Against Tri-Ortho-Cresyl Phosphate-Induced Autophagy“. Frontiers in Molecular Neuroscience 13 (06.03.2020). http://dx.doi.org/10.3389/fnmol.2020.00025.

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Sun, Yan-Yan, und Yi-Jun Wu. „Tri-ortho-cresyl phosphate induces axonal degeneration in chicken DRG neurons by the NAD+ pathway“. Toxicology Letters, Mai 2022. http://dx.doi.org/10.1016/j.toxlet.2022.05.007.

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ZHAO, X. „Tri-ortho-cresyl phosphate (TOCP) decreases the levels of cytoskeletal proteins in hen sciatic nerve“. Toxicology Letters, Juni 2004. http://dx.doi.org/10.1016/j.toxlet.2004.04.012.

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CV, Howard. „Inappropriate Use of Risk Assessment in Addressing Health Hazards Posed by Civil Aircraft Cabin Air“. Open Access Journal of Toxicology 4, Nr. 5 (04.12.2020). http://dx.doi.org/10.19080/oajt.2020.04.555646.

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Annotation:

Toxicological reviews of data on Aerotoxic Syndrome that have been widely referenced by the airline industry tend to use a toxicological endpoint, Organo-Phosphate Induced Neuropathy (OPIDN), that is acknowledged to be the result of a very high dose of organophosphate exposure. Additionally, the reviews tend to only address one chemical, Tri-Ortho Cresyl Phosphate (TOCP), ignoring the presence of other toxic compounds in a complex mixture. In using this to justify the safety of the continued use of unfiltered engine bleed air to ventilate civil aircraft cabins, this represents a misuse of toxicological risk assessment. The approach totally ignores the scientific literature on repeated low-dose exposure to OPs over extended periods, the constant presence of a complex mixture of OPs in engine bleed air and their overall toxicity and the variable susceptibility of individuals to toxicological damage. This paper lists the above-mentioned studies and reviews a sub-set. We present the scientific literature that should be considered to make a realistic risk assessment of the hazards of aircraft engine bleed air.

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Liu, Xiaomei, Linlin Xu, Jingcao Shen, Jinglei Wang, Wenli Ruan, Mei Yu und Jiaxiang Chen. „Involvement of oxidative stress in tri-ortho–cresyl phosphate-induced autophagy of mouse Leydig TM3 cells in vitro“. Reproductive Biology and Endocrinology 14, Nr. 1 (07.06.2016). http://dx.doi.org/10.1186/s12958-016-0165-x.

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C V, Howard. „Inappropriate Use of Risk Assessment in Addressing Health Hazards Posed by Civil Aircraft Cabin Air“. Open Access Journal of Toxicology 4, Nr. 2 (27.02.2020). http://dx.doi.org/10.19080/oajt.2020.04.555634.

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Over decades, the airline industry has published considerable documentation on the potential for inhalation exposure to organophosphates and other toxins sourced to engine oil fumes supplied by “bleed air” systems, which are used on most commercial and military aircraft. Case studies on the subsequent development of neurological and other symptoms reported by crewmembers have also been widely documented. However, airline industry reviews tend to define toxicity of engine oil fumes according to a single toxicological endpoint - Organo Phosphate Induced Delayed Neuropathy (OPIDN) – which is acknowledged to be the result of a very high dose of exposure to a specific chemical, Tri-Ortho Cresyl Phosphate (TOCP). Industry reviews typically argue that the low levels of TOCP in aviation engine oils justifies the safety of continuing to use unfiltered engine bleed air to ventilate civil and military aircraft cabins. In fact, this approach ignores the routine presence and toxicity of a complex mixture of OPs in oil fumes supplied by engine bleed air systems and ignores the type of neurological symptoms that crews report (i.e., not OPIDN). The industry approach also ignores the scientific literature on repeated low-dose exposure to OPs over extended periods (particularly relevant for airline crewmembers) and the variable susceptibility of individuals to toxicological damage. This paper reviews the above-mentioned studies and presents the scientific literature that should be considered to make a realistic risk assessment of the hazards of aircraft engine bleed air.

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