Assessment of neurotoxic effects of tri-cresyl phosphates (TCPs) and cresyl saligenin phosphate (CBDP) using a combination of in vitro techniques

Hausherr, Vanessa; Schöbel, Nicole; Liebing, Julia; Thriel, Christoph van

doi:10.1016/j.neuro.2016.06.005

Cited by 13 publications

(7 citation statements)

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“…Changes in length, number, or branching patterns of axons or dendrites have been linked to psychiatric manifestations in patients, including depression, anxiety, AD, and PD (Marsden, 2013; Rubia et al, 2014; Canu et al, 2015; Negrón-Oyarzo et al, 2016). Axonal length, neurite length, neurite number, and dendritic branching in neuronal culture systems have also been shown to be altered following exposure to a variety of OPs, including CPF (Howard et al, 2005; Yang et al, 2008; Speed et al, 2012), DZ (Pizzurro et al, 2014a,b), parathion (Yousefpour et al, 2006; Berríos et al, 2015), and T O CP (Chen et al, 2013; Duarte et al, 2016; Hausherr et al, 2016). For example, in primary cultures of sympathetic neurons, CPF inhibited axon outgrowth but promoted dendritic arborization (Howard et al, 2005).…”

Section: Mechanisms Of Chronic Op Neurotoxicitymentioning

confidence: 99%

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

et al. 2017

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Organophosphorus (OPs) compounds are widely used as insecticides, plasticizers, and fuel additives. These compounds potently inhibit acetylcholinesterase (AChE), the enzyme that inactivates acetylcholine at neuronal synapses, and acute exposure to high OP levels can cause cholinergic crisis in humans and animals. Evidence further suggests that repeated exposure to lower OP levels insufficient to cause cholinergic crisis, frequently encountered in the occupational setting, also pose serious risks to people. For example, multiple epidemiological studies have identified associations between occupational OP exposure and neurodegenerative disease, psychiatric illness, and sensorimotor deficits. Rigorous scientific investigation of the basic science mechanisms underlying these epidemiological findings requires valid preclinical models in which tightly-regulated exposure paradigms can be correlated with neurotoxicity. Here, we review the experimental models of occupational OP exposure currently used in the field. We found that animal studies simulating occupational OP exposures do indeed show evidence of neurotoxicity, and that utilization of these models is helping illuminate the mechanisms underlying OP-induced neurological sequelae. Still, further work is necessary to evaluate exposure levels, protection methods, and treatment strategies, which taken together could serve to modify guidelines for improving workplace conditions globally.

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Section: Mechanisms Of Chronic Op Neurotoxicitymentioning

confidence: 99%

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

et al. 2017

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“…The commercial TCP products consist of various isomers, in which tri-ortho-cresyl phosphate (ToCP) has been proved most neuroxic due to its irreversible damage to a human's peripheral nerve and spinal cord [2][3][4][5]. ToCP inhibits several vital enzymes, such as acetylcholine esterase [6][7][8] and carboxyesterase [9][10][11]. Acute exposure to ToCP induces nausea, vomiting, diarrhea and abdominal pain, followed by a long asymptomatic period of up to a month.…”

Section: Introductionmentioning

confidence: 99%

Catalytic Hydrolysis of Tricresyl Phosphate by Ruthenium (III) Hydroxide and Iron (III) Hydroxide towards Sensing Application

Zhou

Chin

Simonian

2020

Sensors

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Tricresyl phosphate (TCP) is an organophosphorous neurotoxin that has been detected in water, soil and air. Exposure to TCP in cockpit and cabin air poses a severe threat to flight safety and the health of the aircraft cabin occupants. Conventional methods for the detection of TCP in various samples are gas or liquid chromatography coupled to mass spectrometry, which are complex and expensive. To develop a simple low-cost methodology for the real-time monitoring of TCP in the environment, an effective catalyst is demanded for the hydrolysis of TCP under neutral condition. In this study, Ruthenium (III) hydroxide and Iron (III) hydroxide are found to facilitate the production of the alcoholysis and hydrolysis products of TCP, suggesting their role as a catalyst. With this finding, these metal hydroxides provide new potential to realize not only simple colorimetric or electrochemical detection of TCP, but also a simple detoxication strategy for TCP in environment. In addition, the catalytic capability of Ru (III) or Fe (III) hydroxide for TCP gives a hint that they can potentially serve as catalysts for the hydrolysis of alcolyolysis of many other organophosphate compounds.

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“…15 CBDP is an irreversible inhibitor of both AChE and butyrylcholinesterase (BChE), 16,17 but it also affects carboxyl- esterases and the neuropathy target esterase 18 (NTE). According to in vitro essays the specific affinity of CBDP for NTE would be the primary factor for OPIDN, 14 confirming NTE as the second molecular target of metabolites of OPs. 19 PSP is an analogue of CBDP differing in a single methyl group, known to similarly induce OPIDN by inhibition of NTE.…”

mentioning

confidence: 98%

“…We report here a rotational and computational investigation of cresyl (CBDP, 1, Scheme 2) and phenyl (PSP, 2) saligenin phosphate. CBDP has been involved in OPIDN resulting from exposition to tri-o-cresyl phosphate (ToCP), either by poisoning or contamination with industrial products (as controversially proposed for the aerotoxic syndrome 14 ). The toxicity of ToCP is related to its metabolic activation by conversion into CBDP in vivo.…”

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confidence: 99%

Rotational spectroscopy of organophosphorous chemical agents: cresyl and phenyl saligenin phosphates

Saragi

Juanes

Abad

et al. 2019

Phys. Chem. Chem. Phys.

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Assessment of neurotoxic effects of tri-cresyl phosphates (TCPs) and cresyl saligenin phosphate (CBDP) using a combination of in vitro techniques

Cited by 13 publications

References 46 publications

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

Neurotoxicity in Preclinical Models of Occupational Exposure to Organophosphorus Compounds

Catalytic Hydrolysis of Tricresyl Phosphate by Ruthenium (III) Hydroxide and Iron (III) Hydroxide towards Sensing Application

Rotational spectroscopy of organophosphorous chemical agents: cresyl and phenyl saligenin phosphates

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