Organophosphate induced delayed neuropathy in genetically dissimilar chickens: studies with tri-ortho-cresyl phosphate (TOCP) and trichlorfon

Oliveira, Georgino Honorato de; Moreira, Vanessa Oliveira; Goes, Sheila Patricia Ribeiro

doi:10.1016/s0378-4274(02)00295-3

Cited by 17 publications

(11 citation statements)

References 7 publications

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“…The appearance of OPIDN is associated with chickens strain and dose of TOCP. A dose of 1600 mg/kg TOCP in hy-line w36 chickens strain was not able to induce the characteristic clinical signs of OPIDN [38]. However, if the dose of TOCP is too high, it will result in the acute neurotoxicity and death of chickens.…”

Section: Discussionmentioning

confidence: 91%

“…Nerve function evaluation was performed by an observer blinded to treatments. The clinical signs of delayed neuropathy were assessed by an eightpoint graded scale, namely, 0 score meaned normal ambulation; 1 and 2 score meaned slight and infrequent hindlimb incoordination; 3 and 4 score meaned moderate but definite hindlimb incoordination; 5 and 6 score meaned severe and frequent difficulty in walking and standing erect; 7 and 8 score meaned virtual to complete hindlimb paralysis [21,33].…”

Section: Neurological Testingmentioning

confidence: 99%

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RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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Organophosphate-induced delayed neuropathy (OPIDN) is pathologically characterized by the swollen axon containing aggregations of microtubules, neurofilaments, smooth endoplasmic reticulum and multivesicular vesicles. At present, the exact mechanism of OPIDN is unclear and the effective therapeutic methods is not available to counter this syndrome. Recent studies had shown that the autophagy was involved in OPIDN. The adipocytokine Apelin is a peptide, Apelin and its receptor are abundantly expressed in the nervous system. Recent researches illuminated that Apelin was neuroprotective factor and Apelin could regulate the autophagy in vivo and vitro model. So we investigated the effect of Apelin-13 on the OPIDN induced by Tri-ortho-cresyl phosphate (TOCP) in hens and explored the role of autophagy in Apelin-13 preventing OPIDN. Adult Roman hens were given a single dose of 750 mg/kg TOCP by gavage for 21 days to induce OPIDN, and neural dysfunction were detected, and the formation of autophagosomes in spinal cord neurons was observed by transmission electron microscopy, and the molecular markers of autophagy microtubule-associated protein light chain-3 (LC3) and the autophagy substrates p62/SQSTM1 were determined by Western blot analysis. The results demonstrated that the obvious neurological dysfunction such as hindlimb paralysis and paralysis of gait was present, the number of autophagosomes in the neurons of spinal cords was significantly increased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly increased in the OPIDN model group compared with the control group. Compared with the OPIDN model group, the neurological dysfunction of tens was obviously reduced, the clinical signs scores was significantly decreased, the number of autophagosomes in the neurons of hen spinal cords was significantly decreased, the level of LC3-II and p62 expressions and the ratio of LC3-II/LC3-I in spinal cords and sciatic nerve were significantly decreased in Apelin-13 treatment group. Our results suggested that Apelin-13 prevented against the OPIDN induced by TOCP in hens, which the mechanism might be associated with regulation autophagy flux by Apelin-13.

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Section: Discussionmentioning

confidence: 91%

Section: Neurological Testingmentioning

confidence: 99%

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

et al. 2015

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“…The study of Olajos et al (1979) suggests that trichlorfon is able to cause OPIDN in hens, but some studies have found no sign of delayed neuropathy in hens treated with trichlorfon (Slott and Ecobichon, 1984;Honorato de Oliveira et al, 2002). In addition, there are no studies addressing the delayed effects of acephate in hens or its neuropathic potential in vitro.…”

Section: Introductionmentioning

confidence: 99%

In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

Fernandes

Emerick

Santos

et al. 2015

Toxicology in Vitro

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“…CBDP inhibits acetylcholine esterase (AChE) and butyrylcholinesterase (BuChE), leading to an excess of the neurotransmitter acetylcholine and subsequent cholinergic syndrome. In addition, CBDP can inhibit neuropathy target esterase (NTE), resulting in organophosphate-induced delayed neuropathy (OPIDN) (Honorato de Oliveira et al, 2002;Padilla and Veronesi, 1985;Barrett and Oehme, 1994;Carrington and Abou-Donia, 1988;Carletti et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

In vitro neurotoxic hazard characterization of different tricresyl phosphate (TCP) isomers and mixtures

et al. 2017

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A B S T R A C TExposure to tricresyl phosphates (TCPs), via for example contaminated cabin air, has been associated with health effects including the so-called aerotoxic syndrome. While TCP neurotoxicity is mainly attributed to ortho-isomers like tri-ortho-cresyl phosphate (ToCP), recent exposure and risk assessments indicate that ToCP levels in cabin air are very low. However, the neurotoxic potential of non-ortho TCP isomers and TCP mixtures is largely unknown. We therefore measured effects of exposure (up to 48 h) to different TCP isomers, mixtures and the metabolite of ToCP (CBDP: cresyl saligenin phosphate) on cell viability and mitochondrial activity, spontaneous neuronal electrical activity, and neurite outgrowth in primary rat cortical neurons.The results demonstrate that exposure to TCPs (24-48 h, up to 10 mM) increases mitochondrial activity, without affecting cell viability. Effects of acute TCP exposure (30 min) on neuronal electrical activity are limited. However, electrical activity is markedly decreased for the majority of TCPs (10 mM) following 48 h exposure. Additional preliminary data indicate that exposure to TCPs (48 h, 10 mM) did not affect the number of neurites per cell or average neurite length, except for TmCP and the analytical TCP mixture (Sigma) that induced a reduction of average neurite length.The combined neurotoxicity data demonstrate that the different TCPs, including ToCP, are roughly equipotent and a clear structure-activity relation is not apparent for the studied endpoints. The noobserved-effect-concentrations (1 mM) are well above current exposure levels indicating limited neurotoxic health risk, although exposures may have been higher in the past. Moreover, prolonged and/or repeated exposure to TCPs may exacerbate the observed neurotoxic effects, which argues for additional research.

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Organophosphate induced delayed neuropathy in genetically dissimilar chickens: studies with tri-ortho-cresyl phosphate (TOCP) and trichlorfon

Cited by 17 publications

References 7 publications

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens

In vitro study of the neuropathic potential of the organophosphorus compounds trichlorfon and acephate

In vitro neurotoxic hazard characterization of different tricresyl phosphate (TCP) isomers and mixtures

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