Organophosphorus-induced delayed neuropathy: A simple and efficient therapeutic strategy

Emerick, Guilherme Luz; Peccinini, Rosângela Gonçalves; Oliveira, Georgino Honorato de

doi:10.1016/j.toxlet.2009.10.032

Cited by 41 publications

(29 citation statements)

References 25 publications

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“…The various proteolytic systems within cells require close coordination to maintain intracellular proteostasis. Several evidences suggest that some proteolytic enzymes, such as calcium-dependent cysteine proteases, are associated with the origin and development of OPIDN [8,14]. Autophagy is an evolutionarily conserved process that can lead to degradation of proteins and entire organelles in eukaryotic cells [15,16].…”

Section: Introductionmentioning

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RETRACTED ARTICLE: Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens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

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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“…Chronic exposure to OP pesticides may retard the neurophysiological processes that underlay the development of the early stages of selective attention and late stages of sensory information processing, which includes the evaluation of stimuli and updating of working memory (Dassanayake et al, 2009). OP pesticides and hydraulic fluids can also produce an acute poisoning, known as OP-induced delayed neuropathy (OPIDN), the effects of which require a long recovery time (Emerick, Peccinini, & de Oliveira, 2010). In 2009, Atherton et al studied several horticultural farmers that had been exposed to OPs and several controls to investigate the relationships between OP exposure, DNA damage and oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

Distribution of pesticides in different commonly used vegetables from Hyderabad, India

Sinha

Rao

Vasudev

2012

Food Research International

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“…PNPLA6 encodes for NTE, which is the key protein in the pathogenesis of organophosphorous (OP) compound-induced delayed neuropathy (OPIDN) [26]. In this condition, certain OP esters lead to a degeneration of long axons in the spinal cord and peripheral nerves, either through direct protein inhibition or through generation of neurotoxic complexes.…”

Section: Discussionmentioning

confidence: 99%

Compound heterozygous PNPLA6 mutations cause Boucher–Neuhäuser syndrome with late-onset ataxia

et al. 2014

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PNPLA6 mutations, known to be associated with the development of motor neuron phenotypes, have recently been identified in families with Boucher–Neuhäuser syndrome. Boucher–Neuhäuser is a rare autosomal recessive syndrome characterized by the co-occurrence of cerebellar ataxia, hypogonadotropic hypogonadism, and chorioretinal dystrophy. Gait ataxia in Boucher–Neuhäuser usually manifests before early adulthood, although onset in the third or fourth decade has also been reported. However, given the recent identification of PNPLA6 mutations as the cause of this condition, the determining factors of age of symptom onset still need to be established. Here, we have identified a sporadic Boucher–Neuhäuser case with late-onset gait ataxia and relatively milder retinal changes due to compound heterozygous PNPLA6 mutations. Compound heterozygosity was confirmed by cloning and sequencing the patient’s genomic DNA from coding exons 26–29. Furthermore, both mutations (one novel and one known) fell in the phospholipase esterase domain, where most pathogenic mutations seem to cluster. Taken together, we herein confirm PNPLA6 mutations as the leading cause of Boucher–Neuhäuser syndrome and suggest inquiring about a history of hypogonadism or visual changes in patients presenting with late-onset gait ataxia. We also advocate for neuroophthalmologic evaluation in suspected cases.

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Organophosphorus-induced delayed neuropathy: A simple and efficient therapeutic strategy

Cited by 41 publications

References 25 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

Distribution of pesticides in different commonly used vegetables from Hyderabad, India

Compound heterozygous PNPLA6 mutations cause Boucher–Neuhäuser syndrome with late-onset ataxia

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